Biomedical subjects

S Melnitchuk

Publications and source records attributed to S Melnitchuk.

3 recordsLinked to original sources

PubMed2002

Perfusion-contractility matching during Fontan circulation.

We investigated the relationship between coronary perfusion pressure (CPP) and myocardial contractility and the effects of an acute elevation of right atrial pressure (RAP) on this relationship in an experimental model of Fontan circulation in 6 anesthetized open-chest dogs with isolated perfused coronary arteries. The relationship between CPP and Ees could be described by biphasic J-shaped curves which were nearly identical before and under Fontan circulation. While above a "critical" CPP (72 +/- 9 mmHg vs. 81 +/- 8 mmHg, n.s.) the changes of CPP did not affect Ees, below this level the decrease of CPP resulted in a progressive decrease of Ees. Under Fontan circulation, the progressive increase of RAP did not influence Ees at CPP = 100 mmHg, led to a moderate decrease of Ees at CPP = 75 mmHg and severe decrease at CPP = 60 mmHg. Thus, both coronary arterial and venous pressure affect myocardial contractility after Fontan procedure.

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PubMed2000

Role of neural and humoral factors in hyperdynamic reaction and cardiac dysfunction following brain death.

BACKGROUND: Although hemodynamic instability and cardiac dysfunction after brain death are reported in the potential organ donor, the underlying mechanisms, for example, neurohumoral changes, myocardial injury, and altered loading conditions, have not been differentiated in clinical and experimental settings. In the present study, we performed a load-independent analysis of cardiac function, focusing on the influence of brain death-associated neural and humoral factors. METHODS: In a canine in situ cross-circulated heart model, brain death was induced by inflation of a subdural balloon catheter. Preload, afterload, and coronary perfusion pressure were kept identical in all hearts throughout the experiment. In Group H (humoral factors), the hearts of healthy dogs were perfused with blood from brain-dead support dogs (n = 6). In Group N (neural factors), the hearts of brain-dead dogs were perfused with blood from healthy support dogs (n = 6). In Group H + N (humoral and neural factors), the hearts of brain-dead dogs were perfused parabiotically in situ with the animals' own blood (n = 6). Systolic and diastolic pressure-volume relationships and coronary blood flow were measured. RESULTS: Induction of brain death led to a significant hyperdynamic response in all groups, with a maximal reaction in Group H + N followed by Group H and Group N. After the initial hyperdynamic phase, cardiac function returned to baseline within 15 minutes and remained stable in all groups for the 2-hour observation period. CONCLUSIONS: (1) Both neural and humoral factors contribute to the initial hyperdynamic reaction after brain death, and only in combination do they cause a maximal hemodynamic effect. (2) If loading conditions and perfusion pressure are kept constant, no cardiac dysfunction occurs after brain death. This indicates that poor cardiac function in the potential donor may reflect altered loading conditions and impaired coronary perfusion rather than neurohumorally mediated direct myocardial injury.

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PubMed1998

The role of coronary perfusion changes in cardiac dysfunction associated with brain death.

BACKGROUND: Previous studies described a hemodynamic instability in the potential organ donor which has clinical relevance for cardiac transplantation. The possible pathophysiological link between altered loading conditions, coronary perfusion, and cardiac function after brain death has not been investigated yet. Therefore this study was undertaken to investigate the role of coronary perfusion changes during brain death in cardiac dysfunction. METHODS: Dogs on cardiopulmonary bypass provided iso-volumetric left-ventricular (LV) contractions. By protocol, coronary perfusion pressure was kept at the level of mean aortic pressure. LV pressure, LV dP/dt, the slope of end-systolic pressure-volume relationship (Emax), coronary blood flow (CBF), and myocardial oxygen consumption (MVO2) were measured. Brain death was induced by a subdurally placed balloon-catheter. RESULTS: Induction of brain death led to a transient hyperdynamic response with a significant increase of aortic and LV pressure, dP/dt, Emax, CBF, and MVO2. Thereafter, aortic pressure and, parallelly, LV pressure, dP/dt, Emax, CBF, and MVO2 decreased significantly. However, if coronary perfusion pressure was decoupled from aortic pressure and elevated to pre-brain death level, CBF and myocardial contractility were restored to baseline level. CONCLUSION: The impairment of coronary blood flow may contribute to decreased contractility after brain death.

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