Isotonic versus hypertonic initial hyperkalemic reperfusion after cardioplegic arrest in isolated hearts

• Published in: The Thoracic and cardiovascular surgeon Vol. 43; no. 3; p. 123
• Main Authors: Habazettl, H, Palmisano, B W, Bosnjak, Z J, Graf, B M, Stowe, D F
• Format: Journal Article
• Language: English
• Published: Germany 01.06.1995
• Subjects: Animals; Cardioplegic Solutions - pharmacology; Guinea Pigs; Heart - drug effects; Heart Arrest, Induced; Hypertonic Solutions; Isotonic Solutions - pharmacology; Mannitol - pharmacology; Myocardial Reperfusion - methods; Myocardial Reperfusion Injury - prevention & control; Potassium - pharmacology; Sodium Chloride - pharmacology; Ventricular Function, Left - drug effects
• ISSN: 0171-6425
• DOI: 10.1055/s-2007-1013785

In 24 isolated perfused guinea-pig hearts, 40 min of hyperkalemic arrest and ischemia at 37 degrees C were followed by 5 min of either isotonic or hypertonic initial hyperkalemic reperfusion (HKR). Hearts were divided into 3 groups: HKR, 5 min initial reperfusion with isotonic hyperkalemic Krebs' solution; Mannitol, initial reperfusion with hypertonic (450 mosm für 1 min and 330 mosm for 4 more min) hyperkalemic Krebs' solution modified by addition of mannitol; NaCl, same as Mannitol group but using NaCl instead of mannitol to increase osmolarity. In isotonic HKR hearts, postischemic peak reflow was 98 +/- 11% of pre-ischemic control. Subsequently coronary flow stabilized at 75% of control. Left-ventricular developed pressure (LVDP) recovered to 60% of control. Hypertonic reperfusion increased peak reflow to 141 +/- 11% in the mannitol and to 121 +/- 12% in the NaCl groups, but had no effect on the subsequent reduction of coronary flow to 75% of control. Recovery of LVDP, dP/dtmax, dP/dtmin, the time constant of relaxation, and O2 consumption did not differ between groups. Postischemic flow responses to adenosine, acetylcholine, and nitroprusside were equivalently reduced in all groups. We conclude that the flow increase seen in the hypertonic reperfusion model of the study may be due to direct coronary vasodilation rather than the desired reduction of endothelial or perivascular cell edema by the hypertonic solutions.