Effect of hypercapnia on coronary circulation.
The relative importance of hypercapnia in the control of coronary circulation was examined in 42 anaesthetised open chest rabbits. Coronary blood flow was determined with 15 micron radioactive microspheres. When mean (SD) Paco2 was increased from 38(10) to 76(16) mm Hg in six rabbits, the hypercapnia caused a 62% increase in coronary blood flow. When a similar degree of metabolic acidosis was induced in 12 rabbits for either 15 or 60 min, no changes in coronary blood flow occurred. No increases in coronary blood flow occurred during hypercapnia with propranolol, 2 mg/kg (n = 12), with or without atrial pacing to maintain heart rate. Similarly, carotid denervation prevented the carbon dioxide induced increase in coronary blood flow in six rabbits. Haemodiluted rabbits (n = 6) with a 40% replacement of blood showed no changes in coronary blood flow with hypercapnia. This was due to the 22% decrease in systolic pressure-time index, despite their intact sympathetic nervous system and reduced Bohr shift. Therefore, although carbon dioxide is a coronary vasodilator, both direct vasodilatation and sympathetic adrenergic activation must be intact in order for coronary blood flow to be increased.
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D000138:Acidosis / Q000503:physiopathology; D000818:Animals; D001794:Blood Pressure; D002344:Carotid Body; D003326:Coronary Circulation; D003714:Denervation; D004558:Electric Stimulation; D006339:Heart Rate / Q000187:drug effects; D006438:Hemodilution; D006863:Hydrogen-Ion Concentration; D006935:Hypercapnia / Q000503:physiopathology*; D011433:Propranolol / Q000494:pharmacology; D011817:Rabbits; D014655:Vascular Resistance
D011433:Propranolol