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Conscious Dogs (conscious + dog)
Selected AbstractsEffect of angiotensin II and endothelin-1 receptor blockade on the haemodynamic and hormonal changes after acute blood loss and after retransfusion in conscious dogsACTA PHYSIOLOGICA, Issue 4 2004R. C. E. Francis Abstract Aim:, This study investigates angiotensin II and endothelin-1 mediated mechanisms involved in the haemodynamic, hormonal, and renal response towards acute hypotensive haemorrhage. Methods:, Conscious dogs were pre-treated with angiotensin II type 1 (AT1) and/or endothelin-A (ETA) receptor blockers or not. Protocol 1: After a 60-min baseline period, 25% of the dog's blood was rapidly withdrawn. The blood was retransfused 60 min later and data recorded for another hour. Protocol 2: Likewise, but preceded by AT1 blockade with i.v. Losartan. Protocol 3: Likewise, but preceded by ETA blockade with i.v. ABT-627. Protocol 4: Likewise, but with combined AT1plus ETAblockade. Results:, In controls, haemorrhage decreased mean arterial pressure (MAP) by approximately 25%, cardiac output by approximately 40%, and urine volume by approximately 60%, increased angiotensin II (3.1-fold), endothelin-1 (1.13-fold), vasopressin (116-fold), and adrenaline concentrations (3.2-fold). Glomerular filtration rate and noradrenaline concentrations remained unchanged. During AT1 blockade, the MAP decrease was exaggerated (,40%) and glomerular filtration rate fell. During ETA blockade, noradrenaline increased after haemorrhage instead of adrenaline, and the MAP recovery after retransfusion was blunted. The decrease in cardiac output was similar in all protocols. Conclusions:, Angiotensin II is more important than endothelin-1 for the short-term regulation of MAP and glomerular filtration rate after haemorrhage, whereas endothelin-1 seems necessary for complete MAP recovery after retransfusion. After haemorrhage, endothelin-1 seems to facilitate adrenaline release and to blunt noradrenaline release. Haemorrhage-induced compensatory mechanisms maintain blood flow more effectively than blood pressure, as the decrease in cardiac output , but not MAP , was similar in all protocols. [source] Cardiovascular effects of desflurane following acute hemorrhage in dogsJOURNAL OF VETERINARY EMERGENCY AND CRITICAL CARE, Issue 1 2003Paulo S.P. Santos DVM Abstract Objective: To determine the cardiovascular effects of desflurane in dogs following acute hemorrhage. Design: Experimental study. Animals: Eight mix breed dogs. Interventions: Hemorrhage was induced by withdrawal of blood until mean arterial pressure (MAP) dropped to 60 mmHg in conscious dogs. Blood pressure was maintained at 60 mmHg for 1 hour by further removal or replacement of blood. Desflurane was delivered by facemask until endotracheal intubation could be performed and a desflurane expiratory end-tidal concentration of 10.5 V% was maintained. Measurements and main results: Systolic, diastolic, and mean arterial blood pressure (SAP, DAP and MAP), central venous pressure (CVP), cardiac output (CO), stroke volume (SV), cardiac index (CI), systemic vascular resistance (SVR), heart rate (HR), respiratory rate (RR), partial pressure of carbon dioxide in arterial blood (PaCO2), and arterial pH were recorded before and 60 minutes after hemorrhage, and 5, 15, 30, 45 and 60 minutes after intubation. Sixty minutes after hemorrhage, SAP, DAP, MAP, CVP, CO, CI, SV, PaCO2, and arterial pH decreased, and HR and RR increased when compared with baselines values. Immediately after intubation, MAP and arterial pH decreased, and PaCO2 increased. Fifteen minutes after intubation SAP, DAP, MAP, arterial pH, and SVR decreased. At 30 and 45 minutes, MAP and DAP remained decreased and PaCO2 increased, compared with values measured after hemorrhage. Arterial pH increased after 30 minutes of desflurane administration compared with values measured 5 minutes after intubation. Conclusions: Desflurane induced significant changes in blood pressure and arterial pH when administered to dogs following acute hemorrhage. [source] Comparison of the cardio-respiratory effects of methadone and morphine in conscious dogs,JOURNAL OF VETERINARY PHARMACOLOGY & THERAPEUTICS, Issue 4 2009A. A. MAIANTE The effects of methadone and morphine were compared in conscious dogs. Six animals received morphine sulfate (1 mg/kg) or methadone hydrochloride (0.5 mg/kg [MET0.5] or 1.0 mg/kg [MET1.0]) intravenously (i.v.) in a randomized complete block design. Cardiopulmonary variables were recorded before (baseline), and for 120 min after drug administration. One outlier was not included in the statistical analysis for hemodynamic data. Morphine decreased heart rate (HR) compared to baseline from 30 to 120 min (,15% to ,26%), while cardiac index (CI) was reduced only at 120 min (,19%). Greater and more prolonged reductions in HR (,32% to ,46%) and in CI (,24% to ,52%) were observed after MET1.0, while intermediate reductions were recorded after MET0.5 (,19 to ,28% for HR and ,17% to ,27% for CI). The systemic vascular resistance index (SVRI) was increased after methadone; MET1.0 produced higher SVRI values than MET0.5 (maximum increases: 57% and 165% for MET0.5 and MET1.0, respectively). Compared to morphine, oxygen partial pressure (PaO2) was lower (,12% to ,13%) at 5 min of methadone (0.5 and 1.0 mg/kg), while carbon dioxide partial pressure (PaCO2) did not change significantly. It was concluded that methadone induces cardiovascular changes that are dose-related and is a more potent cardiovascular depressant agent than morphine in conscious dogs. [source] Dual pulse intestinal electrical stimulation normalizes intestinal dysrhythmia and improves symptoms induced by vasopressin in fed state in dogsNEUROGASTROENTEROLOGY & MOTILITY, Issue 5 2007H. Qi Abstract, To assess effects of dual pulse intestinal electrical stimulation (DPIES) on intestinal dysrhythmia and motility, and symptoms induced by vasopressin in conscious dogs. The study was performed in three postprandial sessions (control; vasopressin; DPIES) in six dogs with two pairs of electrodes chronically implanted on the serosal surface of the proximal jejunum and with a chronic duodenal fistula. A manometric catheter was advanced into the small intestine via the intestinal cannula. Motility and intestinal slow waves were recorded. Symptoms were assessed. During vasopressin infusion, the percentage of normal intestinal slow wave frequency was decreased (P < 0.01), reflected as a significant increase in the percentage of both bradygastria and tachygastria; the motility index decreased (P < 0.01) and the symptom score increased (P < 0.01). In the session of DPIES, the percentage of normal slow wave frequency was recovered (P < 0.05 vs vasopressin), attributed to a reduction in both bradyarrhythmia and tachyarrhythmia; the symptom score was reduced (P < 0.05 vs vasopressin); the motility index was not significantly increased. These results suggest that vasopressin induces intestinal dysrhythmia and emetic symptoms and inhibits intestinal motility. Dual pulse intestinal electrical stimulation is capable of improving intestinal dysrhythmia and emetic symptoms but not impaired intestinal motility induced by vasopressin. [source] The peptide hormone xenin induces gallbladder contractions in conscious dogsNEUROGASTROENTEROLOGY & MOTILITY, Issue 3 2007Y. Kamiyama Abstract, Xenin is a 25-amino acid peptide isolated from human gastric mucosa. The biological activities of xenin include modulating intestinal motility and affecting exocrine pancreatic secretion and gastric acid secretion. The physiological effect of xenin on the gastrointestinal tract, however, is incomplete. The objective of this study is to investigate the effects of xenin on the gastrointestinal tract motility of conscious dogs. Gastrointestinal tract and gallbladder contractions were monitored by chronically implanted force transducers. Synthetic xenin was injected intravenously during the interdigestive state with or without pretreatment with cholinergic blockers. The effects of xenin following cholecystectomy and truncal vagotomy were also investigated. Xenin induced gallbladder and jejunal contractions, although a dose-dependent response was shown only with gallbladder contractions. These effects were inhibited by pretreatment with cholinergic blockers, but were not enhanced by truncal vagotomy. The jejunal contractions were completely inhibited by cholecystectomy. The only direct effect of xenin in terms of gastrointestinal motility was to induce gallbladder contractions in conscious dogs. The neural pathway mediating xenin's action was cholinergic, but not the vagal. This novel finding indicates a new role of xenin. [source] Nitrergic and cholinergic vagal pathways involved in the regulation of canine proximal gastric tone: an in vivo studyNEUROGASTROENTEROLOGY & MOTILITY, Issue 4 2000Paterson To better understand the relationship between cholinergic and nitrergic (NO) innervation in the regulation of proximal gastric (fundic) tone in vivo, the effects of nitric oxide synthase blockade on fundic tone were studied in conscious dogs using vagal cooling and an electronic barostat. Vagal cooling, atropine (0.05 mg kg,1 i.v. bolus) and hexamethonium (1 mg kg,1 i.v. bolus) all markedly decreased fundic tone as reflected by increased intragastric volume, indicating a significant contribution of vagal and enteric cholinergic pathways to the maintenance of canine fundic tone. Administration of L -NNA (10 mg kg,1 i.v. bolus) increased fundic tone and the effects of L -NNA were completely prevented by prior vagal cooling or atropine administration, but not by pretreatment with hexamethonium. The relaxation effects of neurally derived NO appear primarily related to inhibition of ongoing vagal cholinergic activity. The data are consistent with the primary site of action of nitrergic mechanisms on gastric fundic tone in conscious dogs being at a presynaptic site on vagal cholinergic efferent nerves. [source] Role of cardiac-renal neural reflex in regulating sodium excretion during water immersion in conscious dogsTHE JOURNAL OF PHYSIOLOGY, Issue 1 2002Kenju Miki The present study was undertaken to determine the role of cardiopulmonary mechanoreceptors in inducing the sustained reduction of renal sympathetic nerve activity (RSNA) and concomitant changes in sodium excretion occurring during water immersion (WI) in intact dogs. Seven cardiac-denervated dogs were chronically instrumented for measuring RSNA, systemic arterial (Pa), central venous (Pcv) and left atrial pressures (Pla). WI initially decreased RSNA in cardiac denervated dogs by 10.0 ± 5.5 %; thereafter the RSNA fell to a nadir of 18.5 ± 5.6 % (P < 0.05) at 40,80 min of WI and then returned toward the pre-immersion level. Renal sodium excretion increased significantly by 211 ± 69 % (P < 0.05) only during the first 20,40 min of WI. WI increased Pa, Pcv and Pla in a step manner from 94 ± 3 to 108 ± 3 mmHg (P < 0.05), from 1.4 ± 0.5 to 12.3 ± 1.0 mmHg (P < 0.05) and from 4.9 ± 0.6 to 15.4 ± 1.2 mmHg (P < 0.05), respectively. These responses in RSNA and sodium excretion to WI in the cardiac-denervated dogs were significantly (P < 0.05) attenuated compared with those in a previous group of intact dogs. These data suggest that the attenuated responses of neural and excretory response to WI observed in cardiac-denervated dogs can be attributed to an interruption of afferent input originating from the cardiopulmonary mechanoreceptors to the central nervous system. [source] Using 20-gauge percutaneous peripheral catheters to reliably collect serial 4-mL blood samples from conscious dogsAUSTRALIAN VETERINARY JOURNAL, Issue 6 2010KF Elliott Objective To determine the reliability of collecting serial 4-mL blood samples over 13 h using a 20-gauge, cephalic catheter in conscious dogs. Design Prospective, observational study. Animals Twelve (6 males, 6 females) healthy, neutered, lean dogs. Procedure Percutaneous placement of a 20-gauge, 1.1 × 30 mm intravenous over-the-needle catheter into the cephalic vein was performed in each dog on three occasions. Catheter patency was maintained by intermittent flushing with 0.9% saline and 1 IU/mL heparinised saline solutions. Blood samples (4 mL) were obtained at 10 time-points over 13 h, with close monitoring of the dogs and the indwelling catheters. Blood volume, resistance on aspirating blood sample (minimal or marked resistance) and the methods used to improve blood flow were recorded. Results A high proportion (93%) of blood sample collections achieved the required 4-mL volume, and the remaining samples were greater than 1.5 mL. Of the 358 collections via the cephalic catheter, 311 (87%) were obtained with ,minimal resistance'. The remaining collections had ,marked resistance' (n=47) and were associated with a loose catheter in 11% (5/47) and of unknown cause in 89% (42/47). After ,marked resistance' had been encountered and the catheter was flushed with saline and heparin solutions, subsequent sampling with ,minimal resistance' was frequently possible from the same catheter. Conclusion Use of a percutaneous, 20-gauge intravenous cephalic catheter allowed reliable serial collection of 4-mL blood samples over 13 h in conscious dogs. [source] Haemodynamic action of B-type natriuretic peptide substantially outlasts its plasma half-life in conscious dogsCLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 5-6 2003Colleen J Thomas Summary 1.,The objective of the present study was to determine the plasma half-life of B-type natriuretic peptide (BNP) in conscious dogs after intravenous administration and to compare this with its haemodynamic effects. In six chronically instrumented dogs, plasma BNP concentrations were measured under basal conditions, during a constant infusion of canine BNP-32 (10 pmol/kg per min; 25 min) to steady state and at nominated time points up to 75 min after stopping the infusion. Concomitant, continuous measurements of mean arterial blood pressure (MAP), heart rate (HR), central venous pressure (CVP) and mesenteric blood flow (MBF) were obtained. 2.,Baseline plasma BNP levels were 15.0 ± 2.3 fmol/mL and rose approximately 10-fold to 159 ± 23 fmol/mL after 20,25 min BNP infusion. When the infusion was turned off, plasma BNP levels declined in a biphasic manner, with an initial half-life of 1.57 ± 0.14 min and a terminal half-life of 301 ± 85 min. The metabolic clearance rate of BNP was 2.29 ± 0.34 L/min. 3.,The infusion of BNP reduced MAP (approximately 10%), CVP (approximately 65%) and MBF (approximately 25%), whereas haematocrit (approximately 4%) and mesenteric vascular resistance (MVR) increased (approximately 40%; all P < 0.05). Plasma BNP levels returned to baseline by 20 min after BNP infusion had been stopped, whereas none of the haemodynamic variables returned to normal by this time. Mean arterial pressure returned to resting levels within 10,15 min after plasma BNP returned to normal. However, CVP, haematocrit and MBF remained substantially below baseline values for more than 20 min after circulating BNP levels had returned to pre-infusion levels. Of these, only mesenteric vascular changes were returned to baseline within 60 min of plasma BNP levels normalizing. 4.,These results demonstrate that the removal of BNP from the canine circulation is rapid, similar to observations made regarding the metabolism of circulating atrial natriuretic peptide in dogs. The half-life of BNP in dogs was shorter than that in rats, sheep or humans. However, the haemodynamic actions of BNP substantially outlasted its plasma half-life. Whether this disparity in plasma level and haemodynamic activity of BNP reflects long-lasting activation of second messenger systems or slow recovery from the hydraulic changes at the capillary level, reflected in the haematocrit and CVP, remains to be answered. [source] | |||||||||||||