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Biomedical subjects

P Macho

Publications and source records attributed to P Macho.

24 records · Page 2Linked to original sources
PubMed1981

Regulation of large coronary arteries by increases in myocardial metabolic demands in conscious dogs.

In order to assess the effects of increasing myocardial metabolic demand on the large epicardial coronary arteries, we measured left circumflex coronary artery diameter (ultrasonic transit time technique) and blood flow in conscious dogs with chronically implanted transducers. Myocardial oxygen consumption was increased by pacing-induced tachycardia and aortic constriction, and monitored by multiplying left circumflex coronary arterial blood flow by coronary arterio-venous oxygen content difference. Increase of heart rate by 90 beats/min caused myocardial oxygen consumption to increase by 34 +/- 4.3% (1 SEM); coronary blood flow at constant arterial pressure to increase by 32 +/- 6.8%; and coronary diameter to increase by 0.07 +/- 0.01 mm, P less than 0.01. Aortic constriction, producing a 53 +/- 5.1% increase of left ventricular systolic pressure, caused myocardial oxygen consumption to increase by 49 +/- 7.2%, coronary blood flow to increase by 50 +/- 6.0%, and coronary diameter to increase 0.03 mm, P less than 0.01. The increases in coronary artery diameter were gradual, not immediate, in onset and not altered by beta-adrenergic blockade. Thus, increased myocardial metabolic demand dilates large epicardial coronary arteries, but with a slower response time than the rapid dilation of the smaller resistance vessels.

Adrenergic beta-Antagonists↗
PubMed1977

Coronary vascular resistance during halothane anesthesia.

To study the effect of halothane on the coronary circulation, the circumflex diastolic coronary vascular resistance was measured in the working heart and total mean coronary resistance (TCR) in the isolated nonworking heart of the dog during administration of 100 per cent oxygen and during administration of 2--3 per cent halothane in oxygen. In the working heart, when the diastolic aortic pressure was kept at a nearly control level, halothane induced decreases of 12 per cent in circumflex diastolic coronary vascular resistance and 18 per cent in left ventricular arteriovenous oxygen content difference and no significant change in diastolic coronary blood flow. This effect occurred in spite of the absence of any significant change of myocardial oxygen consumption. In the nonworking beating, arrested or fibrillating heart, halothane induced a decrease of 24 per cent in total mean coronary resistance. Since the decrease in circumflex diastolic coronary vascular resistance in the working heart connot be attributed to myocardial hypoxia and since the results in the isolated nonworking heart eliminate the influences of mechanical and neurohumoral factors on coronary resistance, it is concluded that the observed decrease in resistance is probably due to vasodilation produced by a direct action of halothane on the coronary vessels. This effect was not modified by beta-adrenergic blockade.

Animals↗
PubMedDate not supplied

Regulation of large coronary vessels by adrenergic mechanisms in conscious dogs.

The effects of alpha and beta adrenergic stimulation were examined in conscious dogs on measurements of left circumflex coronary blood flow and coronary arterial diameter and on calculations of mean coronary resistance (MCR) and left circumflex coronary internal cross-sectional area (CSA). Methoxamine (50 micrograms/kg/min), after transiently increasing left circumflex coronary dimensions, induced sustained reductions in left circumflex coronary diameter (9 +/- 2%) and CSA (27 +/- 5%) at a time when mean arterial pressure rose by 65 +/- 5%, left ventricular (LV) dP/dt had decreased only slightly, and heart rate and mean coronary blood flow were at control levels. Isoproterenol, (0.1 microgram/kg/min), increased heart rate by 66 +/- 8%, LV dP/dt by 58 +/- 5%, and CSA by 17 +/- 3%, while it decreased mean arterial pressure by 12 +/- 1% and MCR by 44 +/- 5%. After beta 1 adrenergic receptor blockade and with heart rate held constant, isoproterenol did not increase LV dP/dt but decreased mean arterial pressure similarly (13 +/- 2%) and induced attenuated increases in CSA (6 +/- 1%), and decreases in MCR (17 +/- 3%). After combined beta 1 and beta 2 adrenergic receptor blockades isoproterenol induced no significant effects. Thus, in the conscious dog, large coronary vessels not only react passively to changes in aortic pressure but also undergo substantial active changes. Alpha adrenergic stimulation is sufficiently powerful to reduce CSA, despite the opposing elevation of distending pressure. Moreover, large vessels appear to be regulated by beta 1 adrenergic mediated increase in myocardial metabolic demands, as well as by beta 2 adrenergic medicated vasodilation.

Animals↗