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Effect of adenosine‐induced controlled hypotension on canine myocardial performance, blood flow and metabolism

The effect of adenosine‐induced controlled hypotension (CH) on myocardial performance, blood flow, and metabolism was studied in nine pentobarbital‐anaesthetized, open‐chest dogs. Adenosine was continuously infused i. v. (0.69 0.06 and 1.36 0.11 mg/kg/min) at two stepwise increased rates (12–14 min‐periods) in order to induce approximately 20 and 40% reduction of the mean arterial pressure (MAP 62 4 and 43 1 mmHg, respectively). The reduction of MAP was associated with decreases in heart rate (6 2%, P<0.05 and 21 4%, P<0.01), left intraventricular systolic pressure (14 3%, P<0.01 and 32 3%, P<0.01), left ventricular end‐diastolic pressure (23 9%, P<0.05 and 42 9%, P<0.01) and ventricular intramyocardial systolic pressure (15 6% n. s. and 27 6%, P<0.01). The rate pressure product was markedly reduced by 49 3% (P<0.01) at the highest infusion rate. The mean coronary vein pressure (20.3 2.8 mmHg) was unaffected by the adenosine infusion. The systolic pressure time index (SPTI) was decreased by 33 3% (P<0.01) during the highest infusion rate of adenosine, while the diastolic perfusion time index (DPTI) was 15.4 2.2 mmHg s and remained unchanged. The DPTI:SPTI ratio increased by 40 13% (P<0.05), suggesting a sufficient endocardial oxygen supply. The coronary sinus blood flow (96 7 ml/min) increased by 40 16% (P<0.05), while the myocardial oxygen uptake (7.2 0.8 ml/min) decreased by 28 5% (P<0.01) during the highest infusion rate. The myocardial lactate uptake and the left ventricular subendocardial ECG (n = 4) were unchanged during CH. In conclusion, adenosine‐induced CH in the canine open‐chest preparation reduced myocardial work as well as oxygen uptake, and increased the total myocardial blood flow. No signs of regional myocardial ischaemia appeared, as judged from the unaffected myocardial lactate uptake and left ventricular sub‐endocardial ECG.