Electrokinetic properties and morphologic characteristics of amphibian gastrula cells.
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Biomedical subjects
Publications and source records attributed to I Brick.
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1. The intravenous infusion of I.C.I. 50172 in doses up to 20 mg reduced, although not significantly, the increase in heart rate produced by the infusion of isoprenaline in healthy volunteers; the response to adrenaline was significantly reduced. The infusion of 1 mg propranolol abolished these responses2. After the pre-treatment of subjects with atropine or hexamethonium, I.C.I. 50172 produced a significant reduction in an isoprenaline tachycardia. This reduction was not competitive and did not exceed 50%.3. The intravenous injection of 4 mg I.C.I. 50172 reduced an exercise tachycardia; its effect was less than that of 4 mg propranolol. This difference became greater as the doses of the two drugs were increased. The dextro isomer of propranolol had no effect on the exercise tachycardia; I.C.I. 45763 reduced it to the same extent as propranolol.4. The intravenous injection of I.C.I. 50172 reduced the increase in heart rate produced by tilting a normal subject from the supine to 80 degrees head-up position. After the administration of atropine, I.C.I. 50172 almost abolished the response. In the presence of atropine, I.C.I. 50172 was as active as propranolol in reducing the increase in heart rate on tilting.5. The reason for the differences in the effects of I.C.I. 50172 on the increases in heart rate brought about by the three procedures is not clear.6. The increase in forearm blood flow produced by the infusion of isoprenaline into the brachial artery was not reduced by the intra-arterial administration of I.C.I. 50172.
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1. Blood flow was simultaneously measured by venous-occlusion plethysmography in both forearms of ten healthy men. 2. Voluntary overbreathing to produce about 8 times the resting ventilation caused a vasodilatation similar in both forearms. 3. When one forearm was treated with an intra-arterialinfusion of propranolol, a beta adrenergic blocking agent, the vasodilator response was reduced by an average of 28%, the reduction was significant (P < 0-01). 4. The failure of propranolol to abolish the vasodilator response was not due to incomplete block of beta adrenergic receptors since the dose of propranolol used reversed the vasodilator response to an intravenous infusion of adrenaline. 5. The results suggest that the vasodilator response to voluntary hyperventilation can be explained partly, but not entirely, by the release to the circulation of an adrenaline-like substance.
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