Abstracts of Posters Presented at the International Anesthesia Research Society; 72nd Clinical and Scientific Congress; Orlando, FL; March 7-11, 1998: Cardiovascular Anesthesia
Introduction: Sodium nitroprusside (SNP) induces vascular relaxation via release of nitric oxide (NO), which diffuses into the vascular smooth muscle cell, where it stimulates guanyl cyclase activity and production of guanosine 3[prime], 5[prime]-cyclic monophosphate (cGMP).  Hemoglobin is a well established scavenger of NO, [2,3] but it is unknown whether this effect limits the coronary vasodilating action of NO donors, such as SNP. The present study tested the hypothesis that hemodilution (HD) enhances SNP-induced coronary vasodilation via a reduction in the NO scavenging capability of the blood.
Methods: After approval from the Instiutional Animal Care Committee, studies were conducted in six anesthetized, open-chest dogs. The left anterior descending coronary artery (LAD) was perfused via an extracorporeal system at a coronary perfusion pressure of 80 mmHg. Coronary blood flow (CBF) was measured with Doppler flow transducer. Mean aortic pressure (MAP) and heart rate (HR) were measured. SNP was infused into the LAD incrementally (20, 40, 80, 160 [micro sign]g/min) under three conditions: 1) control (hematocrit (Hct; 33 +/- 2 %), 2) during intracoronary (i.e.) infusion of adenosine (Aden; 80 [micro sign]g/min), 3) following isovolemic HD with 5 % Dextran-40 (Hct; 19 +/- 3%). The responses to SNP during Aden-induced dilation were used to correct for the higher baseline values for CBF following HD (47 +/- 7 to 81 +/- 9 ml/min). This correction was based on the previously observed linear relation between that the initial vascular resistance and the magnitude of drug-induced coronary vasodilation.  A maximally dilating infusion of Aden was used to assess the flow reserve before and following HD. Statistical analysis was performed using the Student's t test for paired samples.
Results: HD did not alter the dose-dependent increases in CBF caused by SNP: (Figure 1)
The maximal increases in CBF by Aden before and following HD (196 +/- 48 and 174 +/- 59 ml/min, respectively) indicated that the responses during SNP (presented above) were not limited by the flow reserve. Neither HD nor the i.e. infusions of vasodilators altered MAP or HR.
Conclusions: Hemodilution did not enhance SNP-induced coronary vasodilation. The present findings do not support an ability of hemoglobin contained in RBCs to bind exogenous NO and thereby restrict its access to coronary vascular smooth muscle.
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