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Mesenteric
Kinds of Mesenteric Terms modified by Mesenteric Selected AbstractsCYTIDINE 5,-DIPHOSPHOCHOLINE RESTORES BLOOD FLOW OF SUPERIOR MESENTERIC AND RENAL ARTERIES AND PROLONGS SURVIVAL TIME IN HAEMORRHAGED ANAESTHETIZED RATSCLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 5-6 2006M Sertac Yilmaz SUMMARY 1The aim of the present study was to investigate the effect of the intracerebroventricular (i.c.v.) or intravenous (i.v.) administration of cytidine 5¢-diphosphocholine (CDP-choline) on superior mesenteric artery (SMA) and renal artery (RA) blood flow, along with the cardiovascular parameters and survival time of anaesthetized rats under conditions of haemorrhagic shock. 2Rats were anaesthetized with urethane (1.25 g/kg, i.p.) and acute haemorrhage was mimicked by the withdrawal of a total volume of 2,2.1 mL blood/100 g bodyweight over a period of 20 min. The CDP-choline was injected i.c.v. (1.0, 1.5 and 2.0 mmol) or i.v. (250 mg/kg) after the end of haemorrhage. Blood pressure, heart rate, SMA and RA flow values and the survival time of rats were recorded. Changes in blood flow were estimated by laser-Doppler flowmetry. 3The haemorrhage procedure decreased the blood pressures of rats by 60% and limited their survival time to 22 ± 2 min. Both SMA and RA flow decreased to approximately 25% of initial values at the end of the haemorrhage procedure. 4The i.c.v. administration of CDP-choline (1.0, 1.5 and 2.0 mmol) increased blood pressure and partially reversed the hypotension in a dose- and time-dependent manner. At 1.5 and 2.0 mmol, i.c.v., CDP-choline completely restored the decreased flow of the RA and transiently reversed hypoperfusion of the SMA. It also produced an almost fourfold increase in the survival time of rats. 5The i.v. administration of CDP-choline (250 mg/kg) also completely, but transiently, restored SMA and RA flow, whereas it increased blood pressure by only 40% compared with control values. The survival time of rats in the i.v. CDP-choline group was doubled that of control. 6These results indicate that both centrally and peripherally injected CDP-choline can restore SMA and RA flow, together with a partial reversal of hypotension and an increase in the survival time of rats. [source] Mesenteric Complications After Hypothermic Cardiopulmonary Bypass with Cardiac Arrest: Underlying MechanismsARTIFICIAL ORGANS, Issue 11 2002Terézia Bogdana Andrási Abstract: The aim of this study was to determine the pathophysiological mechanisms of postcardiopulmonary bypass (CPB) intestinal dysfunction using an in vivo canine model of extracorporeal circulation. Six dogs underwent a 90 min hypothermic CPB with continuous monitoring of mean arterial blood pressure (MAP) and mesenteric blood flow (MBF). Reactive hyperemia and vasodilator responses of the superior mesenteric artery to acetylcholine and sodium nitroprusside were determined before and after CPB. Mesenteric lactate production, glucose consumption, creatine kinase (CK) release and venous free radicals were determined. CPB induced a significant fall (p < 0.05) in MAP and MBF. After CPB, reactive hyperemia (,26 ± 15% versus ,53 ± 2%, p < 0.05) and the response to acetylcholine (,42 ± 9 versus ,55 ± 6%, p < 0.05) were significantly decreased. Reperfusion increased lactate production (0.8 ± 0.09 mmol/L versus 0.4 ± 0.18, p < 0.05) and the CK release (446 ± 98 U/L versus 5 ± 19 U/L, p < 0.01). Endothelial dysfunction, conversion from aerobic to anaerobic metabolism, and intestinal cell necrosis seem to be responsible for intestinal complications associated with CPB. [source] Changes in reactivity of rat arteries subjected to dynamic stretchACTA PHYSIOLOGICA, Issue 1 2000Dvoretsky The effect of dynamic stretch on the reactivity of the rat tail and mesenteric artery segments was studied. Segments mounted on a myograph were stretched by a computer-controlled motorized micromanipulator. Dynamic stretch (1, 5 or 7 Hz) inhibited the artery constriction induced by noradrenaline (10 ,M), 5-hydroxytryptamine (0.7 ,M), or electrical field stimulation of intramural nerves. In contrast, dynamic stretch enhanced the tetrodotoxin-insensitive dilation induced by electrical field stimulation of noradrenaline-contracted arteries. Maximal increase of dilation evoked by electrical field stimulation (24.5 ± 5.0% in mesenteric and 50.3 ± 15.6% in the tail artery) was observed at a dynamic stretch-frequency of 5 Hz. An inhibitor of nitric oxide synthesis, NG -nitro- L -arginine (100 ,M), abolished the difference in reactivity between static and dynamic conditions. The results indicate that dynamic stretch of the arteries activates nitric oxide synthesis/secretion, thus reducing constrictor and increasing dilator responses to the stimuli used. [source] Methylenetetrahydrofolate reductase gene C677T mutation is related to the defects in the internal elastic lamina of the artery wallEUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 12 2002P. Hämelahti Abstract Background The C677T mutation of the methylenetetrahydrofolate reductase (MTHFR) gene leads to C/C, C/T and T/T genotypes, which affect the plasma homocysteine concentration in humans. In mini-pigs, high serum homocysteine levels are associated with defects in the internal elastic lamina (IEL) of the artery wall, which are apparently related to the migration of smooth muscle cells into the intima during atherogenesis. We studied the association between the MTHFR genotypes and the number of gaps in the IEL in the wall of the five major abdominal arteries. Materials and methods The autopsy study included 123 subjects (90 males and 33 females) aged 18,93. For the light microscopy, a 0·5 cm circular segment of the coeliac, the superior mesenteric, the inferior mesenteric and the renal arteries were cut and embedded in paraffin blocks. The circumference of the IEL, the thickness of the intima and the number of the gaps per millimetre in the IEL were measured by MOP 3 image analysis. Results The T-allele carriers (C/T and T/T) of the MTHFR gene had significantly less gaps in the IEL than the subjects with the C/C genotype in the superior mesenteric and in the left renal arteries (2·02 ± 2·25 vs. 2·53 ± 1·89, P < 0·04 and 0·56 ± 1·09 vs. 1·82 ± 2·66, P < 0·02, respectively). The trend was similar for the coeliac and the right renal arteries. Conclusions Our result suggests that MTHFR polymorphism may be involved in the fragmentation of the IEL. [source] Possible Contribution of Central Gamma-Aminobutyric Acid Receptors to Resting Vascular Tone in Freely Moving RatsEXPERIMENTAL PHYSIOLOGY, Issue 5 2000Yumi Takemoto Previous studies have shown that central administration of GABA (gamma-aminobutyric acid), an inhibitory neurotransmitter, preferentially reduces hindquarters and carotid vascular resistances but not renal and coeliac vascular resistances in conscious rats. This study tested the hypothesis that these preferential actions of central GABA receptors are related to differences between vessels in resting autonomic vascular tone in freely moving rats. Rats were chronically implanted with intracisternal cannulas and/or electromagnetic probes to measure regional blood flows. In response to GABA administration, the changes in vascular resistance (arterial blood pressure/regional blood flow) of the hindquarters (n = 23) and carotid (n = 12) vascular beds were significantly and negatively correlated with basal vascular resistance. No such relationship was found for the renal (n = 21), coeliac (n = 13) and superior mesenteric (n = 23) vascular beds. This finding indicates that the responsiveness to GABA of brainstem pathways controlling the hindquarters and carotid vascular beds co-varies with resting resistance in hindquarters and carotid vessels. A similar analysis was performed, correlating the ongoing vascular resistance of each vessel with its response to ganglionic blockade by chlorisondamine. In this case, a significant negative correlation was also found for the hindquarters (n = 26) and carotid (n = 15) vascular beds, but not for the coeliac (n = 17) or superior mesenteric (n = 19) vessels. Together, these findings suggest that central GABA receptors accessible from the cisterna magna preferentially affect two vascular beds which, in the freely moving rat, show resting autonomic vascular tone. [source] Fatal outcome from extreme acute gastric dilation after an eating bingeINTERNATIONAL JOURNAL OF EATING DISORDERS, Issue 7 2006Endre Gyurkovics MD Abstract Objective: A 22-year-old woman is presented with acute gastric dilation after an eating binge, who died of complications of acute reperfusion syndrome. Method: A young patient was admitted in our clinic with critical condition without any significant previous medical history. Her initial complaints , diarrhea, vomiting and abdominal pain , began after an enormous food intake. There was no history of medications or toxic substances. Physical examination showed a normally-developed, well-nourished female in severe distress with an extremely distended abdomen. Femoral pulses were absent. The US and CT scan showed a dilated stomach, extended into the pelvis, dislocating the intestinal organs and compressed the aorta and mesenteric veins. Results: Urgent laparotomy was performed. An enormously distended stomach was encountered without volvulus, obstruction or adhesions. About 11 liters of gastric content was removed gastrotomy and nasogastric tube. Following the gastric decompression, the mesenteric and femoral pulses reappeared. During the operation, the cardio-respiratory status was stabilized, but in the following 24 hours irreversible shock developed, possibly due to the reperfusion of the retroperitoneal organs and the lower extremities. In the postoperative period disseminated intravascular coagulopathy developed. In an uncontrollable state of diffuse bleeding, 36 hours post-operation, the patient died. In retrospective investigation, the family confessed that previous psychological treatments which aimed at her bulimic attacks. Conclusion: Acute gastric dilatation is very uncommon and is of various etiologies, two of these being anorexia nervosa and bulimia. Several cases documenting complications of gastric dilatation were published; however, such severe complications, involving gastric infarction and compression of the aorta with ischemic injury of the bowels and lower extremities, are rare. © 2006 by Wiley Periodicals, Inc. Int J Eat Disord 2006 [source] Comparison of mesenteric and tissue fat content in relation to sexual cycle of the sardine, Sardina pilchardus (Walb., 1792), in the eastern Middle Adriatic fishery grounds (Croatia)JOURNAL OF APPLIED ICHTHYOLOGY, Issue 5 2009B. Musta Summary The study objective was to analyse Sardina pilchardus (Walb., 1792) for mesenteric fat, which is easier to evaluate than the muscle lipid, for comparisons thereof with the sexual cycle and condition of the examined specimens. Fat reserves, moisture and the sexual cycle of sardines were studied from monthly random samples of purse seine catches from March 2004 to February 2005. A total of 1209 specimens were collected (668 males; 541 females). Total length and mass ranged from 13.0 to 19.0 cm and from 16.7 to 51.5 g, respectively. Lipid analyses in muscle tissues were done using the Soxhlet method. An inverse relation between fat content and the sexual cycle was established. Greatest fat quantities were observed in August (72%) during the gonadal resting phase; lowest values were noted in winter, and in spring during the spawning period peak. Moisture content and sexual cycle were positively correlated (r = 0.7913). Total lipids in sardine tissues were higher in females than in males; however, the moisture content was higher in males than in females. [source] Changes in renal artery resistance after meal-induced splanchnic vasodilatation in cirrhotic patientsJOURNAL OF CLINICAL ULTRASOUND, Issue 9 2001Pascal Perney MD Abstract Purpose A relationship between vasomotor tone changes in mesenteric and renal vessels in cirrhotic patients has been suspected but remains controversial. The aim of this study was to assess by duplex Doppler sonography the changes in the circulatory resistance of the renal arteries and superior mesenteric artery (SMA) following meal-induced splanchnic vasodilatation. Methods Twenty-seven cirrhotic patients and 15 healthy volunteers with no hepatic or renal dysfunction were prospectively included in the study. The resistance index (RI) of the SMA and of the right and left renal arteries was measured by duplex Doppler sonography before and 30 minutes after ingestion of a standard 400-kcal balanced liquid meal. Values in controls and patients and values before and after the meal were compared, and correlations between RIs, Child-Pugh class (liver function), and creatinine clearance were assessed in cirrhotic patients. Results The fasting renal artery RI was greater in cirrhotic patients than in controls (p < 0.0001), but there was no difference in fasting SMA RIs. After the meal, there was a significant decrease in the SMA RI in controls (0.85 ± 0.04 before versus 0.74 ± 0.03 after meal, p = 0.0001) and in cirrhotic patients (0.85 ± 0.04 before versus 0.77 ± 0.04 after, p = 0.0001) and a significant increase in the renal artery RI (0.57 ± 0.06 before versus 0.62 ± 0.05 after in controls, p = 0.001; 0.68 ± 0.07 before versus 0.70 ± 0.07 after in cirrhotic patients, p = 0.001). No correlation was found in cirrhotic patients between the changes in renal artery RI and the postprandial SMA RI decrease, the Child-Pugh class, or the creatinine clearance. Conclusions Meal-induced SMA vasodilatation (RI decrease) is associated with a marked increase in the renal artery RI, worsening the renal vasoconstriction in cirrhotic patients. © 2001 John Wiley & Sons, Inc. J Clin Ultrasound 29:506,512, 2001. [source] Macronodular hepatic tuberculosis associated with portal vein thrombosis and portal hypertensionJOURNAL OF MEDICAL IMAGING AND RADIATION ONCOLOGY, Issue 4 2005SK Venkatesh Summary Tuberculosis (TB) of the liver is usually associated with miliary spread. Macronodular TB of the liver is rare. A case of macronodular TB of the liver in a 31-year-old woman causing portal vein thrombosis and portal hypertension is presented. Ultrasound and CT appearances are described. There was coexistent ileo-caecal TB with extensive mesenteric and retroperitoneal lymphadenopathy. Macronodular TB should be considered in the differential diagnosis when a patient presents with multiple calcified masses in the liver with portal vein thrombosis and portal hypertension. [source] Tezosentan normalizes hepatomesenteric perfusion in a porcine model of cardiac tamponadeACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 2 2009A. ÅNEMAN Background: To investigate endothelin-1 (ET-1)-dependent hepatic and mesenteric vasoconstriction, and oxygen and lactate fluxes in an acute, fixed low cardiac output (CO) state. Methods: Sixteen anesthetized, mechanically ventilated pigs were studied. Cardiac tamponade was established to reduce portal venous blood flow (QPV) to 2/3 of the baseline value. CO, hepatic artery blood flow (QHA), QPV, hepatic laser-Doppler flow (LDF), hepatic venous and portal pressure, and hepatic and mesenteric oxygen and lactate fluxes were measured. Hepatic arterial (RHA), portal (RHP) and mesenteric (Rmes) vascular resistances were calculated. The combined ETA,ETB receptor antagonist tezosentan (RO 61-0612) or normal saline vehicle was infused in the low CO state. Measurements were made at baseline, after 30, 60, 90 min of tamponade, and 30, 60, 90 min following the infusion of tesozentan at 1 mg/kg/h. Results: Tamponade decreased CO, QPV, QHA, LDF, hepatic and mesenteric oxygen delivery, while hepatic and mesenteric oxygen extraction and lactate release increased. RHA, RHP and Rmes all increased. Ninety minutes after tesozentan, QPV, LDF and hepatic and mesenteric oxygen delivery and extraction increased approaching baseline values, but no effect was seen on CO or QHA. Hepatic and mesenteric handling of lactate converted to extraction. RHA, RHP and Rmes returned to baseline values. No changes were observed in these variables among control animals not receiving tesozentan. Conclusion: In a porcine model of acute splanchnic hypoperfusion, unselective ET-1 blockade restored hepatomesenteric perfusion and reversed lactate metabolism. These observations might be relevant when considering liver protection in low CO states. [source] Effects of dofetilide on cardiovascular tissues from normo- and hypertensive ratsJOURNAL OF PHARMACY AND PHARMACOLOGY: AN INTERNATI ONAL JOURNAL OF PHARMACEUTICAL SCIENCE, Issue 5 2002Sheila A. Doggrell The aim was to test whether dofetilide has some potential for use in the treatment of heart failure. Dofetilide at ,3 times 10,5 M had no effect on the quiescent Wistar Kyoto (WKY) rat aorta, mesenteric and intralobar arteries, or the spontaneous contractions of the WKY rat portal vein. Dofetilide at 10,6 to 3 times 10,5 M relaxed the KCl-contracted aorta. Dofetilide at 10,9 -10,7 M augmented the force of contraction of left ventricle strips from 12- and 18-month-old WKY rats at 2 Hz. Spontaneously hypertensive rats (SHRs) at 12 and 17,21 months of age are models of cardiac hypertrophy and failure, respectively. The augmentation of force at 2 Hz with dofetilide was similar on 12-and 18-month-old WKY rats and 12-month-old SHRs but reduced on the 18-month-old SHR left ventricle. At a higher more physiological frequency, 4 Hz, the threshold concentration of dofetilide required to augment the force responses of 21-month-old SHR left ventricles was markedly increased and the maximum augmenting effect was decreased. Dofetilide at 10,7 -10,5 M reduced the rate of the 17-month-old WKY rat right atrium, and had a similar effect on age-matched SHR right atrium. In summary, dofetilide is a positive inotrope and negative chronotrope in the rat. However, as the positive inotropic effect is not observed with clinically relevant concentrations at a physiological rate in heart failure, dofetilide is unlikely to be useful as a positive inotrope in the treatment of heart failure. [source] Age-Related Sympathetic Ganglionic Neuropathology: Human Pathology And Animal ModelsJOURNAL OF THE PERIPHERAL NERVOUS SYSTEM, Issue 3 2002RE. Schmidt Systematic studies of the autonomic nervous system of human subjects and development of well-defined animal models have begun to substantially improve our understanding of the pathogenesis of autonomic dysfunction in aging and may eventually provide strategies for intervention. Neuropathological studies of the sympathetic ganglia of aged human subjects and rodent models have demonstrated that neuroaxonal dystrophy involving intraganglionic terminal axons and synapses is a robust, unequivocal and consistent neuropathological finding in the aged sympathetic nervous system of man and animals. Quantitative studies have demonstrated that markedly swollen argyrophilic dystrophic axon terminals develop in the prevertebral superior mesenteric (SMG) and coeliac, but to a much lesser degree in the superior cervical ganglia (SCG) as a function of age, sex (males more than females) and diabetes. Dystrophic axons were immunoreactive for neuropeptide Y, tyrosine hydroxylase, dopamine-beta-hydroxylase, trkA and p75(NTR), an immunophenotype consistent with their origin from postganglionic sympathetic neurons, and contained large numbers of highly phosphorylated neurofilaments or tubulovesicular elements. The sympathetic ganglia of aged rodents also showed the hallmark changes of neuroaxonal dystrophy as a function of age and location (many more in the SMG than in the SCG). Plasticity-related synaptic remodeling could represent a highly vulnerable target of the aging process. The fidelity of animal models to the neuropathology of aged humans suggests that similar pathogenetic mechanisms may be involved in both and that therapeutic advances in animal studies may have human application. [source] Tuberculosis Caused by Mycobacterium microti in South American CamelidsJOURNAL OF VETERINARY INTERNAL MEDICINE, Issue 6 2009P. Zanolari Background: Infection with Mycobacterium microti can cause chronic disease in animals and threaten human health through its zoonotic potential. Objective: To describe clinical findings, diagnostic investigations, necropsy, and epidemiology results in South American camelids (SAC) infected with M. microti, member of the Mycobacterium tuberculosis complex. Animals: Eleven SAC with tuberculous lesions. Methods: Description of 10 llamas and 1 alpaca, aged 4,18 years, from 6 herds with a history of wasting and weakness admitted to the Vetsuisse-Faculty of Berne over 8 years. Results: Clinical signs included weight loss, recumbency, and anorexia in late stages of the disease. Respiratory problems were seen in 6 animals of 11. No consistent hematologic abnormalities were identified. Suspect animals were examined in detail by abdominal ultrasonography and thoracic radiology. Abnormal findings such as enlarged mediastinal, mesenteric, or hepatic lymph nodes were seen only in animals with advanced disease. Single comparative intradermal tuberculin test with bovine protein purified derivate (PPD) and avian PPD was negative in all animals. At necropsy, typical tuberculous lesions were found, and confirmed by bacteriological smear and culture, molecular methods, or both. Conclusions and Clinical Importance: Infection caused by M. microti should be considered a differential diagnosis in chronic debilitating disease with or without respiratory signs in SAC. Antemortem confirmation of the diagnosis remains challenging at any stage of infection. Because cases of M. microti infection have been reported in immunocompromized human patients, the zoonotic potential of the organism should be kept in mind when dealing with this disease in SAC. [source] Changes in oxyhemoglobin dissociation curve in intrabdominal organs during pig experimental orthotopic liver transplantationLIVER TRANSPLANTATION, Issue 7 2005Georgia Kostopanagiotou Liver transplantation has become a gold standard treatment for irreversible liver disease. Conventional measures of oxygenation are inadequate to understand the dynamics of regional oxygen metabolism during liver transplantation because they represent global markers of tissue dysoxia. Therefore, the addition of an assessment of the hemoglobin O2 binding capacity can give a better insight into systemic and regional tissue oxygenation and can reflect a more accurate estimation of oxygen release to the tissues than can the hemoglobin, the PaO2 and SaO2 alone. This prospective study was designed to evaluate possible alterations in the oxyhemoglobin dissociation curve of vital end organs (small bowel, liver, and kidney) in an experimental liver transplantation model. Fifteen pigs with body weights ranging from 25 to 30 kg were used for the study. Five healthy pigs underwent a sham operation under general anesthesia (group A-control). Ten pigs underwent orthotopic liver transplantation (OLT). Five of them were healthy (group B), whereas the other five were in acute liver failure, which had been surgically induced (group C). Systemic arterial blood pressure, cardiac index, and pulmonary and systemic vascular resistance indexes were measured. Venous blood gas analysis was also performed from pulmonary artery, superior mesenteric, hepatic, and renal veins at well-defined timepoints during the course of the OLT. A statistically significant (P < 0.05) decrease of P50 in groups B and C compared with group A was observed 30 minutes after reperfusion in the systemic circulation, hepatic, and renal veins. This coincided with a decrease in animal temperature 30 minutes after reperfusion. Regarding group C, after reperfusion of the newly transplanted liver there was a significant increase of P50 in the small bowel in comparison to baseline values. In conclusion, these changes in P50 may suggest the occurrence of abnormal tissue oxygenation after reperfusion. (Liver Transpl 2005;11:760,766.) [source] Regional Variations of Contractile Activity in Isolated Rat LymphaticsMICROCIRCULATION, Issue 6 2004ANATOLIY A. GASHEV ABSTRACT Objective: To evaluate lymphatic contractile activity in different regions of the lymphatic system in a single animal model (the rat thoracic duct, mesenteric, cervical, and femoral lymphatics) in response to changes in lymph pressure and flow. Methods: The systolic and diastolic diameters of isolated, cannulated, and pressurized lymphatic vessels were measured. Contraction frequency, ejection fraction, and fractional pump flow were determined. The influences of incrementally increased transmural pressure (from 1 to 9 cm H2O) and imposed flow (from 1 to 5 cm H2O transaxial pressure gradient) were investigated. Results: The authors determined regional differences in lymphatic contractility in response to pressure and imposed flow. They found the highest pumping (at the optimal pressure levels) in mesenteric lymphatics and lowest pumping in thoracic duct. All lymphatics had their optimal pumping conditions at low levels of transmural pressure. Different degrees of the flow-induced inhibition of the pump were observed in the different types of lymphatics. During high flow, the active lymph pumps in thoracic duct and cervical lymphatics were almost completely abolished, whereas mesenteric and femoral lymphatics still exhibited significant active pumping. Conclusions: The active lymph pumps in different regions of the rat body express variable relative strengths and sensitivities that are predetermined by different hydrodynamic factors and regional outflow resistances in their respective locations. [source] The angiotensin II receptor blocker candesartan improves survival and mesenteric perfusion in an acute porcine endotoxin modelACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 2 2004M. Laesser Background:, Blockade of the angiotensin II type 1 (AT1) receptor has been demonstrated to ameliorate splanchnic hypoperfusion in acute experimental circulatory failure. This study focused on hemodynamic changes and survival in pigs treated with AT1 blockade prior to or during acute endotoxinemia. Methods:,Escherichia coli lipopolysaccharide endotoxin was infused in anesthetized and mechanically ventilated pigs. Systemic, renal, mesenteric and jejunal mucosal perfusion as well as systemic oxygen and acid-base balance were monitored. The selective AT1 receptor blocker candesartan was administered prior to as well as during endotoxinemia. Control animals received the saline vehicle. Results:, Pre-treatment with candesartan resulted in higher survival rate (83%, 10 out of 12 animals) compared with 50% (6 of 12) in control animals and 27% (3 of 11) in animals treated during endotoxinemia. Pre-treatment with candesartan resulted in higher cardiac output, mixed venous oxygen saturation, arterial standard base-excess, portal venous blood flow during endotoxin infusion compared with controls and animals treated during endotoxinemia. No adverse effects were found on neither systemic nor renal circulation. Conclusion:, The favorable results of AT1 receptor blockade prior to endotoxinemia are lost when blockade is established during endotoxinemia demonstrating the importance of the renin-angiotensin system and its dynamic involvement in acute endotoxinemic shock. [source] Asbestos fibers in para-aortic and mesenteric lymph nodesAMERICAN JOURNAL OF INDUSTRIAL MEDICINE, Issue 6 2009Toomas Uibu MD Abstract Background Asbestos fibers are known to accumulate in lung parenchyma and thoracic lymph nodes, but their presence and translocation into the extrapulmonary tissues need clarification. We assessed the presence of asbestos in the para-aortic (PA) and mesenteric (ME) lymph nodes. Methods PA and ME lymph nodes and lung tissue from 17 persons who underwent medicolegal autopsy for suspicion of asbestos-related disease and from five controls were analyzed for asbestos fibers using transmission electron microscopy. Results High concentrations of amphibole asbestos fibers were detected in several lung tissue samples and in the respective PA and ME lymph nodes. The mean concentration for the 10 persons with a lung asbestos content of ,1 million fibers/g of dry tissue (f/g) was 0.85 (<0.05,4.36) million f/g in the PA lymph nodes and 0.55 (<0.02,2.86) million f/g in the ME lymph nodes. The respective mean values for the 12 persons with a lung asbestos concentration of <1 million f/g were 0.07 for the PA lymph nodes and 0.03 million f/g for the ME nodes. The lung asbestos burden that predicted the detection of asbestos in abdominal lymph nodes was 0.45 million f/g. Conclusions In addition to their accumulation in lung tissue, asbestos fibers also collect in the retroperitoneal and the mesenteric lymph nodes. Even low-level occupational exposure results in the presence of crocidolite, amosite, anthophyllite, tremolite, or chrysotile in these abdominal lymph nodes. Our results support the hypothesis of lymph drainage as an important translocation mechanism for asbestos in the human body. Am. J. Ind. Med. 52:464,470, 2009. © 2009 Wiley-Liss, Inc. [source] De novo expression of Kv6.3 contributes to changes in vascular smooth muscle cell excitability in a hypertensive mice strainTHE JOURNAL OF PHYSIOLOGY, Issue 3 2009Alejandro Moreno-Domínguez Essential hypertension involves a gradual and sustained increase in total peripheral resistance, reflecting an increased vascular tone. This change associates with a depolarization of vascular myocytes, and relies on a change in the expression profile of voltage-dependent ion channels (mainly Ca2+ and K+ channels) that promotes arterial contraction. However, changes in expression and/or modulation of voltage-dependent K+ channels (Kv channels) are poorly defined, due to their large molecular diversity and their vascular bed-specific expression. Here we endeavor to characterize the molecular and functional expression of Kv channels in vascular smooth muscle cells (VSMCs) and their regulation in essential hypertension, by using VSMCs from resistance (mesenteric) or conduit (aortic) arteries obtained from a hypertensive inbred mice strain, BPH, and the corresponding normotensive strain, BPN. Real-time PCR reveals a differential distribution of Kv channel subunits in the different vascular beds as well as arterial bed-specific changes under hypertension. In mesenteric arteries, the most conspicuous change was the de novo expression of Kv6.3 (Kcng3) mRNA in hypertensive animals. The functional relevance of this change was studied by using patch-clamp techniques. VSMCs from BPH arteries were more depolarized than BPN ones, and showed significantly larger capacitance values. Moreover, Kv current density in BPH VSMCs is decreased mainly due to the diminished contribution of the Kv2 component. The kinetic and pharmacological profile of Kv2 currents suggests that the expression of Kv6.3 could contribute to the natural development of hypertension. [source] Decrease in stearic acid proportions in adipose tissues and liver lipids in fatty liver of dairy cowsANIMAL SCIENCE JOURNAL, Issue 3 2006Hiroshi SATO ABSTRACT Samples of liver and perirenal, mesenteric and subcutaneous fat were collected from 16 sick necropsied dairy cows to evaluate the fatty acid profiles in the hepatic and adipose tissues associated with advanced fatty liver or hepatic lipidosis. Hepatic triglyceride and eight fatty acids were measured in the hepatic and adipose tissues. Six cows had more than 3% triglyceride on fresh weight in their livers and were classified as having fatty liver. Stearic and linoleic acid proportions in the liver decreased markedly with increased hepatic triglyceride levels, while the proportion of palmitic and oleic acids increased. The most striking fluctuations in hepatic lipidosis were manifested as decreased stearic acid in the adipose tissues including subcutaneous fat with the trend of decreasing stearic acid. Palmitic acid was elevated in hepatic and perirenal fat in fatty liver cows. In instances of advanced hepatic lipidosis, palmitoleic acid increased in only subcutaneous fat and not in perirenal or mesenteric fat. In addition to the proportions of hepatic fatty acids in fatty liver, this study also clarified the fluctuations observed in the profiles of fatty acids of the adipose tissues in cows with advanced hepatic lipidosis, particularly the decline in the proportions of stearic acid. [source] SURGICAL OUTCOME OF SUPERFICIAL AND DEEP CASTLEMAN DISEASEANZ JOURNAL OF SURGERY, Issue 5 2007Chih-Hao Chen Background: Castleman disease is a rare lymphoproliferative disease of low malignant potential occurring in two forms, unicentric and multicentric. Surgery, chemotherapy, immunotherapy and radiation therapy have all been used to manage the disease. In this study, we evaluate whether the site of the lesions, that is, superficial or deep, influences the surgical outcome. Methods: We retrospectively reviewed the records of 20 patients operated on for Castleman disease from 1994 to 2003, of whom 11 patients had superficial disease and 9 had deep lesions. The end-points of this study were survival and recurrence. Results: Of the 20 patients, 19 had unicentric (cervical in 8, mediastinal in 5, retroperitoneal in 2, axillary in 2, hepatic in 1, and mesenteric in 1) and 1 had multicentric Castleman disease. Among 19 patients who had complete resection (18 with unicentric and 1 with multicentric disease), there has been no evidence of recurrence. Conclusion: Whether Castleman disease is superficial or deep has no effect on surgical outcome as long as resection is complete. [source] Disseminated Mycobacterium avium infection in a dog with chronic diarrhoeaAUSTRALIAN VETERINARY JOURNAL, Issue 5 2000B HORN A 3-year-old Maltese-cross dog presented with a 4-month history of chronic diarrhoea and inappetence. Poorly regenerative anaemia, leukocytosis and hypoproteinaemia were evident on several occasions. Biopsies of stomach, duodenum and colon revealed marked infiltration of mucosae by macrophages containing many acid-fast bacilli. Similar organisms were numerous in a faecal smear. Melaena, haematochezia and severe abdominal pain developed and were unresponsive to therapy. Following euthanasia and necropsy, histiocytic cells containing acid-fast bacilli were found throughout the gastrointestinal tract, mesenteric and peripheral lymph nodes, spleen, liver, kidney and lungs. The organism was identified as Mycobacterium avium by bacterial culture and polymerase chain reaction testing. [source] ,1A -Adrenoceptors predominate in the control of blood pressure in mouse mesenteric vascular bedAUTONOMIC & AUTACOID PHARMACOLOGY, Issue 3 2007S. G. Martínez-Salas Summary 1,The pressor action of the ,1A -adrenoceptor agonist, A61603 (N -[5-(4,5-dihydro-1H -imidazol-2-yl)-2-hydroxy-5,6,7,8-tetrahydronaphthalen-1-yl] methanesulfonamide) or the ,1 -adrenoceptor agonist phenylephrine, and their blockade by selective ,1 -adrenoceptor antagonists in the mouse isolated mesenteric vascular bed were evaluated. 2,A61603 showed a , 235-fold higher potency in elevating perfusion pressure in mesenteric bed compared to phenylephrine. 3,The ,1A -adrenoceptor selective antagonist RS 100329 (5-methyl-3-[3-[4-[2-(2,2,2,-trifluoroethoxy) phenyl]-1-piperazinyl] propyl]-2,4-(1H)-pyrimidinedione), displaced with high affinity agonist concentration,response curves to the right in a concentration-dependent manner. 4,The ,1D -adrenoceptor selective antagonist BMY 7378 (8-[2-[4-(2-methoxyphenyl)-1-piperazinyl]ethyl]-8-azaspiro[4.5] decane-7,9-dione), did not displace A61603 nor did it block the phenylephrine-induced pressor response. 5,The ,1B/D -adrenoceptor alkylating antagonist chloroethylclonidine (CEC), caused a rightward shift of the phenylephrine concentration,response curve and reduced its maximum response; however, CEC only slightly modified A61603 evoked contraction. 6,The results indicate that the isolated mouse mesenteric vascular bed expresses ,1A -adrenoceptors and suggest a very discrete role for 1B -adrenoceptors. [source] Long-term streptozotocin-induced diabetes alters prostanoid production in rat aorta and mesenteric bedAUTONOMIC & AUTACOID PHARMACOLOGY, Issue 4 2006H. A. Peredo Summary 1 Vascular disease is a major cause of mortality and morbidity in chronic diabetes mellitus. 2 Prostanoids, metabolites of arachidonic acid, include vasoactive substances produced and released from the vascular wall. Alterations in prostanoid production have been reported in the vasculature of diabetic humans and experimental animals. 3 The aim of the present work was to study the influence of three different periods of long-term streptozotocin-induced diabetes, 30, 120 and 180 days in the production of prostanoids in the thoracic aorta and in the mesenteric vascular bed of the rat. The prostanoids released to the incubation medium by the tissues were extracted and measured by reversed-phase HPLC. 4 In the diabetic groups, body weight was reduced and glycaemia was increased when compared with the corresponding non-diabetic controls. 5 In the aorta, 30 days of diabetes did not modify the prostanoid release pattern, meanwhile 120 and 180 days of incubation decreased prostacyclin (PGI2) production. In the mesenteric bed, at 30 days the release of the vasodilators PGI2 and prostaglandin (PGE2) and the vasoconstrictor thromboxane (TXA2) was reduced. At 120 days the vasodilators were reduced and at 180 days such reduction was joined by an increase of the release of vasoconstrictor metabolites. 6 Thirty days of diabetes did not modify the PGI2/TXA2 ratio in the aorta or mesenteric bed. On the other hand, 120 and 180 days of diabetes reduced significantly the ratio when compared with the corresponding controls. 7 In conclusion, the mesenteric bed, a resistance vascular bed, seems to be more sensitive than the aorta, a conductance vessel, to the effects of diabetes on prostanoid production. The observed effects contribute to a displacement of the balance of prostanoid release in favour of the vasoconstrictor metabolites, a phenomenon that could be related to the vascular complications of diabetes mellitus. [source] Oral treatment and in vitro incubation with fructose modify vascular prostanoid production in the ratAUTONOMIC & AUTACOID PHARMACOLOGY, Issue 1 2006H. A. Peredo Summary 1 In the rat, a fructose-enriched diet induces hyperglycaemia, hypertriglyceridaemia, insulin resistance and hypertension; a model which resembles the human metabolic syndrome. 2 Prostanoids, metabolites of arachidonic acid, include vasoactive substances synthesized and released from the vascular wall that have been implicated in the increase of peripheral resistance, one of the mechanisms involved in the fructose-induced hypertension. 3 The aim of the present study was to: (i) analyse the effects of the in vitro incubation with fructose on the production and release of prostanoids in rat thoracic aorta and in rat mesenteric bed and (ii) compare the effects of incubation with those of the in vivo acute and chronic treatment of rats with fructose and with the combination of both in vivo and in vitro procedures. 4 Blood pressure, glycaemia and triglyceridaemia were significantly elevated in both 4- and 22-week fructose-treated groups. Meanwhile, body and heart weight as well as insulinaemia were similar between experimental animals and controls. 5 In aortae, 4 weeks of Fructose treatment did not modify the prostanoid pattern release, but in vitro incubation decreased prostacyclin (PGI2) production. However, after 22 weeks, fructose treatment and incubation exerted the same effect. 6 In mesenteric bed, after 4 weeks, the incubation and the combination of both procedures reduced the release of the vasodilators PGI2 and PGE2, while fructose treatment only diminished the PGE2 release. On the contrary, the production of the vasoconstrictor thromboxane A2 (TXA2) was enhanced by incubation and both the procedures. After 22 weeks, fructose treatment increased PGI2 release, while it was reduced by incubation. The combination of both did not modify this peripheral resistance when compared with controls. Finally, incubation of tissues from treated rats increased the release of the vasoconstrictors, PGF2, and TXA2. 7 In conclusion, the mesenteric bed, a resistance vascular bed, seems to be more sensitive than the aorta, a conductance vessel, to the effects of fructose on prostanoid production. This difference could be related to a more relevant role of resistance vessels in the regulation of peripheral resistance and consequently of blood pressure. The observed effects should contribute to a shift in the balance of the release of prostanoid in favour of vasoconstrictor metabolites. This phenomenon could be related to an increase in the peripheral resistance and the mild hypertension observed in the fructose-treated rats. [source] Opposite effects of endogenous nitric oxide and prostaglandin F2, in the rat mesenteric bedAUTONOMIC & AUTACOID PHARMACOLOGY, Issue 3 2003H. A. Peredo Summary 1 The relationship between the effects of endogenous nitric oxide (NO) and prostanoids on the noradrenaline (NA)-induced contractions and the mechanisms involved were investigated in the rat perfused mesenteric bed, using NG -nitro- l -arginine methyl ester (l -NAME), a NO synthase inhibitor and sodium nitroprusside (SNP), a NO donor. 2 The constrictor responses to NA were reduced to 50% by the cyclooxygenase inhibitor 10 ,m indomethacin as well as by 1 ,m SNP. When indomethacin and SNP were perfused simultaneously the contractions were further reduced. 3 The NA-induced contractions were increased by the addition of 400 ,ml -NAME and the addition of either indomethacin or SNP abolished such increases. The simultaneous perfusion of both agents further reduced the contractions. 4 Removal of the endothelium increased NA-induced contractions to a similar extent as l -NAME and this increase was abolished by indomethacin as well as by SNP. 5 The perfusion of 10 ,m NA augmented the release of prostaglandin (PG) F2, by the mesenteric bed without modifications in any other prostanoid. In the presence of l -NAME, this effect was further increased. However, SNP abolished the NA-induced stimulation of PGF2, release. 6 In de-endothelialized preparations NA also stimulated PGF2, production as observed in intact preparations. This effect was more marked in the presence of l -NAME; in contrast, SNP abolished the stimulation. 7 In conclusion, the present results suggest an opposite action between NO and PGF2, on the NA-induced contractions in the rat mesenteric bed. [source] Inhibition of calcium/calmodulin-dependent protein kinase II normalizes diabetes-induced abnormal vascular reactivity in the rat perfused mesenteric vascular bedAUTONOMIC & AUTACOID PHARMACOLOGY, Issue 1 2003M. H. M. Yousif Summary 1 Calcium/calmodulin-dependent protein kinase II (CaMKII) has an important function in mediating insulin release but its role in the development of diabetes-induced cardiovascular complications is not known. 2 We investigated the ability of a chronic administration of KN-93 (5 mg kg,1alt diem for 4 weeks), an inhibitor of CaMKII, to modulate the altered vasoreactivity of the perfused mesenteric bed to common vasoconstrictors and vasodilators in streptozotocin (STZ)-induced diabetes. 3 The vasoconstrictor responses induced by noradrenaline (NE), endothelin-1 (ET-1), and angiotensin II (Ang II), were significantly increased whereas, vasodilator responses to carbachol and histamine were significantly reduced in the perfused mesenteric bed of the STZ-diabetic rats as compared with non-diabetic controls. 4 Inhibition of CaMKII by KN-93 treatment did not affect blood glucose levels but produced a significant normalization of the altered agonist-induced vasoconstrictor and vasodilator responses. KN-93 did not affect agonist-induced responses in control animals. In addition, KN-93 significantly reduced weight loss in diabetic rats. 5 The present data suggest that CaMKII is an essential mediator in the development of diabetic vascular dysfunction and may also play an important role in signalling pathways leading to weight loss during diabetes. [source] The ,-adrenoceptor antagonist, zolertine, inhibits ,1D- and ,1A-adrenoceptor-mediated vasoconstriction in vitroAUTONOMIC & AUTACOID PHARMACOLOGY, Issue 3 2000M. Ibarra 1 The antagonist effect of zolertine (4-phenyl-1-[2-(5-tetrazolyl)ethyl]piperazine trihydrochloride), on vascular contraction elicited by noradrenaline in aorta, carotid (,1D-adrenoceptors), mesenteric (,1A/D-adrenoceptors) and caudal arteries (,1A-adrenoceptors) from Wistar Kyoto (WKY) and spontaneously hypertensive (SHR) rats and rabbit aorta (,1B-adrenoceptors), was investigated in endothelium-denuded arterial rings. 2 The selective ,1D-adrenoceptor agonist, noradrenaline, elicited concentration-dependent contractions in all arterial rings from both species. Noradrenaline selectivity was: carotid=aorta>>.Gt;mesenteric=rabbit aorta>caudal arteries. 3 The contractile responses induced by noradrenaline were competitively antagonized by zolertine in rat carotid and aorta arteries, yielding pA2 values of WKY, 7.48±0.18; SHR, 7.43±0.13 and WKY, 7.57±0.24; SHR, 7.40±0.08, respectively. Zolertine was a non-competitive antagonist in some blood vessels as Schild plot slopes were lower than unity. The pKb estimates for zolertine were WKY, 6.98±0.16; SHR, 6.81±0.18 in the mesenteric artery, WKY, 5.73±0.11; SHR, 5.87±0.25 in the caudal artery and 6.65±0.09 in rabbit aorta. 4 Competition binding experiments using the ,1-adrenoceptor antagonist [3H]prazosin showed a zolertine pKi of 6.81±0.02 in rat liver (,1B-adrenoceptors) and 6.35±0.04 in rabbit liver (,1A-adrenoceptors) membranes. 5 Zolertine showed higher affinity for ,1D-adrenoceptors compared to ,1A-adrenoceptors, while it had an intermediate affinity for ,1B-adrenoceptors. The ability of the ,1-adrenoceptor antagonist zolertine to block ,1D-adrenoceptor-mediated constriction in different vessels of WKY and SHR rats may explain its antihypertensive efficacy despite its low order of potency. [source] Acute hypertension reveals depressor and vasodilator effects of cannabinoids in conscious ratsBRITISH JOURNAL OF PHARMACOLOGY, Issue 1 2009W-S Vanessa Ho Background and purpose:, The cardiovascular effects of cannabinoids can be influenced by anaesthesia and can differ in chronic hypertension, but the extent to which they are influenced by acute hypertension in conscious animals has not been determined. Experimental approach:, We examined cardiovascular responses to intravenous administration of anandamide and the synthetic cannabinoid, (R)-(+)-[2,3-dihydro-5-methyl-3-(4-morpholinylmethyl)pyrrolo[1,2,3-de]-1,4-benzoxazin-6-yl]-1-naphthalenylmethanone (WIN55212-2), in conscious male Wistar rats made acutely hypertensive by infusion of angiotensin II (AII) and arginine vasopressin (AVP). Rats were chronically instrumented for measurement of arterial blood pressure and vascular conductances in the renal, mesenteric and hindquarters beds. Key results:, Anandamide dose-dependently decreased the mean arterial blood pressure of rats made hypertensive by AII-AVP infusion, but not normotensive rats. Interestingly, acute hypertension also revealed a hypotensive response to WIN55212-2, which caused hypertension in normotensive animals. The enhanced depressor effects of the cannabinoids in acute hypertension were associated with increased vasodilatation in hindquarters, renal and mesenteric vascular beds. Treatment with URB597, which inhibits anandamide degradation by fatty acid amide hydrolase, potentiated the depressor and mesenteric vasodilator responses to anandamide. Furthermore, haemodynamic responses to WIN55212-2, but not to anandamide, were attenuated by the CB1 receptor antagonist, AM251 [N-(piperidin-1-yl)-5-(4-iodophenyl)-1-(2,4-dichlorophen yl)-4-methyl-1H-pyrazole-3-carboxamide]. Conclusions and implications:, These results broadly support the literature showing that the cardiovascular effects of cannabinoids can be exaggerated in hypertension, but highlight the involvement of non-CB1 receptor-mediated mechanisms in the actions of anandamide. [source] Differential effects of glucose on agonist-induced relaxations in human mesenteric and subcutaneous arteriesBRITISH JOURNAL OF PHARMACOLOGY, Issue 3 2008A MacKenzie Background and purpose: Acute periods of hyperglycaemia are strongly associated with vascular disorder, yet the specific effects of high glucose on human blood vessel function are not fully understood. In this study we (1) characterized the endothelial-dependent relaxation of two similarly sized but anatomically distinct human arteries to two different agonists and (2) determined how these responses are modified by acute exposure to high glucose. Experimental approach: Ring segments of human mesenteric and subcutaneous arteries were mounted in a wire myograph. Relaxations to acetylcholine and bradykinin were determined in a control (5 mM) and high glucose (20 mM) environment over a 2 and 6 h incubation period. Key results: Bradykinin-induced relaxation in both sets of vessels was mediated entirely by EDHF whilst that generated by acetylcholine, though principally generated by EDHF, also had contribution from prostacyclin and possibly nitric oxide in mesenteric and subcutaneous vessels, respectively. A 2-h incubation of high glucose impaired bradykinin-induced relaxation of subcutaneous vessels whilst, in contrast, the relaxation generated by bradykinin in mesenteric vessels was enhanced at the same time point. High glucose significantly augmented the relaxation generated by acetylcholine in mesenteric and subcutaneous vessels at a 2 and 6 h incubation point, respectively. Conclusions and implications: Short periods of high glucose exert a variable influence on endothelial function in human isolated blood vessels that is dependent on factors of time, agonist-used and vessel studied. This has implications for how we view the effects of acute hyperglycaemia found in patients with diabetes mellitus as well as other conditions. British Journal of Pharmacology (2008) 153, 480,487; doi:10.1038/sj.bjp.0707592; published online 26 November 2007 [source] Cardiovascular effects of cannabinoids in conscious spontaneously hypertensive ratsBRITISH JOURNAL OF PHARMACOLOGY, Issue 5 2007A J Wheal Background and purpose: In anaesthetized spontaneously hypertensive rats (SHR), there is evidence for up-regulation of cannabinoid (CB1) receptors: antagonism of CB1 receptors causes a rise in blood pressure, and administration of the endocannabinoid, anandamide, or inhibition of anandamide degradation causes hypotension. These findings have led to the suggestion that the endocannabinoid system may be a therapeutic target in hypertension. However, since the cardiovascular responses to cannabinoids are substantially influenced by anaesthesia, the purpose of this study was to assess regional haemodynamic responses to cannabinoid receptor stimulation and inhibition in conscious SHR. Experimental approach: Cardiovascular responses to i.v. administration of anandamide, the cannabinoid receptor agonist, WIN 55212-2, and the CB1 receptor antagonist, AM 251, were measured in male SHR, Wistar Kyoto rats and outbred Wistar rats, chronically instrumented for recording renal, mesenteric and hindquarters haemodynamics in the conscious, freely-moving state. Key results: Hypotensive responses to anandamide and WIN 55212-2 only occurred in SHR, but these were relatively modest and not associated with CB1 receptor-mediated vasodilatation. In SHR only, anandamide caused bradycardia, which was inhibited by AM 251. Furthermore, a pressor response to CB1 receptor antagonism occurred only in SHR, but was not associated with vasoconstriction. Moreover, there was some evidence for CB1 receptor-mediated vasoconstrictor actions of anandamide in SHR, which was not seen in the normotensive strains. Conclusions and implications: The results are consistent with activation of CB1 receptors in SHR by endogenous ligands exerting an antihypertensive effect, but the findings do not indicate enhanced CB1 receptor-mediated vasodilator mechanisms in SHR. British Journal of Pharmacology (2007) 152, 717,724; doi:10.1038/sj.bjp.0707410; published online 13 August 2007 [source] | ||||||||||||||||||||||||||||||||||