一氧化碳系统对慢性肺心病大鼠肺血管重塑的抑制作用
The inhibition of pulmonary vessel remodeling by carbon monoxide system in rats with chronic pulmonary heart disease.
作者信息
Huang Xiaoying, Wang Liangxing, Chen Shaoxian, Xu Zhengjie, Wang Qunji, Fan Xiaofang
机构信息
Department of Respirology First Hospital, Institute of Cor Pulmonale, Wenzhou Medical College, Wenzhou 325003, China.
出版信息
Zhonghua Jie He He Hu Xi Za Zhi. 2002 Jul;25(7):408-11.
OBJECTIVE
To study the effect of carbon monoxide on pulmonary vessel remodeling of chronic pulmonary heart disease.
METHODS
Thirty-six sprague-dawley rats were randomly divided into three groups: control group, and hypoxic hypercapnic group, and hypoxic hypercapnia + hemin group. Blood CO concentration (COHb%), activity of HO-1 in blood serum and lung homogenate, pulmonary arteriole micromorphometric index, HO-1 and HO-1 mRNA were measured.
RESULTS
(1) mPAP and RV/(LV + S) were (20.1 +/- 0.8) mm Hg and (35.5 +/- 1.7)% in hypoxic hypercapnic group, they were significantly higher than those of control group's (15.3 +/- 1.4) mm Hg, (26.7 +/- 1.7)%, and those of hypoxic hypercapnia + hemin (activator of HO-1) group's (16.5 +/- 3.7) mm Hg, (30.2 +/- 1.6)% (P < 0.01). (2) Pulmonary arteriole micromorphometric index in rats of hypoxic hypercapnic group were significantly higher than those of control group and hypoxic hypercapnia + hemin group (P < 0.01). (3) Blood CO concentration, activity of HO-1 in blood serum and lung homogenate, content of HO-1 and HO-1 mRNA in pulmonary arterioles in rats of hypoxic hypercapnic group were (2.1 +/- 0.9)%, (73 +/- 18) nmol.L(-1).h(-1), (1 751 +/- 311) pmol.mg(-1).h(-1), 0.191 +/- 0.012 and 0.301 +/- 0.017, were significantly higher than those of control group: (0.5 +/- 0.3)%, (25 +/- 8) nmol.L(-1).h(-1), (385 +/- 46) pmol.mg(-1).h(-1), 0.059 +/- 0.005, 0.131 +/- 0.011, but were significantly lower than those of hypoxic hypercapnia + hemin group: (4.9 +/- 2.1)%, (132 +/- 39) nmol.L(-1).h(-1), (2 849 +/- 426) pmol.mg(-1).h(-1), 0.272 +/- 0.013, 0.339 +/- 0.020 (P < 0.01). (4) Correlation analysis revealed that the relationship between carbon monoxide system and pulmonary arteriole micromorphometric index was significantly negative (P < 0.01).
CONCLUSION
Up-regulation of endogenous carbon monoxide system can inhibit pulmonary vessel remodeling in rats with chronic pulmonary heart disease induced by hypoxia and hypercapnia.
目的
研究一氧化碳对慢性肺心病肺血管重构的影响。
方法
将36只Sprague-Dawley大鼠随机分为三组：对照组、低氧高碳酸血症组、低氧高碳酸血症+氯高铁血红素组。检测血中一氧化碳浓度（COHb%）、血清及肺匀浆中HO-1活性、肺小动脉形态计量学指标、HO-1及HO-1 mRNA。
结果
（1）低氧高碳酸血症组平均肺动脉压（mPAP）及右心室/（左心室+室间隔）[RV/（LV+S）]分别为（20.1±0.8）mmHg和（35.5±1.7）%，显著高于对照组的（15.3±1.4）mmHg、（26.7±1.7）%，以及低氧高碳酸血症+氯高铁血红素（HO-1激活剂）组的（16.5±3.7）mmHg、（30.2±1.6）%（P<0.01）。（2）低氧高碳酸血症组大鼠肺小动脉形态计量学指标显著高于对照组和低氧高碳酸血症+氯高铁血红素组（P<0.01）。（3）低氧高碳酸血症组大鼠血中一氧化碳浓度、血清及肺匀浆中HO-1活性、肺小动脉中HO-1含量及HO-1 mRNA分别为（2.1±0.9）%、（73±18）nmol·L⁻¹·h⁻¹、（1 751±311）pmol·mg⁻¹·h⁻¹、0.191±0.012、0.301±0.017，显著高于对照组的（0.5±0.3）%、（25±8）nmol·L⁻¹·h⁻¹、（385±46）pmol·mg⁻¹·h⁻¹、0.059±0.005、0.131±0.011，但显著低于低氧高碳酸血症+氯高铁血红素组的（4.9±2.1）%、（132±39）nmol·L⁻¹·h⁻¹、（2 849±426）pmol·mg⁻¹·h⁻¹、0.272±0.013、0.339±0.020（P<0.01）。（4）相关性分析显示，一氧化碳系统与肺小动脉形态计量学指标呈显著负相关（P<0.01）。
结论
内源性一氧化碳系统上调可抑制低氧高碳酸血症诱导的慢性肺心病大鼠肺血管重构。
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