Intracoronary adenosine increased total coronary blood volume by 75%, coronary blood flow by 574%, and myocardial oxygen tension by 122%, but did not significantly affect small-vessel blood volume.
Intracoronary adenosine causes relaxation of arteriolar resistance vessels and larger vessels, but not precapillary sphincters, likely due to the opposing action of increased myocardial oxygen tension.
The effect of a maximally dilating dose of intracoronary adenosine on total (CBV) and small-vessel blood volume (MSVBV, an index of open-capillary density), hematocrit (MSVHct), and related parameters of O2 supply-demand ratio was examined in left ventricular myocardium of anesthetized open-chest dogs. CBV was measured from washout of 51Cr-labeled red blood cells (RBC) and MSVBV and MSVHct from contents of 51Cr-RBC and plasma label, either 131I-serum albumin or 59Fe-siderophilin, in samples of myocardium and blood. Coronary blood flow (CBF) was measured by electromagnetic flowmeter. Myocardial oxygen consumption (MVO2) was computed with the Fick equation. Myocardial oxygen tension (MPO2) was measured with bare-tipped platinum electrodes. Adenosine raised CBV 75%, CBF, 574%, and MPO2 122%, but did not affect significantly MSVBV, MSVHct, or MVO2. These results indicate that infusion of adenosine into a coronary artery perfused at constant pressure causes relaxation of smooth muscle of arteriolar resistance vessels and of other vessels larger than 100 micrometers diam, but not that of the precapillary sphincters. This may be explained by the opposing action of increased MPO2 on the sphincters when flow increases. MSVHct was consistently much less than large-vessel Hct. This warrants combined use of red blood cell and plasma labels for accurate measurements of MSVBV.
Crystal et al. (Sat,) reported a other. intracoronary adenosine was evaluated on total (CBV) and small-vessel blood volume (MSVBV), hematocrit (MSVHct), and related parameters of O2 supply-demand ratio. Intracoronary adenosine increased total coronary blood volume by 75%, coronary blood flow by 574%, and myocardial oxygen tension by 122%, but did not significantly affect small-vessel blood volume.
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