Conway R S, Natelson B H, Chen W H, Ting W
Department of Surgery, UMDNJ-Robert Wood Johnson Medical School, New Brunswick 08903.
Cardiovasc Res. 1994 Mar;28(3):320-4. doi: 10.1093/cvr/28.3.320.
The heart of the young Syrian cardiomyopathic hamster (CMH) displays discrete patches of active myocytolytic necrosis and it has been hypothesised that these lesions are triggered by arteriolar spasm. Accordingly, we tested the theory that the coronary vasoconstrictor response to arginine vasopressin (AVP) infusion is more vigorous in the actively necrotising young (2-3 month old) CMH than in age matched normal hamsters, 5-6 month old CMHs in the histologically quiescent phase of the disease, or 5-6 month old normal hamsters.
An isovolumetric isolated heart preparation was used in which the coronary arteries were perfused with Krebs-Henseleit buffer at constant flow by a syringe pump. Coronary vascular resistance was determined by the ratio of measured perfusion pressure to flow rate during extended diastoles.
There were no significant differences in baseline coronary vascular resistance among the four groups. The increase in resistance with AVP infusion (0.54 pressor units.min-1) was significantly greater (p < 0.01) in the young CMH [6.66(SEM 4.75) mm Hg.ml-1.min-1] than in the old CMH [1.66(0.78)], the young normal [1.10(1.07)], and the old normal [2.72(1.86)] groups.
There is increased vasoconstrictive responsiveness in the young CMH coronary vasculature. The results suggest a broader coronary abnormality in this myopathic model and are consistent with the microvascular spasm hypothesis of myocytolytic lesion formation.
年轻的叙利亚心肌病仓鼠(CMH)心脏呈现出离散的活动性肌细胞溶解坏死灶,有人推测这些病变是由小动脉痉挛引发的。因此,我们检验了这样一种理论,即与年龄匹配的正常仓鼠、处于疾病组织学静止期的5 - 6月龄CMH或5 - 6月龄正常仓鼠相比,在活动性坏死的年轻(2 - 3月龄)CMH中,精氨酸加压素(AVP)输注引起的冠状动脉血管收缩反应更强烈。
采用等容离体心脏制备方法,通过注射泵以恒定流量用Krebs - Henseleit缓冲液灌注冠状动脉。冠状动脉血管阻力通过舒张期延长期间测量的灌注压力与流速的比值来确定。
四组之间的基线冠状动脉血管阻力无显著差异。年轻CMH [6.66(标准误4.75)mmHg·ml⁻¹·min⁻¹] 中AVP输注(0.54升压单位·min⁻¹)引起的阻力增加显著大于(p < 0.01)老年CMH [1.66(0.78)]、年轻正常组 [1.10(1.07)] 和老年正常组 [2.72(1.86)]。
年轻CMH冠状动脉血管系统的血管收缩反应性增强。结果表明在这种肌病模型中存在更广泛的冠状动脉异常,并且与肌细胞溶解病变形成的微血管痉挛假说一致。