Increase In Myocardial Oxygen Demand Research Articles

Myocardial oxygen consumption and blood flow during nicotine infusion: effect of combined alpha- and beta-adrenergic blockade.

The effect of combined alpha- and beta-adrenergic blockade with phenoxybenzamine and propranolol, respectively, on changes in left ventricular myocardial oxygen consumption and blood flow during nicotine administrations (36 micrograms/kg/min, i.v.) was evaluated in anesthetized, open-chest dogs. Myocardial blood flow was estimated by injection of 8 to 10 micrometers diameter radioactive microspheres into the left atrium, and myocardial oxygen consumption was computed from the Fick principle. Before adrenergic blockade, nicotine caused a market (+151%) elevation in myocardial oxygen consumption and a parallel increase in myocardial blood flow. The increase in myocardial blood flow was uniform transmurally. These cardiac changes were accompanied by elevations in systemic arterial and left atrial pressures, peripheral vascular resistance, and heart rate, but by no change in aortic flow or in myocardial contractility. After adrenergic blockade, nicotine caused somewhat lesser, though still marked, elevations in myocardial oxygen consumption (+60%) and blood flow (+43%). Again, myocardial blood flow increases were uniform transmurally. Also, nicotine-induced increases in systemic arterial and left atrial pressure and in peripheral vascular resistance persisted after adrenergic blockade, whereas heart rate remained constant and aortic flow and myocardial contractility declined. The results indicate that nonadrenergic mechanisms contribute significantly to the increase in myocardial oxygen demand during nicotine infusion.

Effect of carbon monoxide on cardiovascular disease

Carbon monoxide exposure from heavy smoking or heavy atmospheric carbon monoxide pollution depresses myocardial function in patients with coronary heart disease, aggravates angina pectoris, aggravates intermittent claudication of the calf or thigh, increases myocardial ischemia in patients with clinical and subclinical coronary heart disease, and contributes to an increased incidence of nonfatal and fatal myocardial infarction and sudden death from coronary heart disease. Carbon monoxide contributes to the increase in nonfatal and fatal myocardial infarction and in sudden death from coronary heart disease in cigarette smokers by (a) carboxyhemoglobin interfering with myocardial oxygen delivery at the time nicotine has caused an increase in myocardial oxygen demand, aggravating an episode of myocardial ischemia, (b) the negative inotropic effect of carboxyhemoglobin aggravating an attack of myocardial ischemia, (c) carboxyhemoglobin reducing the threshold for ventricular fibrillation during an episode of myocardial ischemia, and (d) carboxyhemoglobin increasing platelet stickiness, thereby, increasing a thrombotic tendency. Furthermore, experimental data indicate that exposure to carbon monoxide in concentrations found in heavy tobacco smokers or in persons with heavy occupational exposure to carbon monoxide plays a role in the pathogenesis of cardiovascular disease.

Effects of ouabain on coronary and systemic vascular resistance and myocardial oxygen consumption in patients without heart failure

The effect of digitalis glycosides on vascular resistance varies from one vascular bed to another and is also related to the hemodynamic state of the patient. To determine whether the rate of infusion is also a determinant of the vasoactive response the effect of various infusion rates of ouabain on the coronary and systemic beds was examined and the associated changes in myocardial oxygen consumption in patients without heart failure were quantitated. A 10 second and 2 minute infusion of ouabain (15 μg/kg body weight) produced 18.1 ± 5.6 percent and 7.5 ± 1.7 percent increases in mean arterial pressure and 23.7 ± 9.8 percent and 17.6 ± 7.5 percent increases in systemic vascular resistance, respectively ( P <0.05 for each). A 15 minute infusion produced no statistically significant change in either variable. Coronary vascular resistance increased 13.4 ± 5.2 percent ( P <0.05) after a 10 second infusion but did not change during or after a 15 minute infusion. The 10 second infusion was also associated with transient deterioration of myocardial lactate metabolism. Thirty minutes after ouabain administration mean arterial pressure had returned to control levels, but myocardial oxygen consumption remained increased by 12.5 ± 3.9 percent ( P <0.025), indicating that ouabain produces a net increase in myocardial oxygen demand in patients without heart failure. Rapid intravenous administration of ouabain produces systemic and coronary arteriolar constriction that may lead to clinical deterioration. These effects can be avoided by slower delivery of the drug. Even in patients without heart failure, the increase in myocardial oxygen consumption with full digitalization is small.

ANTAGONISM OF MORPHINE WITH NALOXONE IN DOGS: CARDIOVASCULAR EFFECTS WITH SPECIAL REFERENCE TO THE CORONARY CIRCULATION

The cardiovascular effects of naloxone 15 microgram/kg following morphine 2.0 mg/kg were studied in closed-chest dogs during light nitrous oxide-halothane anaesthesia. The bolus injection of naloxone caused an increase in heart rate (73%), cardiac output (20%) and mean arterial pressure (20%). Total peripheral resistance was unaffected. LV dP/dt max and LV dP/dt max/IP increased by 25% and 14% respectively, but positive inotropic effects could not be shown when load data, heart rate and the decrease in left ventricular ejection fraction (22%) were taken into consideration. The cardiovascular stimulation resulted in an increase in myocardial oxygen demand (66%) which was met by an increase in coronary blood flow (59%). The data suggest that the antagonism of narcotics with high doses of naloxone may impair the myocardial oxygen supply in patients suffering from coronary insufficiency. It is concluded that naloxone should be titrated for each patient to ensure adequate reversal of respiratory depression and to avoid circulatory stress.

Influence of perfusion pressure and heart rate on local myocardial flow in the collateralized heart with chronic coronary occlusion

We studied the influence of controlled changes in perfusion pressure and heart rate on the regional distribution of myocardial flow in normal dogs and in dogs with multiple chronic coronary artery occlusions but without infarctions. Local myocardial blood flow was determined with the tracer microsphere technique. By step-wise altering of systemic blood pressure during maximal vasodilation classical pressure flow relations were obtained. One week after complete chronic occlusion a functionally and anatomically well-defined compartmentation of blood flow was found. The dilatory reserve is clearly compromised not only in the collateral-dependent myocardium but also in the apparently normal myocardium which delivers collateral flow. An “arterio-arterial shunting” mechanism is shown to exist. Several months after coronary occlusion, regional myocardial flow is still non-homogeneous. Although the coronary dilatory capacity of the collateralized myocardium is nearly normal, that of the normal myocardium is found to be higher than normal. Vessel growth in both areas is discussed as being responsible for this phenomenon. Right ventricular pacing during maximal vasodilation produces a flow decrease to the endocardial muscle layers in normal dogs, while the epicardial flow is unchanged. One week after complete chronic coronary occlusion pacing during maximal vasodilation reduces the dilatory capacity in the collateralized areas to such an extent that the supplementary increase in myocardial oxygen demand will induce ischemia because of the compromised oxygen supply.

Coronary circulation during heavy exercise in control subjects and patients with coronary heart disease.

Abstract. Coronary and systemic circulation has been measured in 10 patients with coronary heart disease (CHD) and in 11 control subjects during 2–3 periods of increasing exercise loads. The highest work load was close to the maximal tolerable exercise level. In control subjects the maximal coronary flow during heavy exercise increased to 460% of the resting value. The myocardial (a‐v)O2 difference varied considerably inter‐ and intraindividually with increasing work load, but calculated for the group this (a‐v)O2 difference did not change significantly. The increase in myocardial oxygen demand was thus met almost exclusively by an increase in coronary flow. The myocardial oxygen uptake increased fourfold from rest to heavy exercise with a parallel fourfold increase in the BP8 × HR product, with a linear relationship over the whole range of values, suggesting that this product is a good index of myocardial oxygen uptake. In CHD patients the coronary flow response to moderate exercise was the same as in control subjects. During heavy exercise, however, the coronary flow increase was lower in relation to the BP8 × HR product than in the control subjects. Coronary vascular resistance did not decrease to the same level as in the controls. The demand for increase in oxygen uptake was met through a compensatory increase in myocardial (a‐v)O2 difference, thus making the necessary oxygen delivery possible. During the heaviest exercise, however, a significantly lower myocardial oxygen consumption was recorded in relation to the BP8 × HR product than in the control subjects. This was interpreted as an inadequate oxygen supply, leading to decreased myocardial contractility. The impaired myocardial performance was best demonstrated in two patients with exercise‐provoked angina pectoris who developed rapidly increasing left atrial pressure.