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Biomedical subjects

G Ross

Publications and source records attributed to G Ross.

At least 289 records · Page 16Linked to original sources

Regional circulatory effects of pancreatic glucagon.

1. The effects of close intra-arterial injections and infusions of glucagon on blood flow in the femoral, hepatic and superior mesenteric arteries of anaesthetized cats were studied using non-cannulating electromagnetic flow probes.2. Glucagon dilated the mesenteric vasculature. The threshold dose for rapid injections was less than 1 mug and maximal changes were produced by 10-20 mug. The dilatation began within a few seconds of injection and was unaffected by prior denervation or by pre-treatment with propranolol or atropine.3. Close intra-arterial glucagon increased the resistance of the hepatic arterial bed but had no effect on femoral vascular resistance. Intravenous glucagon failed to alter renal blood flow.4. Glucagon is therefore a potent vasoactive substance with its effect wholly or predominantly confined to the splanchnic area.5. It has been suggested that the cardiac effects of glucagon and isoprenaline resemble each other because both compounds act on the beta-adrenoceptor mechanism. The different regional vascular effects of glucagon and isoprenaline suggest that glucagon vasodilatation may not be mediated via beta-adrenoceptors.

Animals↗

Cholinergic mechanisms on the heart and coronary circulation.

1. The effects of rapid intracoronary injection of acetylcholine (ACh) were studied in anaesthetized open chest dogs. Changes in phasic coronary blood flow were followed with non-cannulating electromagnetic flow probes and in contractile force with isometric strain gauges.2. Increasing doses of ACh from 0.01 to 100 mug produced progressively larger increases in systolic and diastolic coronary blood flow and progressive decreases in end-diastolic vascular resistance which were blocked by atropine but not by propranolol.3. Contractile force showed both negative and positive responses. The negative inotropic effect was small and was blocked by atropine but not by propranolol. The threshold for the negative inotropic response was higher than for the coronary vasodilator effect and the dose response curve was flatter. The positive inotropic response usually showed two components. One component reached its maximum 13 to 18 s after injection, had a high threshold (over 1 mug), was potentiated by atropine and blocked by propranolol. The other reached its maximum 25 to 60 s after the injection, had a threshold between 0.01 and 0.1 mug, and was blocked by atropine but not by propranolol.4. These results suggest that the coronary dilator response, the negative inotropic response and part of the positive inotropic response are mediated through "muscarinic" receptors. The remaining component of the positive inotropic response appears to involve catecholamine release.

Acetylcholine↗