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Ann Thorac Surg 1994;58:200-206
© 1994 The Society of Thoracic Surgeons

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Articles

Adenosine and AICA-riboside fail to enhance microvascular endothelial preservation

Division of Cardiothoracic Surgery, Department of Surgery, Beth Israel Hospital, and Harvard Medical School, Boston, Massachusetts USA

Accepted for publication November 26, 1993.

^_* Address reprint requests to Dr Sellke, Division of Cardiothoracic Surgery, Beth Israel Hospital, Dana 905, 330 Brookline Ave, Boston, MA 02215.

Crystalloid cardioplegia may cause coronary microvascular endothelial dysfunction during cardiopulmonary bypass. The perioperative administration of either adenosine or AICA-riboside (acadesine, 5-aminoimidazole-4-carboxamide-1-ribofuranoside) has been associated with improved myocardial functional preservation and improved coronary blood flow after ischemie arrest. To examine if this enhanced recovery of myocardial function and perfusion may be related to improved endothelial preservation, pigs were placed on cardiopulmonary bypass and the hearts were arrested with plain cold, hyperkalemic (K⁺ = 25 mmol/L) crystalloid cardioplegia, or cardioplegic solution containing either 0.1 mmol/L adenosine or 50 µmol/L AICA-riboside, which causes the release of endogenous adenosine. AICA-riboside (375 mg) also was infused over 30 minutes before cardioplegia in the later group. After 1 hour of ischemic cardioplegia, hearts were reperfused for 1 hour while the pigs were weaned from cardiopulmonary bypass. Coronary arterioles (90 to 190 µm in diameter) from both subepicardial and subendocardial regions of the left ventricle were studied in vitro in a pressurized, no-flow state with videomicroscopy. After contraction of vessels by 25% to 40% of the baseline diameter, drugs were applied extraluminally. Relaxation of control arterioles to serotonin was slightly greater in vessels from the subendocardial region compared with vessels from the subepicardial region, and subendocardial arterioles were more affected by cardioplegia than were subepicardial vessels. In contrast, relaxations of control microvessels to bradykinin and the calcium ionophore A23187 were similar in the two bansmural myocardial regions. Responses to bradykinin and A23187 were significantly and similarly reduced after ischemic arrest with plain crystalloid cardioplegia. The addition of either adenosine or AICA-riboside failed to improve endothelium-dependent relaxation and had minimal effect on transmural differences in vascular responses after crystalloid cardioplegia and blood reperfusion. Endothelium-independent ralaxations of vessels to sodium nitroprusside were similar in all groups. In summary, the addition of either adenosine or AICA-riboside to a crystalloid cardioplegic solution fails to improve preservation of endothelium-dcpendent vascular responses in the subendocardial or subepicaidial porcine coronary microcirculation. Thus, enhanced myocardial recovery after cardioplegia associated with the use of adenosine or AICA-riboside is not due to improved functional preservation of vascular endothelium.

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