CAJ | 학술논문

应用盲肠结扎法制备大鼠败血症休克模型,研究内源性一氧化碳(CO)在败血症休克时低血压发病中的作用.用血红素加氧酶(heme oxygenase,HO)抑制剂2,4-二甘油次卟啉锌(zinc deuteroporphyrin 2,4-bisglycol,ZnDPBG)处理大鼠后,观察动物动脉血压,同时测定主动脉平滑肌组织中HO活性和CO生成量.结果发现:败血症大鼠动脉收缩压、舒张压降低,同时血管平滑肌HO活性和CO生成明显增加.败血症大鼠用ZnDPBG处理后,动脉血压明显回升,同时HO活性和CO生成明显被抑制.实验表明败血症休克时低血压的发生与血管平滑肌细胞HO活性增加和内源性CO生成增多明显相关;应用HO抑制剂阻断HO活性能导致内源性CO生成减少,继而使败血症休克时大鼠血压明显回升.实验提示,内源性CO对血管张力具有重要的调节作用;HO活性和内源性CO生成增加是败血症休克时低血压发生的重要机制之一.
응용맹장결찰법제비대서패혈증휴극모형,연구내원성일양화탄(CO)재패혈증휴극시저혈압발병중적작용.용혈홍소가양매(heme oxygenase,HO)억제제2,4-이감유차계람자(zinc deuteroporphyrin 2,4-bisglycol,ZnDPBG)처리대서후,관찰동물동맥혈압,동시측정주동맥평활기조직중HO활성화CO생성량.결과발현:패혈증대서동맥수축압、서장압강저,동시혈관평활기HO활성화CO생성명현증가.패혈증대서용ZnDPBG처리후,동맥혈압명현회승,동시HO활성화CO생성명현피억제.실험표명패혈증휴극시저혈압적발생여혈관평활기세포HO활성증가화내원성CO생성증다명현상관;응용HO억제제조단HO활성능도치내원성CO생성감소,계이사패혈증휴극시대서혈압명현회승.실험제시,내원성CO대혈관장력구유중요적조절작용;HO활성화내원성CO생성증가시패혈증휴극시저혈압발생적중요궤제지일.
A sepsis model induced by cecal ligation and puncture was used to study the role of endogenous carbon monoxide in hypotension pathogenesis of rats during septic shock. After administration of zinc deuteroporphyrin 2,4-bisglycol (ZnDPBG),an inhibitor of heme oxygenase (HO),blood pressure (BP),HO activity and carbon monoxide (CO) release from vascular muscle tissue were measured. The results showed that BP of sepsis rats,including systolic and diastolic arterial BP,decreased significantly while HO activity and CO content were significantly increased. In contrast,after administration of ZnDPBG,BP of sepsis rats was significantly increased while the HO activity and CO production were significantly decreased. These findings suggest that HO activity and CO release within vascular musculature are increased during septic shock;inhibition of HO may elevate BP of rats during septic shock through a decrease of endogenous CO production. It is concluded that endogenous CO derived from vascular muscle cells plays an important role in regulating vascular tone,and the up-regulation of HO activity followed by subsequent CO production contributes to hypotension pathogenesis during septic shock.