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大鼠对革兰氏阴性菌血症的心肺反应。

Cardiopulmonary response of the rat to gram-negative bacteremia.

作者信息

Pass L J, Schloerb P R, Pearce F J, Drucker W R

出版信息

Am J Physiol. 1984 Mar;246(3 Pt 2):H344-50. doi: 10.1152/ajpheart.1984.246.3.H344.

Abstract

Hemodynamic and respiratory effects of a continuous 5-h intravenous infusion of live Escherichia coli were studied in rats. Control animals were infused with saline. Rats infused with 1.8 +/- 0.4 X 10(10) bacteria/h did not survive a 5-h infusion. These animals developed early hypotension and reduced cardiac output (CO) measured by thermal dilution technique. Rats infused with 8.0 +/- 0.4 X 10(9) bacteria/h survived a 5-h infusion with hypotension and reduced CO occurring later in the course of bacteremia. Heart rate was markedly elevated in both septic groups. Arterial blood gas measurements revealed that partial pressure of O2 was not affected by bacteremia, but partial pressure of CO2 was significantly decreased. Arterial pH remained within the normal range indicating respiratory compensation of a metabolic acidosis. Since hypotension and reduced CO were accompanied by a fall in right atrial pressure (RAP) during bacteremia, a third septic group was studied to evaluate cardiac performance during volume loading. After 3-5 h of bacteremia, a 40% reduction in CO was associated with a significant drop in arterial pressure and RAP. Despite volume loading, ventricular stroke work and arterial pressure were significantly reduced compared with control animals. The results indicate that severe gram-negative bacteremia produces myocardial depression in the rat. This model can be useful for further studies of cardiac dysfunction during sepsis.

摘要

研究了在大鼠中持续5小时静脉输注活大肠杆菌的血流动力学和呼吸效应。对照动物输注生理盐水。每小时输注1.8±0.4×10¹⁰个细菌的大鼠在5小时输注期间未能存活。这些动物出现早期低血压,并通过热稀释技术测量的心输出量(CO)降低。每小时输注8.0±0.4×10⁹个细菌的大鼠在5小时输注期间存活,但在菌血症过程后期出现低血压和CO降低。两个脓毒症组的心率均显著升高。动脉血气测量显示,O₂分压不受菌血症影响,但CO₂分压显著降低。动脉pH值保持在正常范围内,表明存在代谢性酸中毒的呼吸代偿。由于菌血症期间低血压和CO降低伴随着右心房压力(RAP)下降,因此研究了第三个脓毒症组以评估容量负荷期间的心脏功能。菌血症3 - 5小时后,CO降低40%与动脉压和RAP显著下降相关。尽管进行了容量负荷,但与对照动物相比,心室搏功和动脉压仍显著降低。结果表明,严重革兰氏阴性菌血症可导致大鼠心肌抑制。该模型可用于进一步研究脓毒症期间的心脏功能障碍。

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