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Biomedical subjects

K Mobin-Uddin

Publications and source records attributed to K Mobin-Uddin.

At least 19 recordsLinked to original sources
PubMed1986

Vascular anastomosis with Mobin-Uddin vein/graft holder.

A vein/graft holder, designed for use during aortocoronary and peripheral vascular bypass surgery, is described. It holds the opening in a vein or synthetic graft securely during end-to-side and side-to-side anastomosis. The vein/graft holder is atraumatic, simplifies the suturing technique, and facilitates precise anastomosis.

Coronary Artery Bypass↗
PubMed1975

Prophylactic antibiotics in noncardiac thoracic operations.

A high incidence of thoracotomy wound infection and empyema in 1972 was associated with inadequate and irregular administration of prophylactic antibiotics. Beginning with 1973, a strict regimen was adopted that combined systemic cephalosporins and two topical antibiotics (cephalothin and kanamycin). Emphasis was placed on preoperative administration of the systemic agent and on use of the topical drugs before the operative field was contaminated. The patient groups for 1972 and 1973 were similar in most respects, but the wound complication rate was 18.4% in 1972 and 4.8% in 1973.

Administration, Oral↗
PubMed1975

Effect of cardiotonic and vasoactive drugs on transmural flow distribution and ventricular volume in the fibrillating heart on cardiopulmonary bypass.

Subendocardial hemorrhagic necrosis in an important cause of death following cardiopulmonary bypass. The transmural distribution of flow across the left ventricle (LV), septum (SP), and right ventricle (RV) is a complex interaction of vascular resistance and myocardial compressive resistance. We studied the change in transmural blood flow in LV, SP, and RV, and left ventricular volume, following administration of cardiotonic and vasoactive drugs in the fibrillating heart. The drugs studied included calcium with and without ATP-induced vasodilation, isoproterenol, epinephrine, angiotensin, and ouabain. Calcium produced underperfusion of LV subendocardium with or without previous ATP vasodilation. Isoproterenol also caused underperfusion of LV subendocardium. Both calcium and isoproterenol decreased ventricular volume. Angiotensin increased resistance in the subepicardium and increased flow in the subendocardium, with no change in ventricular volume. Epinephrine and ouabain caused no consistent changes in transmural flow. The decreased ventricular volume produced by calcium and isoproterenol restricts flow in the subendocardium because of increased compressive resistance. Increased subendocardial flow with angiotensin indicates that subepicardial vasodilation in the fibrillating heart causes epicardial "steal," which contributes to subendocardial ischemia.

Adenosine Triphosphate↗