Manohar M, Bisgard G E, Bullard V, Will J A, Anderson D, Rankin J H
Am J Physiol. 1978 Dec;235(6):H628-36. doi: 10.1152/ajpheart.1978.235.6.H628.
Hemodynamics, myocardial function, and regional myocardial blood flow (MBF) were measured in 6 closed-chest ponies anesthetized with ketamine hydrochloride before (control) and after creation of acute right ventricular systolic hypertension (RVSH) during normoxia and isocapnic hypoxia. The right ventricular (RV) systolic pressure during each RVSH approached 90 mmHg. There were significant alterations in the pattern of total ventricular MBG distribution in favor of the RV. Because RV myocardium received proportionate increments to its endocardium as well as epicardium, it is concluded that autoregulation in the RV coronary vascular bed had not been abolished even during hypoxia + RVSH. Marked increase in MBF to the right side of the septum during each RVSH with little change in perfusion to other regions suggests that RV contraction is supported by the right side of the septum. Because these increments occurred with decreased RV coronary driving pressure they were the consequence of compensatory coronary vasodilatation. The slow heart rate of the pony in the presence of a large coronary vasodilatory reserve may have been the major factor in allowing large increments in MBF to the stressed regions despite decreased coronary driving pressure.
在6只使用盐酸氯胺酮麻醉的开胸小马中,于常氧和等碳酸血症性低氧条件下,在急性右心室收缩期高血压(RVSH)形成之前(对照)和之后,测量其血流动力学、心肌功能和局部心肌血流量(MBF)。每次RVSH期间右心室(RV)收缩压接近90 mmHg。全心MBG分布模式发生了显著变化,有利于RV。由于RV心肌的心内膜和心外膜均获得了相应的增量,因此得出结论,即使在低氧+RVSH期间,RV冠状血管床的自动调节也未被消除。每次RVSH期间,隔膜右侧的MBF显著增加,而其他区域的灌注变化很小,这表明RV收缩由隔膜右侧支持。由于这些增量是在RV冠状动脉驱动压力降低的情况下发生的,它们是代偿性冠状动脉血管舒张的结果。尽管冠状动脉驱动压力降低,但在存在大量冠状动脉血管舒张储备的情况下,小马的心率缓慢可能是允许向应激区域的MBF大幅增加的主要因素。