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S C Sun

Publications and source records attributed to S C Sun.

133 records · Page 8Linked to original sources

Endocarditis in mice infected with Coxsackie virus B4.

Endocarditis has not been generally considered to be a complication of viral infection. We show that mural and valvular endocarditis can be produced in mice infected with Coxsackie virus B(4). Because this virus commonly infects man and is highly cardiotropic, it is important to know whether it produces valvular lesions in man similar to those we describe in mice.

Animals↗

Specific immune recognition of insect hemolin.

Bacteria entering the body cavities of insects are recognized by hemolymph components and subsequently inactivated by phagocytosis and nodule formation. A hemolymph component called hemolin is apparently involved in the recognition process. It binds to a bacterial surface molecule and forms a stable complex with other hemolymph proteins. Hemolin binding is independent of bacterial lipopolysaccharide (LPS) structure, whereas the complex formation is dependent on the presence of the carbohydrate moiety of LPS molecules. The specificity of immune recognition in insects is discussed.

Animals↗

Ischemic injury before heart transplantation does not cause coronary arteriopathy in experimental isografts.

In this study we investigated whether the duration of ischemia before heart transplantation was related to coronary arteriopathy. Heterotopic cardiac isografts were done in 24 Lewis rats. Group 1 hearts (n = 4) were transplanted immediately after harvesting. Hearts in groups 2 (n = 8), 3 (n = 6), and 4 (n = 6) were implanted after preservation at 4 degrees C for 1, 2, or 3 hours, respectively. No immunosuppressive drugs were given. After 120 days, grafts were removed and evaluated by means of light microscopy for coronary artery intimal proliferation. Minimal intimal thickening was noted throughout, and no differences among the groups were found. Pretransplant ischemia in the absence of other factors does not cause coronary arteriopathy after heart transplantation.

Abdomen↗

Thromboxane A2 mediates reperfusion injury after heart preservation.

To assess the role of the eicosanoid thromboxane A2, a potent vasoconstrictor and platelet activator, in reperfusion injury after heart preservation, donor rats (n = 18) were anesthetized, and their hearts were rapidly excised, arrested with cardioplegic solution, and fitted with a left ventricular balloon. Seven hearts were subjected to 45 minutes of ischemia at 15 degrees C, simulating implantation, (group 1) during which the carotid and jugular vessels of support rats were cannulated for ex vivo blood reperfusion. Remaining hearts were preserved in 4 degrees C saline solution for 3 hours followed by 45 minutes at 15 degrees C (group 2, n = 11). Before reperfusion of group 2 hearts, support rats received either vehicle (group 2a, n = 6) or thromboxane A2 receptor antagonist SQ29548 (0.2 mg/kg) (group 2b, n = 5). After 1 hour of reperfusion, left ventricular peak-systolic pressure and end-diastolic pressure were measured in all hearts at incremental ventricular volumes. The slope of the peak-systolic pressure-volume relation and the volume-axis intercept of the end-diastolic pressure-volume relation were also measured. No significant differences were noted in mean peak-systolic pressure, at any left ventricular volume, nor slope of the peak-systolic pressure-volume relation between groups, indicating that neither preservation nor SQ29548 treatment affected systolic contractile performance in this model. Through all left ventricular volume, however, end-diastolic pressure was significantly lower (p < 0.05) in group 2b compared to group 2a, and overall did not differ significantly from group 1.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗