Isoproterenol and cardiovascular performance

Krasnow, Norman; Rolett, Ellis L.; Yurchak, Peter M.; Hood, William B.; Gorlin, Richard

doi:10.1016/0002-9343(64)90065-8

Cited by 201 publications

(38 citation statements)

References 44 publications

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“…This is speculation, for detailed studies have not been made in any of these patients. In normal man the intravenous infusion of isoprenaline in small doses (08 53 ,ug/min) increases heart rate (Krasnow, Rolett, Yurchak, Hood & Gorlin, 1964); in conscious dogs larger doses (0 4 aLg/kg) increase heart rate but do not produce cardiac arrhythmias, (Shanks, unpublished). In anaesthetized cats much larger doses (1 mg/kg) did not cause death (Butterworth, 1963).…”

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The cardio‐toxicity of isoprenaline during hypoxia

Collins¹,

McDevitt²,

Shanks³

et al. 1969

British J Pharmacology

102

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The effects of the intravenous injection of isoprenaline on heart rate and arterial pressure has been studied in dogs artificially respired with room air or with 12% oxygen—88% nitrogen. In dogs breathing room air, isoprenaline in doses from 0.02 to 500 μg/kg increased heart rate and reduced arterial pressure. Ventricular fibrillation was produced in one out of three dogs given 250 μg/kg. This was the only dog breathing room air which was killed by isoprenaline. In dogs breathing room air the repeated intravenous injection at 5‐min intervals of 2.5 μg/kg increased heart rate and reduced arterial pressure. No ill effects were produced by six doses. In dogs respired with 12% oxygen—88% nitrogen the Pao2 was reduced from 84 to 38 mm Hg with no changes in Paco2. In these dogs death was produced by doses of isoprenaline which in dogs breathing room air produced normal responses. The fatal dose of isoprenaline (10–50 μg/kg) reduced heart rate and arterial and pulse pressures; sinus rhythm persisted until arterial pressure was less than 50 mm Hg. Ventricular fibrillation did not occur; death occurred from cardiac asystole. Death was produced in a similar way in dogs with hypoxaemia by giving four or five doses of isoprenaline (2.5 μg/kg) at 5‐min intervals or by two doses of 25 μg/kg. The final reduction in arterial pressure during a fatal response resulted from a reduction in cardiac contractility. These lethal effects of isoprenaline could be prevented by pretreatment with propranolol.

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confidence: 99%

The cardio‐toxicity of isoprenaline during hypoxia

Collins¹,

McDevitt²,

Shanks³

et al. 1969

British J Pharmacology

102

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“…An increased heart rate itself is inotropic, but because it tends to decrease left ventricular volume the increase in oxygen consumption is less than would occur in isolated muscle strips. This may be why Jorgensen et al 47 observed equally good prediction of myocardial oxygen consumption during exercise before and after propranolol had been given, and why Krasnow et al 49 showed that myocardial oxygen consumption per unit of SPTI increased by only 25% during maximal stimulation with isoproterenol. The effect that this would have would be to raise the critical DPTI: SPTI ratio from about 0.4-0.5 to about 0.5-0.6.…”

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confidence: 99%

Determinants and prediction of transmural myocardial perfusion.

Hoffman¹

1978

Circulation

204

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“…It is of interest that practolol, in a dose not affecting the peripheral vascular changes caused by isoprenaline, blocked the effects of isoprenaline on coronary flow and coronary fraction of cardiac output, but only attenuated its effect on coronary vascular resistance. This observation may be explained by the fact that cardiac output was still raised and that this increase in cardiac output might have caused secondary coronary vasodilatation (Hashimoto, Shigei, Imai, Saito, Yago, Uei & Clark, 1960;Krasnow, Rolett, Yurchak, Hood & Gorlin, 1964;Somani & Laddu, 1969;Lioy, 1967).…”

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confidence: 99%

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1971

British J Pharmacology

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Summary1. The effects of three /3-adrenoceptor blocking agents on isoprenaline induced changes in systemic and regional blood flow have been investigated in rats anaesthetized with pentobarbitone. The blood flow to the principal vascular beds was measured by the "Rb fractionation method.2. Isoprenaline infusion at a rate of 0 3 (1,g/kg)/min intravenously caused an increase in cardiac output and a decrease in peripheral resistance which affected different vascular fields unevenly. The coronary and carcass fractions of cardiac output increased while the cutaneous, renal and splenic fractions decreased. 3. Pretreatment with propranolol (2 mg/kg intravenously) blocked all isoprenaline effects. Practolol (8 mg/kg intravenously) lessened the effect on cardiac output but did not prevent the vascular effects except those on the coronary circulation. LB 46 (0-2 mg/kg) had less marked P-adrenoceptor blocking activity than propranolol (2-0 mg/kg).

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Isoproterenol and cardiovascular performance

Cited by 201 publications

References 44 publications

The cardio‐toxicity of isoprenaline during hypoxia

The cardio‐toxicity of isoprenaline during hypoxia

Determinants and prediction of transmural myocardial perfusion.

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