Low cardiac output abolishes cardiovascular responses to infra-renal aortic cross-clamping in the pig

被引:6
|
作者
SeemanLodding, H
Biber, B
Ponten, J
Sundeman, H
Winso, O
机构
[1] GOTHENBURG UNIV,SAHLGRENS HOSP,DEPT ANESTHESIOL,S-41685 GOTHENBURG,SWEDEN
[2] UMEA UNIV HOSP,DEPT ANESTHESIOL,S-90185 UMEA,SWEDEN
关键词
pigs; low cardiac output; infra-renal aortic clamping; pericardial pressure; portal blood flow; preportal vascular resistance; renal blood flow; renal vascular resistance;
D O I
10.1111/j.1399-6576.1997.tb04671.x
中图分类号
R614 [麻醉学];
学科分类号
100217 ;
摘要
Background: Previous data suggest that preoperative myocardial dysfunction is associated with an altered cardiac response to infra-renal aortic cross-clamping (AXC). This study was designed to further explore how acute reductions in stroke volume and cardiac output influence the systemic, preportal and renal circulatory responses to AXC. Methods: In chloralose-anesthetized normoventilated pigs, graded increases in pericardial pressure (P-PERICARD) were obtained by local infusions of dextran. Measurements included cardiac output (CO, thermodilution), mean blood pressure proximal to the aortic clamping site (MAP(PROX)) and ultrasonic flowmetry for portal (Q(PORT)) and renal (Q(REN)) blood flows. In all animals, measurements were made a) prior to AXC, b) at the end of a 5 min AXC period and, c) 5 min following declamping. These recordings were repeated during control (P-PERiCARD 0 cmH(2)O) and during stages with increased P-PERICARD (4 and 8 cmH(2)O, respectively). Results: Pericardial infusions of dextran produced hemodynamic responses that in magnitude were proportional to P-PERICARD levels. Stroke volume, CO and mean arterial pressure decreased, while systemic vascular resistance (SVR) increased. In the preportal tissues, vascular resistance increased and Q(PORT) decreased. Similarly, in the kidney, vascular resistance and Q(REN) decreased, but only at a P-PERICARD of 8 cmH(2)O. At control, AXC increased SVR, MAP(PROX), Q(PORT) and both renal and preportal vascular resistances. When P-PERICARD was increased to 4 cm H2O, the responses to AXC concerning SVR and MAP(PROX) were not significantly altered, while renal and preportal circulatory responses were blunted. At stages with a P-PERICARD of 8 cmH(2)O, we could not demonstrate any circulatory responses to AXC. Conclusions: AXC-induced systemic, preportal and renal circulatory responses are inhibited during a condition of acutely lowered cardiac output. (C) Acta Anesthesiologica Scandinavica 41 (1997).
引用
收藏
页码:232 / 238
页数:7
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