Department of Medicine, Medical College of Wisconsin, Milwaukee, WI, USA.
Cardiovascular Center, Medical College of Wisconsin, Milwaukee, WI, USA.
Physiol Rep. 2021 Feb;9(3):e14507. doi: 10.14814/phy2.14507.
The objective of this study was to measure flow-mediated dilation (FMD) prior to and following transient increases in intraluminal pressure (IILP) in resistance arterioles isolated from subjects with and without coronary artery disease (CAD) (CAD and non-CAD) and non-CAD subjects with hypertension.
Arterioles were isolated from discarded surgical tissues (adipose and atrial) from patients without coronary artery disease (non-CAD; ≤1 risk factor, excluding hypertension), with CAD, and non-CAD patients with hypertension (hypertension as the only risk factor). To simulate transient hypertension, increased IILP was generated (150 mmHg, 30 min) by gravity. Arterioles were constricted with endothelin-1, followed by FMD and endothelial-independent dilation prior to and following exposure to IILP.
IILP reduced FMD in non-CAD and CAD arterioles relative to pre-IILP (p <.05 at 100 cmH O). In contrast, arterioles from non-CAD hypertensive subjects exhibited no reduction in maximal FMD following IILP (p = .84 at 100 cmH O). FMD was reduced by L-NAME prior to IILP in non-CAD hypertensive patients (p < .05 at 100 cmH O); however, following IILP, FMD was inhibited by peg-cat (p < .05 at 100 cmH O), indicating a switch from NO to H O as the mechanism of dilation.
Acute exposure (30 min) to IILP (150 mmHg) attenuates the magnitude of FMD in non-CAD and CAD resistance arterioles. The presence of clinically diagnosed hypertension in non-CAD resistance arterioles preserves the magnitude of FMD following IILP as a result of a compensatory switch from NO to H O as the mechanism of dilation.
本研究旨在测量患有和不患有冠状动脉疾病（CAD）的患者（CAD 和非 CAD）以及非 CAD 合并高血压患者的阻力小动脉在腔内压力（IILP）短暂升高前后的血流介导的扩张（FMD）。
从小动脉中分离出来自无冠状动脉疾病（非 CAD；≤1 个危险因素，不包括高血压）、CAD 和非 CAD 合并高血压患者（高血压为唯一危险因素）的废弃手术组织（脂肪组织和心房组织）。通过重力产生升高的 IILP（150mmHg，30min）来模拟短暂性高血压。用内皮素-1使小动脉收缩，然后在暴露于 IILP 之前和之后测量 FMD 和内皮非依赖性扩张。
与 IILP 前相比，非 CAD 和 CAD 小动脉中的 IILP 降低了 FMD（p<.05，在 100cmH2O 时）。相比之下，非 CAD 合并高血压患者的小动脉在 IILP 后 FMD 没有降低（在 100cmH2O 时 p=0.84）。在非 CAD 合并高血压患者中，L-NAME 在 IILP 前降低了 FMD（p<.05，在 100cmH2O 时）；然而，在 IILP 后，peg-cat 抑制了 FMD（p<.05，在 100cmH2O 时），表明扩张的机制从 NO 切换为 H2O。
急性暴露（30min）于 IILP（150mmHg）会降低非 CAD 和 CAD 阻力小动脉的 FMD 幅度。在非 CAD 阻力小动脉中存在临床诊断的高血压会导致 FMD 在 IILP 后保持不变，这是由于扩张机制从 NO 切换为 H2O 所致的代偿性变化。
