Leg edema following the harvest of great saphenous vein (SV) is sometimes recognized after coronary artery bypass surgery (CABG). Maximum venous outflow (MVO) is one of the parameters of leg venous function which is measured by straingauge plethysmography. To clarify the mechanism of the development of leg edema after CABG, we measured the perioperative MVO. Six patients had leg edema afer CABG (group I), 4 patients had no edema after CABG (group II). Six patients without edema after cardiac surgery, apart from CABG, were selected as controls (group III). The MVO of both legs was measured before and after the operation. In group I, venous echo or venography of the leg, or both, were performed after the operation. The MVO of legs from which SV had been harvested in group I decreased from 35.0±13.6 (ml/min/ 100ml tissue) to 23.9±7.6 (p=0.04) after the operation, but did not differ from the MVO of the contralateral leg. The preoperative MVO of legs from which SV had been harvested in group I was slightly higher than the legs of other groups. There was no significant change of MVO in group II or III after surgery. No deep vein thrombosis was shown in group I by venous echo and venography. Left ventricular ejection fraction, blood cell count and serum chemistry indicated no changes in any of the three groups after the operation except for the hemoglobin level in group I. These results suggested that the leg which had edema had a relatively high MVO before the operation. This MVO significantly decreased to the level of leg from which SV had not been harvested after the operation, and the edema appeared. In conclusion, postoperative edema in the leg from which SV was harvested was the result of a decrease in venous function due to removal of the SV. SV which causes leg edema might play the greater part of the venous return than others and the total function of the venous return was higher than normal at the point of preoperation.

Objective To infect human pulmonary artery smooth muscle cells with different HIV-based vectors, and introduce foreign genes into the cells with HIV-based lentivirus vectors.MethodsThe human pulmonary artery smooth muscle cells, U87.CD4.CCR5 and U87.CD4.CXCR4, were infected with ADA/Luc, HXB2/Luc, VSV-G/Luc and VSV-G/GFP.ResultsU87.CD4 with corresponding coreceptors could be infected by ADA/Luc and HXB2/Luc, however, the human pulmonary artery smooth muscle cells could not be infected by ADA/Luc and HXB2/Luc, even pseudotypes. VSV-G/Luc and VSV-G/GFP could be transfered into the human pulmonary artery smooth muscle cells. After 3 days post-infection, the relative proportion of positive cells of human pulmonary artery smooth muscle cells expressing VSV-G/GFP was 18%.ConclusionHIV-based lentivirus vectors can introduce foreign genes into the human pulmonary artery smooth muscle cells.