大鼠快速性心律失常诱发低血压期间的心肌和脑血流动力学

Myocardial and cerebral hemodynamics during tachyarrhythmia-induced hypotension in the rat.

作者信息

Hagendorff A, Dettmers C, Danos P, Pizzulli L, Omran H, Manz M, Hartmann A, Lüderitz B

机构信息

Department of Cardiology, University of Bonn, Germany.

出版信息

Circulation. 1994 Jul;90(1):400-10. doi: 10.1161/01.cir.90.1.400.

DOI:10.1161/01.cir.90.1.400

PMID:8026025

Abstract

BACKGROUND

The different vulnerabilities of heart and brain to hypotension and hypoxia have been discussed. Hemorrhagic or cardiogenic hypotension appears to cause greater cerebral lesions than drug-induced hypotension. The present model was established to evaluate myocardial blood flow (MBF) and function of the heart and cerebral blood flow (CBF) during tachyarrhythmias and to characterize the capacity of blood flow regulation in the heart and brain during tachycardia-induced borderline hypotension.

METHODS AND RESULTS

MBF and CBF were determined with radiolabeled microspheres. Coronary and central venous oxygen tensions were measured to estimate myocardial and cerebral oxygen consumption (MVO2 and CVO2). Measurements were performed in 62 Sprague-Dawley rats during sinus rhythm and high-rate left ventricular pacing and after hemorrhage. In control rats, MBF and CBF were 5.08 +/- 1.07 and 1.09 +/- 0.29 mL.g-1.min-1. MBF increased (7.21 +/- 1.98 mL.g-1.min-1, P < .05), whereas CBF decreased (0.99 +/- 0.29 mL.g-1.min-1, P = NS) during normotensive high-rate pacing. MBF and CBF dropped to 4.27 +/- 2.24 mL.g-1.min-1 (P = NS) and 0.68 +/- 0.29 mL.g-1.min-1 (P < .05) during pacing-induced borderline hypotension and decreased further during severe hypotension (1.77 +/- 0.81 mL.g-1.min-1, P < .01; 0.45 +/- 0.18 mL.g-1.min-1, P < .01). During borderline hypotension due to hemorrhage, MBF and CBF were 4.05 +/- 0.95 mL.g-1.min-1 (P = NS) and 0.71 +/- 0.23 mL.g-1.min-1 (P < .05). MVO2 and CVO2 were 72.7 +/- 15.4 and 12.7 +/- 3.3 mL.100 g-1.min-1 in control rats. MVO2 increased during normotensive pacing (100.3 +/- 27.4 mL.100 g-1.min-1, P = NS). Mean MVO2 was reduced during pacing-induced borderline hypotension (64.1 +/- 35.6 mL.100 g-1.min-1, P = NS) and severe hypotension (29.8 +/- 15.4 mL.100 g-1.min-1, P < .05). CVO2 decreased in correlation to CBF. Coronary and cerebrovascular resistance and autoregulation indexes indicated a maintenance of MBF regulation and a failure of CBF regulation during borderline hypotensive tachycardias. These results show a dissociation of MBF and CBF after onset of hypotensive tachycardias. Thus, brain tissue appears to be jeopardized at an earlier stage than myocardial muscle during tachyarrhythmias.

CONCLUSIONS

The proposed hypotension model is suitable to analyze tachyarrhythmia-induced hemodynamic changes and end-organ perfusion in the presence of myocardial dysfunction. It has the potential to test therapeutic strategies in the treatment of tachycardias.

摘要

背景

心脏和大脑对低血压和缺氧的不同易损性已被讨论。出血性或心源性低血压似乎比药物性低血压导致更严重的脑损伤。建立本模型是为了评估快速心律失常期间的心肌血流量（MBF）和心脏功能以及脑血流量（CBF），并表征心动过速诱发的临界低血压期间心脏和大脑的血流调节能力。

方法与结果

用放射性微球测定MBF和CBF。测量冠状动脉和中心静脉氧分压以估计心肌和脑氧消耗（MVO2和CVO2）。在62只Sprague-Dawley大鼠的窦性心律、高速率左心室起搏期间及出血后进行测量。在对照大鼠中，MBF和CBF分别为5.08±1.07和1.09±0.29 mL·g-1·min-1。在血压正常的高速率起搏期间，MBF增加（7.21±1.98 mL·g-1·min-1，P<.05），而CBF降低（0.99±0.29 mL·g-1·min-1，P=无显著性差异）。在起搏诱发的临界低血压期间，MBF和CBF分别降至4.27±2.24 mL·g-1·min-1（P=无显著性差异）和0.68±0.29 mL·g-1·min-1（P<.05），在严重低血压期间进一步降低（1.77±0.81 mL·g-1·min-1，P<.01；0.45±0.18 mL·g-1·min-1，P<.01）。在出血引起的临界低血压期间，MBF和CBF分别为4.05±0.95 mL·g-1·min-1（P=无显著性差异）和0.71±0.23 mL·g-1·min-1（P<.05）。对照大鼠的MVO2和CVO2分别为72.7±15.4和12.7±3.3 mL·100 g-1·min-1。在血压正常的起搏期间MVO2增加（100.3±27.4 mL·100 g-1·min-1，P=无显著性差异）。在起搏诱发的临界低血压期间平均MVO2降低（64.1±35.6 mL·100 g-1·min-1，P=无显著性差异），在严重低血压期间降低更明显（29.8±15.4 mL·100 g-1·min-1，P<.05）。CVO2与CBF呈相关性降低。冠状动脉和脑血管阻力及自动调节指数表明在临界低血压性心动过速期间MBF调节得以维持而CBF调节失败。这些结果表明低血压性心动过速发作后MBF和CBF出现分离。因此，在快速心律失常期间脑组织似乎比心肌更早受到损害。