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Biomedical subjects

J C Kerr

Publications and source records attributed to J C Kerr.

At least 55 records · Page 3Linked to original sources
PubMed1977

Influence of vasopressin on colon blood flow in monkeys.

Inferior mesenteric arterial blood flow was measured with an electromagnetic blood flowmeter in five anesthetized rhesus monkeys. The effects of vasopressin on this vasculature were determined to evaluate the optimal, safe concentration of this agent during its clinical application in the management of hemorrhagic lesions of the colon. Control flow was 29 +/- 3 (SE) ml min-1; aortic pressure was 124 +/- 4 mm Hg. Intraarterial injections of vasopressin, in doses ranging logarithmically from 5 X 10(-5) to 5 X 10(-2) U kg-1, caused dose-dependent decreases in flow. At the highest dose, vasopressin reduced flow by 50% and increased arterial pressure by 9 mm Hg. When infused, at a rate of 5 X 10(-3) U kg-1 min-1, vasopressin produced a significant and sustained reduction in inferior mesenteric arterial blood flow. Autoregulatory escape was not observed. At this rate, vasopressin increased arterial pressure 10 mm Hg, by the 6th minute of infusion. This hypertension was unaccompanied by significant bradycardia. After cessation of the infusion, flow gradually returned to control values over a period of minutes. These observations indicate that vasopressin is a potent constrictor in the inferior mesenteric arterial circulation of the monkey, and support the use of this agent to control lower intestinal bleeding in man. At a dose of 5 X 10(-3) U kg-1 min-1, vasopressin causes a significant reduction in flow without adverse systemic side effects.

Animals↗
PubMed1977

Adrenergic mechanisms in the hepatic arterial circulation of baboons.

The effects of intra-arterial injections and infusions of three adrenergic amines upon hepatic arterial blood flow were measured in anesthetized baboons before and after alpha and beta adrenergic blockade with intravenous phenoxybenzamine and propranolol. Injections of norepinephrine or epinephrine caused dose-dependent decreases in hepatic arterial blood flow. These responses were attenuated by alpha adrenergic blockade and were unchanged by beta adrenergic blockade. Injections of isoproterenol caused dose-dependent increases in hepatic arterial flow. These increases were relatively small and were reversed to constriction at low doses and attenuated at high doses of the agonist by beta adrenergic blockade. Intrahepatic arterial infusions of constrictors were unaccompanied by autoregulatory excape. The degree of constriction was attenuated by alpha adrenergic blockade but was not potentiated by beta adrenergic blockade. Intrahepatic arterial infusion of a relatively large dose of isoproterenol was required to evoke a relatively modest, but sustained, increase in hepatic arterial blood flow. This response was not potentiated by alpha adrenergic antagonism, but was attenuated by beta adrenergic blockade. These observations suggest an apparent and relative decrease in beta adrenergic receptor activity in the hepatic arterial bed of the baboon when compared to other regional circulations such as the mesenteric and femoral beds. These beta receptors are relatively resistant to both stimulation and blockade.

Animals↗
PubMed1976

Primate gastric circulation: effects of catecholamines and adrenergic blockade.

The effects of intra-arterial injections and infusions of epinephrine, norepinephrine, and isoproterenol on gastric blood flow were studied in anesthetized baboons. Blood flow was measured electromagnetically before and after adrenergic blockade. The results for injected epinephrine and norepinephrine indicate these agents to be pure vasoconstrictors in the primate gastric circulation, and this response is attenuated by alpha-adrenergic blockade with phenoxybenzamine. Isoproterenol is a pure vasodilator, and its response is attenuated following beta-adrenergic blockade with propranolol. Intra-arterial infusions of epinephrine and norepinephrine (.05 mug kg-1 min-1) resulted in sustained vasoconstriction with no evidence of autoregulatory escape and no postinfusion "over-shoot." This study suggests that epinephrine and norepinephrine might provide alternatives to vasopressin as a vasoconstrictor for the control of upper gastrointestinal bleeding.

Animals↗
PubMed1976

Distribution and arteriovenous shunting of gastric blood flow in the baboon: effect of epinephrine and vasopressin infusions.

The effects of 60-min intraarterial infusion of vasopressin (0.005 U per kg-min) and epinephrine (0.05 mu per kg-min) on gastric hemodynamics were studied in anesthetized baboons. Total gastric blood flow was measured electromagnetically and radioactive microspheres (15 +/- 5 mu) with three labels were used to determine regional distribution of gastric blood flow and arteriovenous shunting. Control flow was 55 +/- 8 ml per min, with 77.4 +/- 2.7% of flow going to the gastric mucosa and 1.7 +/- 0.4% of injected spheres appearing in the liver. Epinephrine infusion resulted in a sustained vasoconstriction to 18 +/- 5 ml per min with no autoregulatory escape and no changes in arterial pressure or cardiac output. Vasopressin resulted in a decrease in flow to 14 +/- 3 ml per min with no excape. Whereas cardiac output did not change, there was a singificant hypertensive effect during the vasopressin infusion. There was neither redistribution of flow nor change in arteriovenous shunting with either epinephrine or vasopressin. Transmucosal electrical potential difference was 62 +/- 8 mv and did not change significantly with either infusion.

Animals↗
PubMed1975

Adrenergic mechanisms in canine gastric circulation.

The effects of adrenergic stimulation and blockade on the gastric circulation were studied in anesthetized dogs. Blood flow through the right and left gastric artery was measured electromagnetically. Norepinephrine and isoproterenol were injected intra-arterially and intravenously before and after alpha- and beta-adrenergic blockade. Isoproterenol caused vasodilation of both right and left gastric circulations and this effect was attenuated by beta blockade. Epinephrine and norepinephrine induced constriction followed by dilation in both circulations. The constrictor components were attenuated or abolished by alpha-adrenergic blockade and the dilator components were attenuated by beta-adrenergic blockade. The right and left gastric vascular beds demonstrated quantitatively different responses to the same dose of each adrenergic amine. The left gastric circulation had a greater vasodilator response than did the right gastric circulation. These data support the classical concepts that epinephrine and norepinephrine are "mixed" adrenergic agonists and isoproterenol is a "pure" beta-adrenerigic agonist. The data further suggest that there is a differential in beta-adrenergic receptor distribution with the left gastric vasculature demonstrating greater dilator responses than the right.

Adrenergic Agonists↗
PubMed1975

Hemodynamics of experimental portal venous occlusion in dogs.

The effects of graded occlusion of the portal vein upon hepatic arterial blood flow were studied in anesthetized dogs to evaluate the so-called "reciprocal relationship" between portal venous flow and hepatic arterial flow in maintaining oxygenation of the liver. An obstruction that increased portal venous pressure to 20 mm Hg was accompanied by a transient increase in hepatic arterial blood flow without changing the other hemodynamic parameters. Release of portal venous occlusion was accompanied by a transient fall in hepatic arterial blood flow in this group of experiments. Increasing portal venous pressure to 30 mm Hg caused a gradual but progressive fall in arterial pressure accompanied by a significant fall in hepatic arterial blood flow. With complete obstruction of the portal vein there is a reduction in arterial pressure to the same level of portal venous pressure and a significant and sustained diminution in hepatic arterial blood flow. These observations conflict with previously described theories of a relationship between diminution in portal venous flow and increases in hepatic arterial blood flow.

Animals↗
PubMed1975

Hemodynamic effects of intra-arterial infusions of catecholamines on the canine gastric circulation.

The effects of intra-arterial infusions of epinephrine, norepinephrine, and isoproterenol upon right and left gastric blood flow were studied in anesthetized dogs. Blood flow was measured electromagnetically before and after adrenergic blockade. Infusion of epinephrine (0.05 mug Kg.(-1) min.(-1)) resulted in vasoconstriction (-50 +/- 6 ml. min.(-1)) with autoregulatory escape in the right gastric artery (RGA) and constriction (-41 +/- 8 ml. min.(-1)) followed by significant dilation (+ 56 +/- 10 ml. min.(-1)) in the left gastric artery (LGA). Alpha adrenergic blockade with phenoxybenzamine produced only a dilator response in both RGA and LGA to epinephrine infusion and beta adrenergic blockade resulted in a constrictor response with no autoregulatory escape. Norepinephrine infusions produced a constrictor response of similar magnitude as epinephrine but with little evidence of autoregulatory escape in either RGA and LGA. Alpha adrenergic blockade significantly attenuated this response in both circulations. Isoproterenol is a dilator in both circulations and its response is attenuated only by beta adrenergic blockade. This study demonstrates that the canine stomach has two regionally distinct circulations with the fundus and body exhibiting a greater dilator response than the antrum and pylorus.

Adrenergic alpha-Antagonists↗
PubMedDate not supplied

Acute ischemia-reperfusion injury in the canine hindlimb.

A canine arterial ligation preparation was used to produce whole limb ischemia-reperfusion injury. Alterations in the distribution of arterial blood flow as well as the morphology of skeletal muscle ischemia-reperfusion have not been investigated completely in this setting. Five anesthetized adult mongrel dogs underwent multiple infrarenal aortic branch ligations; one randomly selected hindlimb was subjected to six hours of ischemia and two hours of reperfusion, while the opposite limb served as control. Distribution of arterial blood flow was analyzed by injection of radiolabeled microspheres. Electromagnetically measured femoral arterial blood flow was 92 +/- 10 ml/min during control, and increased significantly (p less than 0.05) to 254 +/- 94 ml/min during reperfusion. Flow distribution to skin, muscle, and bone was 9 +/- 2%, 68 +/- 7%, and 8 +/- 1% during control, and 7 +/- 3%, 65 +/- 8%, and 9 +/- 4% after reperfusion, which did not represent significant changes. Arteriovenous shunting was 11 +/- 4% during control, and was 13 +/- 5% during reperfusion, which was not significantly different. Subcellular injury in the ischemic and reperfused hindlimb was demonstrated by light and electron microscopy. These findings further characterize whole limb ischemia-reperfusion injury in the canine hindlimb.

Acute Disease↗