Hinojosa-Laborde C, Greene A S, Cowley A W
Department of Physiology, Medical College of Wisconsin, Milwaukee 53226.
Hypertension. 1988 Jun;11(6 Pt 2):685-91. doi: 10.1161/01.hyp.11.6.685.
Autoregulation of blood flow in various organ systems is a well-documented phenomenon. However, the net effect of these regional autoregulatory responses on the systemic circulation has not been studied in conscious rats despite the now extensive use of rats in cardiovascular research. The ability of the systemic circulation to autoregulate cardiac output has been proposed to play an important role in the development of increased vascular resistance in volume-dependent forms of hypertension. To better understand these events, we characterized responses to acute increases and decreases in blood volume in conscious areflexic rats that were chronically instrumented with arterial and venous catheters and an electromagnetic flow probe around the ascending aorta. Neurohumoral blockade was achieved with chlorisondamine (10 mg/kg), methscopolamine (0.5 mg/kg), captopril (1.0 mg/kg), and d(CH2)5Tyr(Me)arginine vasopressin (10 micrograms/kg). Mean arterial pressure was restored to normal levels with a constant i.v. norepinephrine infusion, which resulted in normal values of cardiac output, total peripheral resistance, and blood gases. Blood volume expansion (0.9 ml i.v. blood infusion for 6 minutes) increased cardiac output 9 +/- 1% and mean arterial pressure 30 +/- 3% and caused a 22 +/- 2% increase in total peripheral resistance (n = 7). Blood volume contraction (6-minute withdrawal of 0.9 ml of blood) decreased cardiac output 12 +/- 1% and mean arterial pressure 26 +/- 4%, which resulted in a 16 +/- 4% decrease in total peripheral resistance (n = 8). The slopes of the pressure-flow relationships during volume expansion were 0.24 and 0.41 during volume contraction, as compared with a nonautoregulating system (slope = 1) and a completely autoregulating system (slope = 0).(ABSTRACT TRUNCATED AT 250 WORDS)
各种器官系统中血流的自动调节是一个有充分文献记载的现象。然而,尽管目前大鼠在心血管研究中被广泛应用,但这些局部自动调节反应对体循环的净效应在清醒大鼠中尚未得到研究。有人提出,体循环自动调节心输出量的能力在容量依赖性高血压形式中血管阻力增加的发展中起重要作用。为了更好地理解这些事件,我们对长期植入动脉和静脉导管以及升主动脉周围电磁流量探头的清醒无反射大鼠对血容量急性增加和减少的反应进行了表征。通过使用氯筒箭毒碱(10毫克/千克)、甲基东莨菪碱(0.5毫克/千克)、卡托普利(1.0毫克/千克)和d(CH2)5Tyr(Me)精氨酸加压素(10微克/千克)实现神经体液阻断。通过持续静脉输注去甲肾上腺素将平均动脉压恢复到正常水平,这导致心输出量、总外周阻力和血气值正常。血容量扩张(静脉输注0.9毫升血液,持续6分钟)使心输出量增加9±1%,平均动脉压增加30±3%,并使总外周阻力增加22±2%(n = 7)。血容量收缩(抽取0.9毫升血液,持续6分钟)使心输出量减少12±1%,平均动脉压减少26±4%,导致总外周阻力减少16±4%(n = 8)。与非自动调节系统(斜率 = 1)和完全自动调节系统(斜率 = 0)相比,血容量扩张期间压力-流量关系的斜率在血容量收缩期间分别为0.24和0.41。(摘要截断于250字)