Hagendorff A, Dettmers C, Omran H, Pizzulli L, Hartmann A, Lüderitz B
Department of Cardiology, University of Bonn, Germany.
Res Exp Med (Berl). 1994;194(3):147-55. doi: 10.1007/BF02576375.
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.
在20只Sprague-Dawley大鼠的窦性心律期间以及稳定但血流动力学受损的室性心动过速期间，使用放射性微球测定心肌和脑血流量。此外，在10只动物中，在放血诱导的低血压状态下进行测量。在对照组（n = 10）中，心肌和脑血流量分别为每分钟5.14±0.6和1.03±0.3 ml/g。在心外膜起搏诱导心动过速发作后，心肌血流量值的范围明显扩大。心动过速发作1分钟后心肌血流量的平均值为每分钟5.80±1.9 ml/g（无统计学意义），5分钟后为每分钟7.46±3.9 ml/g（无统计学意义）。然而，脑血流量在1分钟后（每分钟0.57±0.1 ml/g，P<0.01）和5分钟后（每分钟0.71±0.3 ml/g，P<0.05）显著降低。相比之下，放血1分钟后心肌血流量显著降低（每分钟4.03±1.5 ml/g，P<0.05），5分钟后恢复（每分钟6.06±1.2 ml/g，无统计学意义）。由于放血导致低血压发作1分钟后脑血流量低于对照水平（每分钟0.70±0.2 ml/g，P<0.05），并在接下来的4分钟内恢复到正常值（每分钟0.90±1 ml/g，无统计学意义）。结果表明，稳定但血流动力学受损的室性心动过速显著影响脑血流量，而在大多数情况下，心肌血流量保持在正常范围内，甚至增加。从自动调节指数可以推断心肌自动调节增强。这种调节能力的维持可能是由于心动过速期间冠状动脉灌注压降低时心肌氧消耗增加。相比之下，在低血容量性低血压期间，心肌和脑血流量均降低。在稳定但血流动力学受损的室性心动过速期间，脑血流量最初急剧下降，并在接下来的5分钟内缓慢恢复。这一发现与低血容量性和药物性低血压模型的结果形成对比。
