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Influence of adenosine–induced hypotension on the canine myocardium rendered acutely ischaemic by artificial stenosis
Author(s) -
ÖWall A.,
Rudehill A.,
Sylvén C.,
Sollevi A.
Publication year - 1988
Publication title -
acta anaesthesiologica scandinavica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.738
H-Index - 107
eISSN - 1399-6576
pISSN - 0001-5172
DOI - 10.1111/j.1399-6576.1988.tb02738.x
Subject(s) - medicine , cardiology , adenosine , blood flow , heart rate , stenosis , anesthesia , ischemia , blood pressure
An open–chest preparation was carried out in 14 pentobarbitone anaesthetized dogs in order to evaluate the myocardial effects of controlled hypotension induced by adenosine in the presence of a severe coronary stenosis that caused ischaemia of the left anterior ventricular wall. Myocardial performance, blood flow and metabolism were studied before and during a 78 ± 3% reduction of flow in the left anterior descending coronary artery (LAD) and during adenosine–induced hypotension (approximately 40% reduction of the mean arterial pressure) in the presence of the LAD stenosis. The LAD stenosis decreased the myocardial lactate uptake ( P <0.01), increased ST–T segment depression ( P <0.05) of the left ventricular subendocardial ECG, and reduced cardiac output by 10% ( P <0.05). In the presence of stenosis, the mean arterial pressure was reduced by adenosine from 10.4 ± 0.6 kPa to 6.3 ± 0.2 kPa for 15 min. Heart rate decreased by 22% ( P <0.01). There was no change in cardiac output during hypotension, while the rate–pressure product decreased by 47% ( P < 0.01) and myocardial oxygen consumption decreased by 30 ±7%,. Adenosine increased the coronary sinus blood flow by 52% ( P <0.01), while the LAD flow distal to the stenosis was not significantly reduced. Myocardial lactate uptake was not further reduced and subendocardial ECG signs of ischaemia were not aggravated by the hypotension. In conclusion, adenosine–induced hypotension did not aggravate the subendocardial ECG signs of acute poststenotic myocardial ischaemia. Nor did myocardial lactate determinations indicate aggravation of myocardial ischaemia. Reduced myocardial oxygen demand, as indicated by a reduced rate–pressure product and reduced myocardial oxygen consumption and heart rate, probably counteracted aggravation of ischaemia during the induced hypotension.