Myocardial Blood Flow and Oxygen Consumption during Isovolemic Hemodilution Alone and in Combination with Adenosine-Induced Controlled Hypotension

Abstract

CRYSTAL GJ, ROONEY MW, SALEM MR. Myocardial blood flow and oxygen consumption during isovolemic hemodilution alone and in combination with adenosine-induced controlled hypotension. Anesth Analg 1988:67:53947.Recent reports have proposed combining isovolemic hemodilution and controlled hypotension to limit blood loss during surgery. Before such a technique can be considered for clinical use, it must be demonstrated that it does not endanger maintenance of adequate myocardial oxygenation. Accordingly, measurements of left ventricular myocardial blood flow and oxygen consumption were obtained during isovolemic hemodilution alone and in combination with adenosine-induced controlled hypotension in ten pentobarbital-anesthetized, open chest dogs with normal corona y circulation. Hemodilution to a hematocrit of 21.7% was produced by isovolemic exchange of whole blood for 5% dextran. In the presence of hemodilution, adenosine was infused intravenously at a rate sufficient to decrease mean aortic pressure to 51 mm Hg. Myocardial blood flow was measured with radioactive microspheres and used to calculate global left ventricular myocardial oxygen consumption and oxygen supply. Hemodilution alone increased aortic blood flow (+43%) but had no effect on aortic pressure, left atrial pressure, heart rate, or left ventricular dPldt,,; an increase in myocardial blood flow (+130%) maintained oxygen supply and consumption at the baseline level. Adenosine-induced hypotension during hemodilution decreased heart rate (-35%), left ventricular dPldt max (-28%), and aortic blood flow (-14%). These systemic responses were accompanied by reduced myocardial oxygen consumption (-29%) and increased myocardial blood flow (+54%) and myocardial oxygen supply (+72%). These latter effects resulted in reduction in the coronary arteriovenous oxygen content difference and in an attendant rise in coronary sinus Po, (+66%), which are signs of luxuriant myocardial perfusion. The present study demonstrated in anesthetized dogs that 1) myocardial oxygenation is well maintained during isovolemic hemodilution alone and, 2) myocardial oxygenation is influenced favorably when isovolemic hemodilution is combined with adenosine-induced controlled hypotension. Further studies are required to evaluate the safety of the latter condition in hearts with stenotic coronary arteries.Adenosine, a metabolic breakdown product of adenosine triphosphate, is an endogenous vasodilator that has been implicated in local regulation of coronary blood flow (1). The drawbacks of currently used hypotensive drugs, halothane, nitroglycerin, nitroprusside, and trimethaphan, which include cyanide toxicity, tachyphylaxis, reflex tachycardia, rebound hypertension, and excessive cerebral vasodilation (2-5), have stimulated interest in the use of exogenous adenosine to induce controlled hypotension (2,7-9).Intravenous infusion of adenosine causes arterial hypotension that is rapidly achieved, easily controlled, short-lived and, furthermore, is not associated with any apparent hematologic or...

Cardiac mechanoenergetic cost of elevated plasma viscosity after moderate hemodilution

“…Hemodilution decreases blood intrinsic oxygen carrying capacity and blood viscosity, which leads to increased CO and sustains oxygen delivery to tissues [9, 29]. In our experimental model, oxygen carrying capacities for both PE were identical due to similar Hct, and oxygen delivery to tissues improved as CO increased.…”

“…Isolated heart studies have demonstrated that higher viscosity, with the perfusion solution, induced the NO production [17]. Several studies have reported that an increase in endothelial NO synthase levels augments venous return or preload [9, 20, 27], and an enhancement of shear stress by increasing fluid viscosity at a given shear rate increases eNOS expression in endothelial cell culture and in vivo [34, 36–38]. Our results after hemodilution demonstrated that an equivalent wall shear stress is higher in an HVPE group than that in a LVPE group, leading to increased venous return (V ed ) and reduced systemic vascular resistance.…”

“…In response to the decrease in Hct, cardiac output (CO) increases due to reduction in vascular resistance and to maintain oxygenation [9, 11, 14, 19]. Changes in blood viscosity directly affect vascular wall shear stress, and the synthesis of vascular endothelial shear dependent mediators, such as nitric oxide (NO) [17, 21, 22, 34, 37].…”

Tissue oxygenation after exchange transfusion with ultrahigh-molecular-weight tense- and relaxed-state polymerized bovine hemoglobins

“…The compensatory mechanisms responding to the acute decrease in Hct involve the increase of cardiac output due to a reduction in vascular resistance due to a lower blood viscosity (10,14,18,23). During hemodilution, blood viscosity is an important factor in the responses of the cardiovascular system, as it affects endothelial shear stress, which activates the synthesis of vascular autocoids, such as prostacyclin and NO (22,26,27,35,42).…”

Exogenous intravascular nitric oxide enhances ventricular function after hemodilution with plasma expander

“…The role of NO in the regulation of cardiac function and circulatory system has been remarkably studied in both normal and pathological conditions (Bolli, et al 1998,Fellet, et al 2003,Kojda, et al 1997,Colley and Sivarajan 1984,Crystal, et al 1988). The principal reported effect of NO on cardiac function describes bimodal effects on inotropy with positive inotropic effects at reduced NO availability, and negative inotropic effects at increased NO availability (Kojda, et al 1997,Preckel, et al 1997,Brady, et al 1993).…”