进行性肺损伤中肺血管舒缩控制的机制失衡
Mechanistic imbalance of pulmonary vasomotor control in progressive lung injury.
作者信息
Fullerton D A, Hahn A R, McIntyre R C
机构信息
Department of Surgery, University of Colorado, Denver, USA.
出版信息
Surgery. 1996 Jan;119(1):98-103. doi: 10.1016/s0039-6060(96)80220-0.
BACKGROUND
Pulmonary hypertension is the major hemodynamic feature of progressive lung injury. We hypothesized that the mechanisms of pulmonary vasorelaxation become progressively impaired in progressive lung injury. The purpose of this study was to examine the following mechanisms of pulmonary vasorelaxation in a rat model of monocrotaline-induced progressive lung injury: endothelial-dependent cyclic guanosine monophosphate-mediated relaxation (response to acetylcholine), endothelial-independent cyclic guanosine monophosphate-mediated relaxation (response to nitroprusside), beta-adrenergic cyclic adenosine monophosphate-mediated relaxation (response to isoproterenol), and hypoxic pulmonary vasoconstriction.
METHODS
Rats were studied 2, 7, and 14 days after monocrotaline injection (100 mg/kg intraperitoneally). Pulmonary vasomotor control mechanisms were studied in isolated pulmonary artery rings. Controls were studied 14 days after saline injection. Statistical analysis was by ANOVA; p < 0.05 was considered significant.
RESULTS
A progressive impairment of pulmonary vasorelaxation was observed. By 14 days after monocrotaline injection acetylcholine produced only 25% +/- 5% relaxation versus 95% +/- 5% in controls (p < 0.05), nitroprusside produced 46% +/- 5% relaxation versus 100% in controls (p < 0.05), and isoproterenol produced only 18% +/- 5% relaxation versus 94% +/- 4% in controls (p < 0.05). At the same time hypoxic pulmonary vasoconstriction became progressively exaggerated.
CONCLUSIONS
Progressive dysfunction of pulmonary vasomotor control may contribute to the pulmonary hypertension seen in progressive lung injury.
背景
肺动脉高压是进行性肺损伤的主要血流动力学特征。我们推测在进行性肺损伤中，肺血管舒张机制会逐渐受损。本研究的目的是在野百合碱诱导的进行性肺损伤大鼠模型中，研究肺血管舒张的以下机制：内皮依赖性环磷酸鸟苷介导的舒张（对乙酰胆碱的反应）、非内皮依赖性环磷酸鸟苷介导的舒张（对硝普钠的反应）、β-肾上腺素能环磷酸腺苷介导的舒张（对异丙肾上腺素的反应）以及低氧性肺血管收缩。
方法
在腹腔注射野百合碱（100mg/kg）后2天、7天和14天对大鼠进行研究。在离体肺动脉环中研究肺血管运动控制机制。对照组在注射生理盐水14天后进行研究。采用方差分析进行统计学分析；p<0.05被认为具有统计学意义。
结果
观察到肺血管舒张进行性受损。在野百合碱注射后14天，乙酰胆碱产生的舒张仅为25%±5%，而对照组为95%±5%（p<0.05）；硝普钠产生的舒张为46%±5%，而对照组为100%（p<0.05）；异丙肾上腺素产生的舒张仅为18%±5%，而对照组为94%±4%（p<0.05）。同时，低氧性肺血管收缩逐渐加剧。
结论
肺血管运动控制的进行性功能障碍可能导致进行性肺损伤中出现的肺动脉高压。
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