Pharmacologic- vs. ischemia-induced coronary artery vasodilation.
Responses of total coronary and regional myocardial blood flow to ischemia- or drug-induced coronary artery vasodilation were studied in open-chest anesthetized dogs. Systolic, diastolic, and mean coronary blood flow after addition of chromonar (8 mg/kg iv), adenosine triphosphate (400 micrograms/min intracoronary), or adenosine (500 micrograms/min intracoronary) exceeded the respective flow at the peak of reactive hyperemia (90-s occlusion period). Whereas the regional distribution of total coronary flow favored the subendocardium of the left ventricle during reactive hyperemia, flow was preferentially distributed to subepicardium during drug-induced maximal coronary artery vasodilation. These results were independent of type of anesthesia, vasodilator agent, or degree of autonomic innervation. These data indicate that total coronary vasodilator reserve is greater than that observed at the peak of reactive hyperemia and that there is a transmural gradient of vasodilator reserve within the left ventricle. A greater regional vasodilator reserve is present in subepicardial than in subendocardial layers.[1]References
- Pharmacologic- vs. ischemia-induced coronary artery vasodilation. Warltier, D.C., Gross, G.J., Brooks, H.L. Am. J. Physiol. (1981) [Pubmed]
Annotations and hyperlinks in this abstract are from individual authors of WikiGenes or automatically generated by the WikiGenes Data Mining Engine. The abstract is from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.About WikiGenesOpen Access LicencePrivacy PolicyTerms of Useapsburg
