Hexobendine demonstrates anti-anginal properties in animal models by increasing myocardial blood flow and protecting against hypoxia without antagonizing catecholamine effects.
Answers are grounded in this paper and cite their sources.
Hexobendine merits evaluation in ischemic models; leaves open any role in human angina therapy.
In cats anaesthetized with pentobarbitone sodium, hexobendine (0.25 mg/kg) markedly increased myocardial blood flow (measured using a heat clearance technique) and usually decreased myocardial metabolic heat production, without influencing cardiac contractility or systemic arterial blood pressure. These effects lasted for about 45 min.2. Larger doses (0.5 and 1.0 mg/kg) decreased systemic arterial blood pressure and the rate of rise of the left ventricular pressure pulse (dp/dt), although left ventricular end-diastolic pressure was usually increased. This is indicative of a decrease in myocardial contractility.3. In a concentration of 5 x 10(-6) g/ml., hexobendine protected isolated rabbit atria against the decrease in contractility that follows the removal of oxygen.4. Hexobendine did not antagonize the systemic and myocardial effects of infusions of adrenaline and noradrenaline, nor (except in concentrations of 10(-5) g/ml.) the increase in contractility induced by these catecholamines on isolated rabbit atria.
No takes yet. Share an insight, caveat, or question.
McINNES et al. (1969) studied this question.
Synapse has enriched 10 related papers. Consider them for comparative context: