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Splanchnic Circulation (splanchnic + circulation)
Selected AbstractsAcute exercise causes an enhancement of tissue renin,angiotensin system in the kidney in ratsACTA PHYSIOLOGICA, Issue 1 2005S. Maeda Abstract Aims:, Initially, the renin,angiotensin system (RAS) produced through the classical endocrine pathway was well known for its regulation of blood pressure. However, it was revealed that a local autocrine and/or paracrine RAS may exist in a number of tissues (such as kidney). Exercise causes a redistribution of tissue blood flow, by which the blood flow is greatly increased in active muscles, whereas it is decreased in the splanchnic circulation (such as in the kidney). We hypothesized that exercise causes an enhancement of tissue RAS in the kidney. Methods:, We studied whether exercise affects expression of angiotensinogen and angiotensin-converting enzyme (ACE) and tissue angiotensin II level in the kidney. The rats performed treadmill running for 30-min. Immediately after this exercise, kidney was quickly removed. Control rats remained at rest during this 30-min period. Results:, The expression of angiotensinogen mRNA in the kidney was markedly higher in the exercise rats than in the control rats. ACE mRNA in the kidney was significantly higher in the exercise rats than in the control rats. Western blot analysis confirmed significant upregulation of ACE protein in the kidney after exercise. Tissue angiotensin II level was also increased by exercise. Conclusion:, The present study suggests that the exercise-induced enhancement of tissue RAS in the kidney causes vasoconstriction and hence decreases blood flow in the kidney, which are helpful in increasing blood flow in active muscles, thereby contributing to the redistribution of blood flow during exercise. [source] Reversal of portal hypertension and hyperdynamic splanchnic circulation by combined vascular endothelial growth factor and platelet-derived growth factor blockade in rats,HEPATOLOGY, Issue 4 2007Mercedes Fernandez Vascular endothelial growth factor (VEGF) and platelet-derived growth factor (PDGF) pathways are crucial to angiogenesis, a process that contributes significantly to the pathogenesis of portal hypertension. This study determined the effects of inhibition of VEGF and/or PDGF signaling on hyperdynamic splanchnic circulation and portosystemic collateralization in rats with completely established portal hypertension, thus mimicking the situation in patients. Portal vein,ligated rats were treated with rapamycin (VEGF signaling inhibitor), Gleevec (PDGF signaling inhibitor), or both simultaneously when portal hypertension was already fully developed. Hemodynamic studies were performed by transit-time flowmetry. The extent of portosystemic collaterals was measured by radioactive microspheres. The expression of angiogenesis mediators was determined by Western blotting and immunohistochemistry. Combined inhibition of VEGF and PDGF signaling significantly reduced splanchnic neovascularization (i.e., CD31 and VEGFR-2 expression) and pericyte coverage of neovessels (that is, ,-smooth muscle actin and PDGFR-, expression) and translated into hemodynamic effects as marked as a 40% decrease in portal pressure, a 30% decrease in superior mesenteric artery blood flow, and a 63% increase in superior mesenteric artery resistance, yielding a significant reversal of the hemodynamic changes provoked by portal hypertension in rats. Portosystemic collateralization was reduced as well. Conclusions: Our results provide new insights into how angiogenesis regulates portal hypertension by demonstrating that the maintenance of increased portal pressure, hyperkinetic circulation, splanchnic neovascularization, and portosystemic collateralization is regulated by VEGF and PDGF in portal hypertensive rats. Importantly, these findings also suggest that an extended antiangiogenic strategy (that is, targeting VEGF/endothelium and PDGF/pericytes) may be a novel approach to the treatment of portal hypertension. (HEPATOLOGY 2007.) [source] Effect of porto-systemic shunting on NOS expression after extended hepatectomy in ratsHEPATOLOGY RESEARCH, Issue 1 2009Hironori Hayashi Aim:, Several surgical procedures have been developed for reducing portal vein pressure to prevent postoperative liver injury. Nitric oxide synthase expression (NOS) induced by elevation of portal vein pressure is thought to play an important role in liver regeneration, but the details are not well understood. Methods:, Rats in the control group and in the subcutaneous splenic transposition (SST) group underwent 90% partial hepatectomy. Survival and portal vein pressure were analyzed. The serum IL-6 and TNF-, levels were measured by enzyme-linked immunosorbent assay (ELISA). Hepatocyte proliferation and apoptosis 12 hours after hepatectomy were analyzed immunohistochemically. The protein and messenger RNA expression of inducible and endothelial NOS were analyzed using Western blotting and quantitative reverse transcriptase polymerase chain reaction, respectively. Results:, The survival rate of the SST group was significantly higher. Portal vein pressure, TNF-, level and the apoptotic index were significantly lower in the SST group. Twelve hours after surgery, liver inducible NOS (iNOS) protein expression was significantly lower in the SST group. However, protein expression of endothelial NOS was not significantly different between the groups. Conclusion:, Inducible NOS expression after extended hepatectomy is related to the effects of porto-systemic shunting on the splanchnic circulation. Also, iNOS induction and concomitant nitric oxide generation appear to participate in the cytotoxicity of excessive portal pressure after extended hepatectomy. [source] Effects of levosimendan on indocyanine green plasma disappearance rate and the gastric mucosal,arterial pCO2 gradient in abdominal aortic aneurysm surgeryACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 6 2008H. LEPPIKANGAS Background: Levosimendan has a dual mechanism of action: it improves myocardial contractility and causes vasodilatation without increasing myocardial oxygen demand. In a laboratory setting, it selectively increases gastric mucosal oxygenation in particular and splanchnic perfusion in general. The aim of our study was to describe the effects of levosimendan on systemic and splanchnic circulation during and after abdominal aortic surgery. Methods: Twenty abdominal aortic aneurysm surgery patients were randomized to receive either levosimendan (n=10) or placebo (n=10) in a double-blinded manner. Both the mode of anaesthesia and the surgical procedures were performed according to the local guidelines. Automatic gas tonometry was used to measure the gastric mucosal partial pressure of carbon dioxide. Systemic indocyanine green clearance plasma disappearance rate (ICG-PDR) was used to estimate the total splanchnic blood flow. Results: The immediate post-operative recovery was uneventful in the two groups with a comparable, overnight length of stay in the intensive care unit. Cumulative doses of additional vasoactive drugs were comparable between the groups, with a tendency towards a higher cumulative dose of noradrenaline in the levosimendan group. After aortic clamping, the cardiac index was higher [4(3.8,4.7) l/min/m2 vs. 2.6(2.3,3.6) l/min/m2; P<0.05] and the gastric mucosal,arterial pCO2 gradient was lower in levosimendan-treated patients [0.9(0.6,1.2) kPa vs. 1.7(1.2,2.1) kPa; (P<0.05)]. However, the total splanchnic blood flow, estimated by ICG-PDR, was comparable [29(21,29)% vs. 20(19,25)%; NS]. Organ dysfunction scores (sequential organ dysfunction assessment) were similar between the groups on the fifth post-operative day. Conclusion: Levosimendan favours gastric perfusion but appears not to have a major effect on total splanchnic perfusion in patients undergoing an elective aortic aneurysm operation. [source] KICG value, a reliable real-time estimator of graft function, accurately predicts outcomes in adult living-donor liver transplantation,LIVER TRANSPLANTATION, Issue 4 2006Tomohide Hori Reliable monitoring enabling evaluation of graft function is crucial after living-donor liver transplantation (LDLT). A method to identify poor graft function at an early postoperative period would allow opportune intensive clinical management to bring about further improvements in LDLT outcomes. This study assessed the reliability of the indocyanine green (ICG) elimination rate constant (KICG) value as an estimator of graft function and determined the actual temporal changes of KICG after LDLT. KICG values were measured using a noninvasive method in 30 adult recipients up to 28 days after LDLT. The receptor index (LHL15) based on liver scintigraphy, and graft parenchymal damage score based on histopathological findings were evaluated after LDLT and correlated well with simultaneous KICG. Thus, KICG measured by noninvasive method was confirmed as accurately evaluating graft function. Changes of KICG after LDLT in recipients with good graft function were maintained, after some falls in the early periods, and had a significant difference compared with those for recipients without good graft function; moreover, there were already significant differences in KICG 24 hours after LDLT. Mean transit time reflecting systemic hemodynamics revealed that recipients without good outcomes fell into an unstable systemic hemodynamic state, and effective hepatic blood flow has a large influence on liver regeneration after LDLT. In conclusion, we suggested that KICG values can predict clinical outcomes at the early postoperative period after LDLT by sharply reflecting the influence of systemic dynamics on splanchnic circulation. Liver Transpl 12:605,613, 2006. © 2006 AASLD. [source] Comparison of liver hemodynamics according to doppler ultrasonography in alcoholic patients subtyped by Cloninger classification and non-alcoholic healthy subjectsACTA NEUROPSYCHIATRICA, Issue 1 2006Z. Sumru Cosar Background:, The aim of this study was to search for morphological and hemodynamic changes in hepatic and splanchnic vasculature in alcoholic patients without the signs of hepatic damage and subtyped by Cloninger classification by means of sonography, and compare the subtypes among themselves and with nonalcoholic healthy subjects. Methods:, Thirty alcohol dependent patients and 30 healthy subjects with no alcohol problem or hepatic impairment were included in the study. Patients were subtyped by Cloninger classification and all patients were evaluated by gray-scale and spectral Doppler ultrasound. The diameter of the portal vein, portal venous velocity, peak systolic and end diastolic velocities of hepatic and superior mesenteric arteries were assessed. RI, PI and systolic/diastolic velocity ratios were also calculated. Results:, Portal vein diameter (PV diameter), portal vein cross sectional area (PV area), portal vein velocity (PV PSV), hepatic artery peak systolic velocity (HA PSV), hepatic artery end diastolic velocity (HA EDV), hepatic artery resistive index (HA RI), hepatic artery pulsatility index (HA PI), and systolic/diastolic velocity ratios (HA S/D), superior mesenteric artery peak systolic velocity (SMA PSV), superior mesenteric artery end diastolic velocity (SMA EDV), superior mesenteric artery resistive indices (SMA RI), pulsatility index (SMA PI), and systolic/diastolic velocity rates (SMA S/D) showed no significant difference among the groups (P > 0.01). Although there is no significant difference in PV PSV, HA PSV, SMA PSV, SMA EDV values between the groups, mean values of Type II alcoholics is greater than other groups. Portal vein cross-sectional area was greater in alcoholic patients (Type I, II and III) compared to the control group (P = 0.000). Portal vein velocity, hepatic artery peak systolic and end diastolic velocity, superior mesenteric artery peak systolic and end diastolic velocity were significantly greater in alcoholic patients than in the control group (P < 0.001). No statistical difference was detected between other parameters evaluated. Conclusion:, In alcohol dependent patients, some hemodynamic and morphologic changes occur in hepatic and splanchnic circulation, even before the signs of hepatic damage develop, which can be detected by means of Doppler and gray-scale sonography. But as there is no significant difference between the Doppler ultrasonographic findings among alcoholics subtyped by a Cloninger classification, which is a clinical classification, it suggests that psychiatric classification doesn't show any correlation with biological parameters, and because of this Cloninger classification a psychiatric classification cannot be considered as a characteristic determinative factor in the prognosis of hepatic disorder due to alcohol use. However, higher values of Type II alcoholics can be attributed to the longer alcohol intake of this subtype. [source] | ||||||||||