The effect of catecholamine infusions on myocardial blood flow, metabolic heat production and on general haemodynamics, before and after alprenolol (H56/28), in anaesthetized cats

1974

1Haemodynamic changes have been studied in cats after the chronic oral administration of oxyfedrine (14 mg/kg for 3-4 weeks) or of placebo (lactose). The initial part of the study was carried out under double-blind conditions. The arterial blood pressure was between 19 mmHg (diastolic) and 27 mmHg (systolic) higher in the oxyfedrine treated animals, but there were no differences between the two groups with regard to cardiac output, left ventricular dP/dt max, heart rate or systolic ejection time. 2 In cats similarly treated with propranolol (4 mg/kg) there was a slight (12%), but significant, reduction in cardiac output. 3 Isoprenaline dose-response curves were shifted to the right in the cats administered oxyfedrine as well as in those administered propranolol. The degree of shift was five-fold (positive chronotropic response) and 20-fold (decrease in diastolic blood pressure) in the oxyfedrine group and 10-and 80-fold, respectively, in the propranolol group. 4 In contrast to the partial blockade of the effects of isoprenaline, the haemodynamic response to oxyfedrine was largely unaltered, both in the cats pretreated with propranolol and in those pretreated with oxyfedrine. The pressor response to noradrenaline was potentiated in the cats pretreated with oxyfedrine. 5 These results provide an explanation for the anti-anginal action of oxyfedrine. Some degree of 3-adrenoceptor blockade is achieved without a reduction in cardiac output or left ventricular dP/dt max. The relevance of these findings to the haemodynamic situation in angina is discussed.

Section: Discussionsupporting

confidence: 56%

The HAEMODYNAMIC EFFECTS OF PROLONGED ORAL ADMINISTRATION OF OXYFEDRINE, a PARTIAL AGONIST AT Β‐ADRENOCEPTORS: COMPARISON WITH PROPRANOLOL

1974

“…Sometimes, however, noradrenaline had a slight vasodilator effect, while in other experiments a mild vasoconstrictor action was noted in the myocardial bed. These results are similar to those obtained by Parratt & Wadsworth (1970b). The effects of an infusion of noradrenaline in one experiment are illustrated in Figure In this cat an infusion was administered before (upper panel) and after (lower panel) dipyridamole (1 mg/kg).…”

Section: Noradrenalinesupporting

confidence: 85%

“…Thus /82-adrenoceptor antagonists reduce the myocardial vasodilator action of isoprenaline by inhibiting the direct effect,; /1 antagonists can also reduce isoprenaline dilatation, but in this case by inhibiting the indirect effect (Parratt & Wadsworth, 1970a). The constrictor actions of noradrenaline become apparent after ,B-receptor blockade, which removes the indirect dilator component of action of the amine (Parratt & Wadsworth, 1970b). These direct and indirect effects have also been clearly distinguished in isolated hearts (Broadley, 1970).…”

Section: Discussionmentioning

confidence: 95%

The effects of dipyridamole on the myocardial vasodilator actions of noradrenaline, isoprenaline and adenosine

Wadsworth

1972

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Summary1. In anaesthetized cats, intravenous adenosine infusions decreased resistance to blood flow in the myocardial vascular bed. This effect of adenosine was augmented during the 60 min following the intravenous injection of dipyridamole(1 mg/kg).2. In different experiments, intravenous infusions of noradrenaline caused either a slight increase or a slight decrease in myocardial vascular resistance. The dilator component of the action of noradrenaline was not augmented by dipyridamole.3. Isoprenaline infusions decreased the resistance of the myocardial bed. This effect was unaltered after dipyridamole. 4. These results do not support the hypothesis that part of the effect of catecholamines on myocardial vascular resistance involves the release of adenosine from hypoxic myocardial cells.

“…Experiments were therefore performed to test this hypothesis. In four cats the effects of phentolamine infusions were examined before and after alprenolol, a 8-adrenoceptor blocking agent, in a dose (0 5 mg/kg) previously found markedly to reduce the cardiovascular effects of infused catecholamines (Parratt & Wadsworth, 1970). The results are summarized in Table 2.…”

Section: Resultsmentioning

confidence: 99%

Myocardial and haemodynamic effects of phentolamine

Das

1971

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Summary In cats anaesthetized with pentobarbitone, intravenous infusions of phentolamine ((10–50 μg/kg)/min for 5 min) increased heart rate, left ventricular dp/dt max (without increasing end‐diastolic pressure), aortic dp/dt, cardiac output, myocardial blood flow and metabolic heat production. Phentolamine‐induced increases in myocardial contractility occurred irrespective of the direction or magnitude of the blood pressure change and were maintained well beyond the actual infusion period. In cats treated with alprenolol, bretylium or reserpine there was no evidence of increased cardiac contractility following phentolamine administration. It is concluded that phentolamine, in doses less than those required to produce significant α‐adrenoceptor blockade, increased myocardial contractility through an effect on the sympathetic nervous system.