Influence of hypertonic mannitol on regional myocardial blood flow during myocardial ischemia in awake, unsedated, and in anesthetized dogs

1974 ◽  
Vol 33 (1) ◽  
pp. 145 ◽  
Author(s):  
Ian Hutton ◽  
John T. Watson ◽  
Gordon H. Templeton ◽  
David E. Fixler ◽  
W.L. Sugg ◽  
...  
Keyword(s):  
Blood Flow ◽  
Myocardial Ischemia ◽  
Myocardial Blood Flow ◽  
Regional Myocardial Blood Flow ◽  
Anesthetized Dogs ◽  
Regional Myocardial Blood

Effects of histamine receptor stimulation on regional myocardial blood flow

1983 ◽  
Vol 245 (3) ◽  
pp. H461-H467 ◽  
Author(s):  
C. W. Christensen ◽  
G. J. Gross ◽  
H. F. Hardman ◽  
H. L. Brooks ◽  
D. C. Warltier
Keyword(s):  
Blood Flow ◽  
Myocardial Blood Flow ◽  
Histamine Receptor ◽  
Regional Myocardial Blood Flow ◽  
Intracoronary Infusion ◽  
H2 Antagonist ◽  
Tracer Microspheres ◽  
Anesthetized Dogs ◽  
H1 Antagonist ◽  
Regional Myocardial Blood

The effect of histamine (H) and specific H1 and H2 agonists and antagonists on regional myocardial blood flow was studied in anesthetized dogs by use of tracer microspheres. Intracoronary infusion of histamine (15 and 34 micrograms/min) produced a dose-related increase in transmural myocardial blood flow (from 0.82 to 1.36 and 2.25 ml X min-1 X g-1) without alteration of heart rate or blood pressure. Infusion of the H1 agonist 2-(2-thiazolyl)ethylamine (135 and 442 micrograms/min) produced an increase in transmural perfusion (from 0.69 to 1.22 and 1.65 ml X min-1 X g-1) and a significant (P less than 0.05) increase in the ratio of flow between subendocardium and subepicardium (endo/epi from 0.97 to 1.31 and 1.54). Infusion of the H2 agonist dimaprit (195 and 390 micrograms/min) produced an increase in transmural myocardial blood flow (from 0.97 to 1.49 and 2.00 ml X min-1 X g-1) without a change in endo/epi. The H1-mediated increase in regional myocardial perfusion and endo/epi was blocked by the H1 antagonist diphenhydramine but not by the H2 antagonist cimetidine. These results suggest that stimulation of H1 coronary receptors preferentially distributes flow to the subendocardium, whereas H2 receptors mediate vasodilation in subepicardium as well as subendocardium.

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