Effect of hyperosmotic perfusion on rate of oxygen consumption of isolated guinea pig and rat hearts during cardioplegia.
OBJECTIVE
The aim was to determine the metabolic consequence of increasing the osmolality of a crystalloid cardioplegic solution during periods of cardiac arrest.


METHODS
Isolated hearts of guinea pig and rat were Langendorff perfused with Krebs-Henseleit solution at 37 degrees C and arrested by an increase in KCl. The rate of oxygen consumption was measured under standard isosmotic conditions and with the osmolality of the perfusate increased by addition of sucrose.


RESULTS
Increased osmolality stimulated the rate of myocardial oxygen consumption in a dose dependent manner. At optimal dose (about twice normal osmolality), the oxygen consumption of the arrested heart approximated that of the beating, non-working heart measured prior to arrest. Potentiation of cardiac resting metabolism was greater in the rat than in the guinea pig, whether expressed in absolute terms or relative to the metabolism of the beating heart. Metabolic potentiation was accompanied by an increase of passive or diastolic left ventricular pressure in the rat but not in the guinea pig. The metabolic response was unaffected by coronary vasodilation (adenosine) and by inhibition of Ca2+ channels (verapamil); it was moderately diminished by perfusion with Ca(2+)-free solution. Procaine inhibited the hyperosomotic potentiation of oxygen consumption in a dose dependent manner.


CONCLUSIONS
From the absence of passive force development in the guinea pig heart, it appears that the hyperosmotic stimulation of cardiac resting metabolism primarily reflects increased activity of the sarcoplasmic reticular Ca(2+)-ATPase subsequent to release of Ca2+ through a procaine inhibitable channel. Blunting of both the metabolic and mechanical responses in the guinea pig vis-a-vis the rat heart is attributed to the greater capability of the former to buffer myoplasmic Ca2+ via the energetically neutral Na(+)-Ca2+ exchange mechanism.
Hanley
P J
PJ
Department of Physiology, School of Medicine, University of Auckland, New Zealand.
Cooper
P J
PJ
Loiselle
D S
DS
D000241:Adenosine / Q000494:pharmacology; D000818:Animals; D002118:Calcium / Q000378:metabolism; D002314:Cardioplegic Solutions; D004305:Dose-Response Relationship, Drug; D005260:Female; D006168:Guinea Pigs; D006324:Heart Arrest, Induced; D008297:Male; D009206:Myocardium / Q000378:metabolism*; D009994:Osmolar Concentration; D010101:Oxygen Consumption / Q000187:drug effects / Q000502:physiology*; D010477:Perfusion; D011343:Procaine / Q000494:pharmacology; D051381:Rats; D013045:Species Specificity; D013268:Stimulation, Chemical; D013395:Sucrose / Q000494:pharmacology; D014700:Verapamil / Q000494:pharmacology
D002314:Cardioplegic Solutions; D011343:Procaine; D013395:Sucrose; D014700:Verapamil; D000241:Adenosine; D002118:Calcium