Cogswell T L, Bernath G A, Raff H, Hoffmann R G, Klopfenstein H S
Am J Physiol. 1986 Nov;251(5 Pt 2):R916-22. doi: 10.1152/ajpregu.1986.251.5.R916.
During progressive cardiac tamponade in conscious dogs, cardiac output falls continuously while arterial blood pressure is maintained until cardiovascular decompensation by increases in total peripheral resistance (TPR). Plasma renin activity (PRA) is known to increase at decompensation. We hypothesized that the increase in TPR during cardiac tamponade was mediated by alpha-adrenergic and renin-angiotensin mechanisms. Twelve adult dogs were instrumented to measure cardiac output (electromagnetic flow probe), aortic and right atrial blood pressures, and intrapericardial pressure (IPP). TPR was calculated as the conscious euvolemic animals underwent cardiac tamponade induced by intrapericardial saline infusion at 20 ml/min. Six dogs underwent cardiac tamponade in the control condition (no medications) and during independent alpha- and beta-adrenergic and angiotensin-converting enzyme (ACE) inhibition. PRA and angiotensin II (ANG II) were measured during control tamponade. We found that TPR increased continuously to levels of greater than 200% of base line as IPP rose during cardiac tamponade (P less than 0.01). This increase in TPR was unaffected by beta-adrenergic or ACE blockade but was blunted by alpha-adrenergic blockade. PRA and ANG II increased only at decompensated tamponade (P less than 0.05) when arterial blood pressure had fallen by 30%. These changes in PRA and ANG II during tamponade were not altered by beta-blockade in six separate animals. We conclude that cardiac tamponade stimulates renin release and ANG II generation by a non-beta-receptor-mediated mechanism. The increase in TPR during cardiac tamponade is primarily dependent on alpha-adrenergic mechanisms, with a limited late contribution from the renin-angiotensin system.
在清醒犬进行性心脏压塞过程中，心输出量持续下降，而动脉血压在总外周阻力（TPR）增加导致心血管失代偿之前保持稳定。已知血浆肾素活性（PRA）在失代偿时会升高。我们假设心脏压塞期间TPR的增加是由α-肾上腺素能和肾素-血管紧张素机制介导的。对12只成年犬进行仪器植入，以测量心输出量（电磁血流探头）、主动脉和右心房血压以及心包内压（IPP）。在清醒的血容量正常动物以20 ml/min的心包内输注生理盐水诱导心脏压塞时计算TPR。6只犬在对照条件下（未用药）以及独立进行α-和β-肾上腺素能及血管紧张素转换酶（ACE）抑制时进行心脏压塞。在对照性心脏压塞期间测量PRA和血管紧张素II（ANG II）。我们发现，随着心脏压塞期间IPP升高，TPR持续增加至基线水平的200%以上（P<0.01）。TPR的这种增加不受β-肾上腺素能或ACE阻断的影响，但被α-肾上腺素能阻断所减弱。仅在失代偿性心脏压塞（动脉血压下降30%时，P<0.05）时PRA和ANG II才升高。在6只单独的动物中，心脏压塞期间PRA和ANG II的这些变化不受β-阻断的影响。我们得出结论，心脏压塞通过非β受体介导的机制刺激肾素释放和ANG II生成。心脏压塞期间TPR的增加主要依赖于α-肾上腺素能机制，肾素-血管紧张素系统的后期贡献有限。
