In patients undergoing aortic valve replacement, allograft valves stored at 4 degrees C in a nutrient medium have been associated with excellent immediate and long-term results. The effects of this method of prolonged storage on the antigenic, immunological and cellular characteristics of these grafts are incompletely understood. This study was designed to study these phenomena in rat aortic valves subjected to antibiotic sterilization and stored for up to 3 weeks in RPMI containing 10% fetal calf serum. Selected valves from Brown Norway rats were implanted heterotopically into the abdominal aorta of Lewis rats. Other valves were studied prior to transplantation. Antigenicity was determined by immunocytochemical staining using monoclonal mouse antibodies directed at Class I and Class II rat antigens. Immunogenicity was determined by duration of second-set skin graft survival following heterotopic aortic valve implant. Endothelial cell viability was determined by flow cytometric analysis of endothelial cells harvested from aortic valve allografts by collagenase digestion. Only fresh valves and valves stored for 1 day were positive for Class I antigens; no valves were positive for Class II antigens. Duration of skin graft survival was prolonged with greater duration of storage, but grafts remained immunogenic after 21 days of storage. Endothelial cell viability declined from 95% in the fresh valves to 64% after 21 days of storage. With prolonged duration of allograft valve storage at 4 degrees C, there is an attenuation of antigenicity, immunogenicity, and endothelial cell viability. Loss of endothelial cells may contribute to the changes in immunological responses to the valve allografts. The expression of antigens on the endothelial surface is not a reliable predictor of immunological response.

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Studies were performed to determine the pressure at the origin of the native coronary collaterals (Pstem) and thus assess the contribution of collaterals arising from proximal conduit coronary vessels vs. those arising from distal microvessels. Nine isolated blood-perfused dog hearts were studied. Aortic pressure was maintained at 80 mmHg. Collateral flow to the circumflex perfusion field was measured (radioactive microspheres) repeatedly before and after successive 25-micron nonradioactive microsphere embolization of the circumflex vasculature. After each microembolization, collateral flow decreased and peripheral coronary pressure (PCP) increased. After all embolizations collateral flow decreased from an initial value of 17 +/- 4 to 2 +/- 0.4 ml X min-1 X 100 g-1 and PCP increased from an initial value of 15 +/- 3 to 65 +/- 3 mmHg. The relationship between decreasing collateral flow and increasing PCP was linear with a pressure intercept of 74 +/- 3 mmHg. This pressure intercept predicts the PCP that would be observed if microembolization produced complete cessation of collateral flow. Accordingly, this pressure intercept allowed an accurate estimate of Pstem. This estimate of Pstem was similar to left anterior descending pressure (75 +/- 2 mmHg). These studies show that Pstem may be accurately estimated by measuring pressure in a nonoccluded large epicardial vessel. The contribution of microvascular anastomoses to total collateral flow is likely small.

The present studies were performed to examine the role of beta-adrenergic receptors in modulating smooth muscle tone in mature coronary collaterals. To examine the beta-adrenergic receptor population present, radioligand binding-cover slip autoradiographic studies were performed on sections of native canine coronary vessels and sections of coronary collaterals developed after placement of Ameroid constrictors. Specific binding of the nonselective beta-adrenergic antagonist [125I]iodopindolol to vascular smooth muscle in segments of both collaterals and native coronary arteries was saturable and stereospecific. Maximal binding and the potency of beta-adrenergic subtype-selective antagonists were similar in all segments. Beta-adrenergic relaxation of native coronary vessels and collateral vessels were studied in isolated organ chambers after preconstriction with prostaglandin F2 alpha. Both native coronary arteries and collateral segments demonstrated beta-adrenergic-mediated relaxation with affinities for both agonists and antagonists compatible with a mixed population of beta 1- and beta 2-adrenergic receptors. These studies indicate that during development, the new collateral vascular smooth muscle expresses a functional population of beta-adrenergic receptors, comparable to that in native vessels.