Coronary flow response after myocardial ischemia may predict level of functional recovery.
Is there a quantity, potentially measurable in the operating theater, which predicts rapid recovery of heart power output after surgical intervention with ischemia? We have enhanced our blood-perfused, ejecting, isolated rat heart model for use inside the magnet of an NMR spectrometer, in order to conduct fundamental research into cardioprotective techniques. To provide a baseline, we investigated the effect of normothermic ischemic insults of varying duration. Hemodynamic and metabolic data were collected, and analyzed to seek measures predictive of rapid recovery of aortic power output, which was selected as the most important measure of function. The presence of erythrocytes in the perfusate ensures that oxygen supply is sufficient to support a physiological workload, and that there is reserve coronary flow. On reperfusion, reactive hyperemia occurs: coronary flow increases to a peak, then declines to a steady value. This response was mathematically modeled, and the data for each of fifteen experiments were fitted to the model. Correlating power output recovery against time to reach peak coronary flow yielded the following equation: R = -0.45 log10tp + 1.74 where R is the ratio of power output ten minutes after reperfusion to that before the ischemic insult, and tp is the time taken to reach peak coronary flow, in seconds. The correlation is very significant (p = 0.005). In the clinic, coronary flow response on reperfusion could be used to predict the patient's need for post-operative support.
Houston
R J
RJ
Physiology Department, Faculty of Medical Sciences, University of Nijmegen, The Netherlands.
Skotnicki
S H
SH
Heerschap
A
A
Oeseburg
B
B
D000818:Animals; D003326:Coronary Circulation / Q000502:physiology*; D004912:Erythrocytes / Q000378:metabolism; D006324:Heart Arrest, Induced / Q000009:adverse effects / Q000379:methods*; D066298:In Vitro Techniques; D009682:Magnetic Resonance Spectroscopy; D008297:Male; D008955:Models, Cardiovascular; D009200:Myocardial Contraction / Q000502:physiology; D017202:Myocardial Ischemia / Q000503:physiopathology*; D015428:Myocardial Reperfusion Injury / Q000503:physiopathology / Q000517:prevention & control*; D010101:Oxygen Consumption; D010477:Perfusion; D051381:Rats; D017208:Rats, Wistar