INTERACTION OF PRESSURE-INDUCED AND FLOW-INDUCED RESPONSES IN PORCINE CORONARY RESISTANCE VESSELS
INTERACTION OF PRESSURE-INDUCED AND FLOW-INDUCED RESPONSES IN PORCINE CORONARY RESISTANCE VESSELS
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DOI：
10.1152/ajpheart.1991.261.6.h1706
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发表时间：
1991-12-01
影响因子：
--
通讯作者：
DAVIS, MJ
中科院分区：
文献类型：
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作者：
KUO, L;CHILIAN, WM;DAVIS, MJ
压力诱导的肌源性反应和流量诱导的血管舒张反应已被记录在冠状动脉阻力小动脉，但这两种机制的相互作用和流量介导的反应的性质还没有得到很好的理解。实验旨在定量研究压力和流量诱导的反应的相互作用，并表征在孤立的冠状小动脉中负责流量介导的扩张的物质的性质。从猪分离心外膜下小动脉（40-80 μ m），用两个玻璃微量移液管插管，然后通过独立的储液器系统加压。通过在相等和相反的方向上同时移动储液器来启动流动，从而产生压力梯度（Δ P）而不改变平均腔内压力（IP）。通过在相同方向上移动两个储液器来改变IP，以在没有流动的情况下改变肌源性张力（Δ P = 0）。当流量和压力升高时，流量介导的扩张与肌源性收缩竞争。此外，当IP减少时，流量增强肌源性扩张。流量引起的扩张的幅度是最大的血管张力（IP = 60 cmH 2 O）的中间水平，但在较高和较低水平的张力衰减。在存在流量（Δ P = 4 cmH 2 O）的情况下，压力-直径关系向上移动，肌源性反应的幅度减弱。双血管生物测定研究表明，可转移的物质从完整的内皮细胞释放的流量。吲哚美辛不影响血流诱导的扩张，但N（G）-单甲基-L-精氨酸或机械去除内皮可消除血流诱导的扩张。我们的研究结果表明，压力和流量引起的反应密切相互作用的竞争或添加剂，这取决于局部血管压力变化的方向。此外，流动诱导的扩张是由可转移的硝基血管扩张剂，而不是前列腺素类从内皮细胞的释放介导的。
Pressure-induced myogenic responses and flow-induced vasodilatory responses have been documented in coronary resistance arterioles, but the interaction of these two mechanisms and the nature of the flow-mediated response are not well understood. Experiments were designed to quantitatively study the interaction of pressure- and flow-induced responses and to characterize the nature of the substance responsible for flow-mediated dilation in isolated coronary arterioles. Subepicardial arterioles (40-80-mu-m) were isolated from pigs and cannulated with two glass micropipettes and then pressurized via independent reservoir systems. Flow was initiated by simultaneously moving the reservoirs in equal and opposite directions thus generating a pressure gradient (DELTA-P) without changing the mean intraluminal pressure (IP). IP was changed by moving both reservoirs in the same direction to alter myogenic tone in the absence of flow (DELTA-P = 0). Flow-mediated dilation competed with myogenic constriction when flow and pressure were elevated. Also, flow potentiated myogenic dilation when IP was decreased. The magnitude of flow-induced dilation was greatest at an intermediate level of vascular tone (IP = 60 cmH2O) but was attenuated at higher and lower levels of tone. In the presence of flow (DELTA-P = 4 cmH2O), pressure-diameter relationships were shifted upward, and the magnitude of myogenic responsiveness was attenuated. Double-vessel bioassay studies indicated that a transferable substance was released from intact endothelium in response to flow. Flow-induced dilation was not affected by indomethacin but was abolished by N(G)-monomethyl-L-arginine or by mechanical removal of endothelium. Our results indicate that pressure- and flow-induced responses closely interact either competitively or additively, depending on the direction of local vascular pressure changes. Moreover, flow-induced dilation was mediated by the release of a transferable nitrovasodilator rather than a prostanoid from endothelial cells.