Transmural distribution of myocardial blood flow during systole in the awake dog.

Abstract

This study was designed to quantitate transmural myocardial blood flow when coronary arterial inflow was limited to systole and during the subsequent reactive hyperemic response. Studies were performed in 10 awake dogs chronically prepared with electromagnetic flowmeters and pneumatic occluders on the left circumflex coronary artery. Intermittent coronary perfusion, confined to the interval of left ventricular systole or an equivalent period during diastole, was effected by an R wave-triggered solenoid valve connected to the occluder. To measure regional myocardial blood flow we injected radionuclidelabeled microspheres, 7-10 fim in diameter, into the left atrium. When arterial inflow was limited to systole, flow was normal in the subepicardial layers and was decreased as a linear function of tissue depth in the subendocardial layers. When coronary arterial inflow was limited to an equivalent interval in diastole, the transmural distribution of flow was uniform. When coronary flow was confined to systole for more than 20 seconds, the blood flow debt incurred elicited a reactive hyperemia similar to that following a total occlusion of equivalent blood flow debt. However, regional myocardial blood flow during the peak of reactive hyperemia following systolic perfusion was preferentially directed to the subendocardium, where underperfusion was most marked, whereas reactive hyperemia flow following a total occlusion of equiva-

A study of the routes by which protein passes from the pericardial cavity to the blood in rabbits.

“…This is surprising for any intrathoracic tissue since not only does the heart drain into the right lymph duct (Eliskova & Eliska, 1974a,b;lTlal, Kluge, Kerth & Gerbode, 1972), but so also do the pleural cavity (Courtice & Simmonds, 1949, 1954 and most of the lungs (Meyer, 1968; Leeds, thley, Sampson & Friedman, 1959). This particular route suggests a drainage of protein through the parietal pericardium, a conclusion in agreement with that ofKluge (1968 b) (Morgan, Guntheroth & iDillard, 1965; Banchero, Rutishauser, Tsakiris & Wood, 1967), whereas intramyocardial pressure is positive and fluctuates with the heart beat to reach levels as high as systolic blood pressure in systole (D'Silva, Mendel & Winterton, 1964;Kirk & Honig, 1964a, b;Hess & Bache, 1976;Baird, Adiseshiah & Okumori, 1976).…”

Doppler Estimation of Reduced Coronary Flow Reserve in Mice with Pressure Overload Cardiac Hypertrophy

“…However, the heart has to generate systolic pressure, and one would expect that the gradient between coronary arterial pressure and intramyocardial pressure during systole would remain low at least in the subendocardium. Indeed, when coronary flow is restricted to occur only during systole in dogs, there is relative under-perfusion of the subendocardium (Hess and Bache, 1976). In patients, we have observed similarly high systolic/diastolic velocity ratios in the right coronary arteries which supply mainly the right ventricle and both atria where the systolic compressive forces are lower (Cole and Hartley, 1977).…”

Doppler velocity measurements from large and small arteries of mice

“…The systolic component of coronary flow is more difficult to measure and is often ignored by coronary physiologists because systolic flow cannot perfuse actively contracting myocardium (54,61). Thus the significant increase in systolic coronary flow following TAC may indicate a redistribution of flow away from contracting myocardium or from endocardium to epicardium as the heart hypertrophies (27,28,60). CFR is relatively easy to measure in mice, appears to be reduced by most forms of heart disease, and could be used in place of ejection fraction as an index of global cardiac reserve in mice.…”