Reoperation in patients with closed SVG and patient LITA-LAD graft: T-graft approach.

Selection of the bypass graft that the patient has demonstrated will remain patent and free from critical atherosclerosis is a most important part of coronary artery bypass reoperations. Sixteen patients in whom a patent left internal thoracic artery-left anterior descending coronary artery bypass graft and obstructed or closed saphenous vein grafts to other coronary arteries were visualized underwent reoperation. To reach the inadequately perfused circumflex and right coronary arteries, the right internal thoracic artery was anastomosed to the left internal thoracic artery as a T graft and then was attached to the circumflex and right coronary artery branches. All patients survived the procedure and are free from angina. There were no perioperative myocardial infarctions, and there was no suggestion of hypoperfusion by the grafts. We believe this technique may reduce the incidence of graft failure in patients undergoing reoperative coronary artery bypass grafting.

Responses of cerebral arteries after ischemia and reperfusion in cats.

Our goal was to determine whether responses of cerebral arteries are altered after cerebral ischemia and reperfusion. We measured diameter of cerebral arteries (150-180 micron) in cats in response to topical application of acetylcholine (ACh) and serotonin, which release endothelium-derived relaxing factor (EDRF), and adenosine and angiotensin, which do not release EDRF. Diameter of arteries was measured before and after 10 or 30 min of cerebral ischemia, when base-line diameter had returned to control levels. Under control conditions, serotonin and angiotensin constricted cerebral arteries by 16 +/- 2 and 23 +/- 3% (means +/- SE), respectively, and ACh and adenosine dilated cerebral arteries by 22 +/- 2 and 23 +/- 3%, respectively. During reperfusion after 10 min of cerebral ischemia, constrictor responses of cerebral arteries were preserved. Vasodilator responses of arteries to ACh after 10 min of ischemia were heterogeneous. In 6 of 15 cats, vasodilatation in response to ACh was preserved. In contrast, in 9 of 15 cats, vasodilatation in response to ACh was impaired (7 +/- 3%). In both groups, vasodilatation in response to adenosine was not impaired after 10 min of ischemia. During reperfusion after 30 min of cerebral ischemia, constrictor responses of cerebral arteries were preserved. In contrast, dilatation of cerebral arteries in response to ACh and adenosine was impaired. We speculate that impaired cerebral vasodilatation after ischemia, with maintenance of vasoconstriction, may contribute to impaired reperfusion after cerebral ischemia.