Cardiovascular effects of S 2620 in dogs anesthetized with pentobarbital]

In the dog under pentobarbitone anesthesia, the intravenous infusion of 1 mg/kg S 2620 results in tachycardia and systemic arterial hypertension. The same attenuated effects are caused by a second injection of the drug after cervical vagotomy and chemoreceptors denervation. Tachycardia and peripheral vaso constriction can account for elevation of arterial pressure.     

The effects of ethanol on pancreatic blood flow in awake and anesthetized dogs

The pathophysiology of alcohol-induced acute pancreatitis is not clear. Ischemic injury has been suggested as a possible mechanism. To examine the effects of ethanol on pancreatic and splanchnic blood flow, measurements were made in fasted, conditioned awake dogs before and after iv infusion of ethanol (1.7 g/kg). At 30 min blood ethanol concentration ranged between 60 and 150 mg/dl and at 60 min between 166 and 350 mg/dl. Although cardiac output, aortic pressure, left atrial pressure, and arterial pH did not change, pancreatic flow declined by 39 +/- 12 ml/min/100 g, P less than 0.05 (from 173 +/- 10 ml/min/100 g) at 30 min and was still depressed (by 27 +/- 12 ml/min/100 g, P less than 0.05) at 60 min. Concomitantly, hepatic arterial flow increased. While hepatic and pancreatic flow changed inversely, the correlation (r = -0.17) of these changes was not significant. At comparable blood ethanol concentrations in pentobarbital-anesthetized dogs hepatic arterial flow increased by 11 +/- 3 ml/min/100 g, P less than 0.01 (from 24 +/- 5 ml/min/100 g), but pancreatic flow did not change. Thus, in the awake dog at blood levels that would produce mild to moderate alcoholic intoxication in man, ethanol reduces pancreatic flow. Although hepatic flow increases concomitantly, the relationship of these changes appears to be independent.     

Effect of d-1 propranolol on urinary osmolarity after furosemide in anesthesized dog]

The effects of propranolol (l mg/kg/H infused in the renal artery) on the diuretic action of furosemide (20 mg/kg i.v.) have been studied in pentobarbital anesthetized dogs. We obtained the 3 following results : the urine remained isotonic to the plasma during the 6 hours following the furosemide injection ; the urinary output of sodium and water, measured during 6 hours after furosemide injection, was increased ; the renin hypersecretion was inhibited.     

Investigations on the circulation of anesthetized dogs.

In the present experiments arterial blood pressure, cardiac output, heart rate, oxygen consumption, AVO2 difference values and their changes were investigated in 64 anesthetized dogs in four periods for altogether 60 min. Blood flows of the renal, commune carotid and femoral arteries were measured in parallel and the changes were recorded throughout the 60 min of the experimental period. Urine was collected separately from both kidneys, in order to determine whether the measurement of the blood flow of the renal artery disturbed renal functions. Total peripheral vascular resistance and the vascular resistance of the territories of the commune carotid and femoral arteries were calculated from the parameters measured. In the present experiments the equation of the regression line between cardiac output and body weight was y = 0.102x + 0.9411. The equation of the regression line between cardiac output an body surface proved to be y = 2.996x + 0.653. The relationship between total oxygen consumption and body weight could be characterized by the y = 5.815x + 24.227 equation. Our data were in accordance with data of the Biology Data Book obtained in dogs anesthetized by pentobarbital. Our present data can be found but partially in the Biology Data Book, so the results obtained in the present study may serve as basis of future comparisons. In this work proper care was taken to maintain the same conditions and, thus ruling out possible artefacts. The experiments were carried out on mongrel dogs of different sexes; nevertheless, the animals were attempted to be kept under the same conditions for the 14 days preceding the experiments.     

The effects of serum osmolarity on cerebrospinal fluid volume flow

The effects of changes in serum osmolarity on cerebrospinal fluid (CSF) formation were studied in cats. CSF production rates were measured by ventriculocisternal perfusion both before and after intravenous infusion of glucose solutions.Infusion of glucose, hyperosmolar with respect to serum, increased serum osmolarity and caused a decrease in CSF formation rate; conversely, infusion of hypoosmolar solutions lowered serum osmolarity and increased CSF formation. CSF production and serum osmolarity were found to be linearly related. A 1% serum osmolarity change resulted in a 6.7% change in CSF formation. CSF formation increased by 130% with a serum osmolarity of 265 m0sm/1 and was undetectable with serum of 380 m0sm/1.     

A microsphere study on the effects of somatostatin and secretin on regional blood flow in anesthetized dogs

The endogenous peptides somatostatin and secretin are effective in the therapy of upper gastrointestinal tract bleeding and acute pancreatitis. The clinical effects may be partly brought about by changes in the regional blood flow. To evaluate the effects of somatostatin (50 and 100 μg/min over 6–8 min) and secretin (0.1 and 0.5 U · kg^?1 · min^?1 over 3–5 min) on tissue blood flow, particularly of the gastrointestinal tract, the tracer microsphere reference sample method was used in anesthetized dogs.Infusion of somatostatin significantly diminished gastric and pancreatic blood flow whereas no changes of duodenal and ileal blood flow could be obtained. Blood flow through spleen, kidneys and adrenal glands was increased but no changes were observed in the blood flow of other tissues. Cardiac hemodynamics remained unchanged.Secretin increased the blood flow of the duodenum, the kidneys and the adrenal glands and diminished gastric blood flow without changing pancreatic, ileal, hepatic, pulmonary and muscle blood flow. Cerebral, pituitary and myocardial blood flow was increased by a higher dose of secretin. It also evoked a slight but significant positive ino- and chronotropic effect. Since secretin and somatostatin differ in their respective effects on gastrointestinal blood flow it is suggested that the previously reported beneficial effects of both peptides on upper gastrointestinal bleeding cannot solely be attributed to changes in regional blood flow.     

The effects of clonidine on the kidney function in the anesthetized dog

Studies were performed to determine the mechanism by which the antihypertensive agent clonidine increased urine flow. The response of the kidney has been examined in four combinations. The parameters of renal function have been compared during volume expansion by 1.5-2.0% body weight Ringer solution. In the control animals, volume expansion by 2% body weight, resulted in a slight increase in sodium excretion and urine flow. In 10 anesthetized dogs 1.0 microgram/kg/min of clonidine infused i.v. during 30 minutes (the total amount of clonidine infused was 30 micrograms/kg) decreased the arterial blood pressure from 136 +/- 13 mmHg to 127 +/- 12 mmHg and elevated urine flow from 2.95 +/- 1.65 ml/min to 4.34 +/- 1.77 ml/min while the urine osmolality diminished from 399 +/- 107 mosm/l to 265 +/- 90 mosm/l and the glomerular filtration remained constant. In 5 animals 0.1 microgram/kg/min of clonidine was infused into the left renal artery (this dose is corresponding to the renal fraction of the cardiac output) without any effects in the left kidney. 1.0 microgram/kg/min of clonidine infused directly into the left renal artery produced vasoconstriction in the ipsilateral kidney, decreased the glomerular filtration rate and the urine flow. By contrast in the right kidney the urine flow rose without hemodynamic changes, and the urine osmolality became hypoosmotic compared to the plasma. In ten dogs 1.0 microgram/kg/min of clonidine and 1 mU/kg/min of arginine-vasopressin were infused intravenously. The vasopressin infusion superimposed on the clonidine could not inhibit the increase of the urine excretion, and the fall of the urine osmolality. The results suggest that the clonidine increases the renal medullary blood flow possibly via a direct mechanism, decreases the sympathetic outflow to the kidney and via an indirect pathway, mediated by the renin-angiotensin system. The renal medullary flow increase produces a washout of the medullary osmotic gradient, and the water reabsorption diminishes.     

The effects of 15AU81, a chemically stable prostacyclin analog, on the cardiovascular and renin-angiotensis systems of anesthetized dogs

15AU81 is a chemically stable tricyclic benzindene analog of prostacyclin. Prostaglandins, PGI2 and PGE2, and their analogs have demonstrated acute hemodynamic benefit in congestive heart failure. The purpose of this study was to evaluate the cardiovascular effects of 15AU81 in anesthetized dogs in order to assess this agent's potential for clinical study in the treatment of congestive heart failure. Four hour intravenous infusions of 15AU81 at 0.1, 0.3, 1.0, or 3.0 micrograms/kg/min produced dose-dependent decreases in mean arterial blood pressure of 10%, 43%, 55% and 68% respectively with associated decreases in total peripheral resistance of 20%, 32%, 56% and 73%, respectively. 15AU81 dilated the pulmonary circulation; however, the effects of 15AU81 on the pulmonary vascular bed were not dose dependent and not stable over time. Maximal decreases in mean pulmonary artery blood pressure achieved were 9%, 23%, 22%, and 18% with an associated decrease in pulmonary vascular resistance of 9%, 33%, 30% and 23%, at doses of 15AU81 of 0.1, 0.3, 1.0 and 3.0 micrograms/kg/min respectively. The onset of vasodilator effects were rapid, reaching a maximum within 5-10 min with an equally rapid recovery when the infusion was discontinued. Cardiac and hormonal effects associated with 15AU81 treatment included decreases in inotropy, and lusitropy and increases in heart rate and plasma angiotensin II concentration. The increase in plasma angiotensin II concentrated correlated significantly with the decrease mean arterial blood pressure. These effects are interpreted to be generally secondary to the potent and profound vasodilator activity of 15AU81 and not likely due to direct cardiac or neurohumoral effects. The hemodynamic profile of 15AU81 suggests that, through its rapid onset and ability to reduce loading conditions of the right and left ventricles and its chemical stability over natural prostacyclin, this prostacyclin analog may have utility in the management of chronic congestive heart failure.     

The effects of ph, osmolarity and urine contamination on equine spermatozoal motility

Urospermia has been reported as a cause of infertility in numerous species. The detrimental effects of urine on spermatozoa are due, at least in part, to changes in pH and osmolarity. Semen was collected and subjected to conditions of varying pH (Experiment 1), of varying osmolarity (Experiment 2), and various quantities and concentrations of urine (Experiment 3) and effects on motility were recorded. Finally, semen was contaminated with urine and then either of 2 semen extenders was added, with or without centrifugation, in an attempt to alleviate the detrimental effect of urine on motility (Experiment 4). The results of these experiments showed that alterations in pH and osmolarity negatively affected stallion sperm motility. Optimal pH and osmolarity appeared to be approximately 7.7 and 315, respectively. Contamination of the ejaculate with urine significantly decreased sperm motility. Smaller quantities of dilute urine were less detrimental than larger quantities of dilute urine, and dilute urine was less detrimental than more concentrated urine. The addition of semen extender restored the motility of urine contaminated semen to that of the uncontaminated control, however centrifugation to remove urine provided no significant advantage.     

Effects of dihydroergotamine on hemodynamic molsidomine actions in anesthetized dogs

In pentobarbital-anesthetized mongrel dogs the intravenous actions of 0.50 mg/kg molsidomine on pulmonary artery and left ventricular (LV) end-diastolic pressures and internal heart dimensions (preload), left ventricular systolic and peripheral blood pressures, and total peripheral resistance (afterload), as well as on heart rate, dP/dt, stroke volume, and cardiac output (heart performance) were studied for 2 h. Hemodynamic molsidomine effects were influenced by increasing amounts of intravenously infused dihydroergotamine solution (DHE, 1-64 micrograms X kg-1 X min-1). Molsidomine decreased preload, stroke volume, and cardiac output for over 2 h but decreased ventricular and peripheral pressures for 45 min. Systemic vascular resistance showed a tendency to decrease while heart rate and LV dP/dtmax were not altered. DHE infusion reversed molsidomine effects on the preload and afterload of the heart. The diminished stroke volume was elevated so that cardiac output also increased. Total peripheral resistance increased while heart rate fell in a dose-dependent fashion. The LV dP/dtmax remained unchanged until the highest dose of 64 micrograms X kg-1 X min-1 DHE elevated the isovolumic myocardial contractility. These experiments indicate that DHE can reverse the intravenous molsidomine effects on hemodynamics. Most likely, this is mediated through peripheral vasoconstriction of venous capacitance vessels, thereby affecting molsidomine's action on postcapillary beds of the circulation.     

Cardiovascular effects of intravenous and intracoronary administration of atrial natriuretic peptide in halothane anesthetized dogs

Cardiovascular actions of synthetic 1-28 human natriuretic peptides (hANP) were examined in dogs anesthetized with halothane. In seven closed-chest dogs a Swan-Ganz catheter was inserted for measurement of cardiac output. Intravenous infusion of increasing doses of hANP (0.1, 0.3, 0.9 microgram/kg/min) lowered mean aortic pressure without affecting heart rate significantly. Cardiac output and pulmonary wedge pressure were markedly decreased while total peripheral resistance was increased significantly. All these parameters returned to control levels after 1 hr of recovery with an 100-150ml of saline infusion to increase pulmonary capillary wedge pressure to the preinfusion value. Intracoronary infusion of hANP (0.05 and 0.1 microgram/kg/min) did not cause any significant changes in coronary flow and regional contraction. These results indicate that the hypotensive action of hANP is due to a decrease in cardiac output mediated by reduced preload but not by negative inotropic action.     

Hemodynamic and renal effects of acute and progressive nitric oxide synthesis inhibition in anesthetized dogs

This study evaluated the effects of progressive nitric oxide (NO) inhibition in the regulation of systemic and regional hemodynamics and renal function in anesthetized dogs. The N(G)-nitro-L-arginine methyl ester group (n = 9) received progressive doses of 0.1, 1, 10, and 50 microg. kg(-1). min(-1). Renal (RBF), mesenteric (MBF), iliac (IBF) blood flows, mean arterial pressure (MAP), pulmonary pressures, cardiac output (CO), and systemic and pulmonary vascular resistances were measured. During N(G)-nitro-L-arginine methyl ester infusion, MAP and systemic vascular resistances increased in a dose-dependent manner. Mean pulmonary pressure and pulmonary vascular resistances increased in both the N(G)-nitro-L-arginine methyl ester and the control group, but the increase was more marked in the N(G)-nitro-L-arginine methyl ester group during the last two infusion periods. CO decreased progressively, before any significant change in blood pressure was noticeable in the N(G)-nitro-L-arginine methyl ester group. IBF decreased significantly from the first N(G)-nitro-L-arginine methyl ester dose, whereas RBF and MBF only decreased significantly during the highest N(G)-nitro-L-arginine methyl ester dose. Urinary volume and sodium excretion only increased significantly in the time control group during the two last time periods. The pulmonary vasculature was more sensitive than the systemic vasculature, whereas skeletal muscle and renal vasculatures showed a greater sensitivity to the inhibition of NO production than the mesenteric vasculature. NO synthesis inhibition induces a progressive antidiuretic and antinatriuretic effect, which is partially offset by the increase in blood pressure.