Myocardial and cerebral blood flow were determined with radiolabeled microspheres in 20 Sprague-Dawley rats during sinus rhythm and during stable but hemodynamically compromising ventricular tachycardias. In addition, in 10 animals the measurements were performed at hypotension induced by exsanguination. In controls (n = 10), myocardial and cerebral blood flow were 5.14 +/- 0.6 and 1.03 +/- 0.3 ml/g per minute, respectively. The range of myocardial blood flow values was markedly enlarged after onset of tachycardia induced by epicardial pacing. The mean values of myocardial blood flow were 5.80 +/- 1.9 ml/g per minute (n.s.) after 1 min and 7.46 +/- 3.9 ml/g per minute (n.s.) after 5 min. Cerebral blood flow, however, significantly decreased after 1 min (0.57 +/- 0.1 ml/g per minute, P < 0.01) and after 5 min (0.71 +/- 0.3 ml/per minute, P < 0.05). In contrast, 1 min after exsanguination myocardial blood flow significantly decreased (4.03 +/- 1.5 ml/g per minute, P < 0.05) and recovered after 5 min (6.06 +/- 1.2 ml/g per minute, n.s.) Cerebral blood flow was below control levels 1 min (0.70 +/- 0.2 ml/g per minute, P < 0.05) after onset of hypotension due to exsanguination and returned to normal values with the next 4 min (0.90 +/- 1 ml/g per minute, n.s.). The results suggest that stable but hemodynamically compromising ventricular tachycardias markedly affect cerebral blood flow, whereas in most cases myocardial blood flow is maintained within normal ranges, or even increases. An augmented myocardial autoregulation can be concluded from the autoregulatory index. This maintainance of regulatory ability might be due to the increase of myocardial oxygen consumption at decreased coronary perfusion pressure during tachycardias. In contrast, during hypovolemic hypotension, myocardial as well as cerebral blood flow decreased. During stable but hemodynamically compromising ventricular tachycardias, cerebral blood flow initially drops drastically and recovers slowly over the next 5 min. This finding contrasts with the results of hypovolemic and drug-induced hypotension models.