Magder S
Division of Critical Care Medicine, Royal Victoria Hospital, Montreal, Quebec, Canada.
Circ Res. 1990 Jul;67(1):209-20. doi: 10.1161/01.res.67.1.209.
Arterial pressure at zero flow (Pz = 0) that is higher than venous pressure (Pv) in dynamic pressure-flow relations has been explained by the presence of an arteriolar Starling resistor (SR) mechanism (i.e., vascular waterfall) or the discharge of vascular capacitance. To determine which was predominant, I studied in vivo hind limbs of 18 anesthetized dogs in which femoral arteries were cannulated with in-line electromagnetic flow probes to measure inflow (Qin), Pv was controlled, and collateral flow was eliminated with a tourniquet. Pz = 0 was obtained by turning flow to zero. Three tests were applied: 1) Pv was raised in steps with either constant Qin or constant arterial pressure (Pa) to determine the pressure at which upstream vascular characteristics were affected by a change in Pv, 2) the time to reach Pz = 0 was varied to determine compliance effects, and 3) an equation was developed to determine if experimentally derived parameters could explain Pz = 0 without invoking an SR. With constant Qin and a Pz = 0 of 56.9 +/- 11.7 mm Hg (time to Pz = 0, 3 seconds), Pv could be raised by 9.6 +/- 6.2 to 16.3 +/- 6.0 mm Hg before Pa increased, and with constant Pa, Pv could be raised by 6.8 +/- 7.3 to 14.0 +/- 8.0 mm Hg before Qin decreased. With increasing times to reach Pz = 0, Pz = 0 initially dropped precipitously, but then decreased by only a small amount over the next 5-10 seconds even though arterial pressure was much above Pv. This could be explained by an SR mechanism with a critical pressure of 42.3 +/- 11.4 mm Hg and an arterial compliance of 0.0104 +/- 0.0023 ml.mm Hg-1 (n = 6). There was no value for the compliance that described the results when the arterial outflow pressure was Pv. Thus, this study supports the hypothesis that an SR mechanism is present in the vascular system. It is most likely precapillary, and in the resting limb, it has a value of 40-50 mm Hg. However, Pz = 0 in dynamic pressure-flow studies of less than 4 seconds is also greatly influenced by capacitance effects and the initial Pa.
在动态压力-流量关系中,零流量时的动脉压(Pz = 0)高于静脉压(Pv),这已通过存在小动脉的斯塔林电阻器(SR)机制(即血管瀑布)或血管顺应性的释放来解释。为了确定哪种机制占主导,我对18只麻醉犬的后肢进行了体内研究,在这些犬的股动脉中插入在线电磁流量探头以测量流入量(Qin),控制Pv,并使用止血带消除侧支血流。通过将流量调至零来获得Pz = 0。应用了三项测试:1)在Qin恒定或动脉压(Pa)恒定的情况下逐步提高Pv,以确定上游血管特性受Pv变化影响时的压力;2)改变达到Pz = 0的时间以确定顺应性的影响;3)建立一个方程以确定实验得出的参数是否可以在不引入SR的情况下解释Pz = 0。在Qin恒定且Pz = 0为56.9±11.7 mmHg(达到Pz = 0的时间为3秒)的情况下,在Pa升高之前,Pv可以升高9.6±6.2至16.3±6.0 mmHg,在恒定Pa的情况下,在Qin降低之前,Pv可以升高6.8±7.3至14.0±8.0 mmHg。随着达到Pz = 0的时间增加,Pz = 0最初急剧下降,但在接下来的5 - 10秒内仅少量下降,尽管动脉压远高于Pv。这可以用临界压力为42.3±11.4 mmHg且动脉顺应性为0.0104±0.0023 ml·mmHg⁻¹的SR机制来解释(n = 6)。当动脉流出压为Pv时,没有描述结果的顺应性值。因此,本研究支持血管系统中存在SR机制的假设。它很可能位于毛细血管前,在静息肢体中,其值为40 - 50 mmHg。然而,在小于4秒的动态压力-流量研究中,Pz = 0也受到顺应性效应和初始Pa的极大影响。