Why the study?
Does acute right ventricular systolic hypertension alter myocardial perfusion and function in anesthetized ponies?
Does acute right ventricular systolic hypertension alter myocardial perfusion and function in anesthetized ponies?
In a pony model, acute right ventricular systolic hypertension leads to compensatory coronary vasodilatation and increased myocardial blood flow to the right ventricle and right side of the septum, preserving autoregulation even during hypoxia.
Indicates preferential RV perfusion during acute systolic hypertension; leaves open translation from pony models to human right heart disease.
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.
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Manohar et al. (1978) studied this question.
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