The severity and duration of ischemia-reperfusion injury is hypothesized to play an important role in the ability of the heart subsequently to recover contractility. Permeabilized trabeculae were prepared from a rat model of ischemia-reperfusion injury to examine the impact on force generation. Compared with the control perfused condition, the maximum force (F(max)) per cross-sectional area and the rate of tension redevelopment of Ca(2+)-activated trabeculae fell by 71% and 44%, respectively, during ischemia despite the availability of a high concentration of ATP. The reduction in F(max) with ischemia was accompanied by a decline in fiber stiffness, implying a drop in the absolute number of attached cross bridges. However, the declines during ischemia were largely recovered after reperfusion, leading to the hypothesis that intrinsic, reversible posttranslational modifications to proteins of the contractile filaments occur during ischemia-reperfusion injury. Examination of thin-filament proteins from ischemic or ischemia-reperfused hearts did not reveal proteolysis of troponin I or T. However, actin was found to be glutathionylated with ischemia. Light-scattering experiments demonstrated that glutathionylated G-actin did not polymerize as efficiently as native G-actin. Although tropomyosin accelerated the time course of native and glutathionylated G-actin polymerization, the polymerization of glutathionylated G-actin still lagged native G-actin at all concentrations of tropomyosin tested. Furthermore, cosedimentation experiments demonstrated that tropomyosin bound glutathionylated F-actin with significantly reduced cooperativity. Therefore, glutathionylated actin may be a novel contributor to the diverse set of posttranslational modifications that define the function of the contractile filaments during ischemia-reperfusion injury.

In patients with venous thrombotic disease and in whom anticoagulation or thrombolytic therapy is inappropriate, ineffective, or even contraindicated, insertion of vena caval filters or venous thrombectomy must be considered. The primary indication for the placement of vena caval filters is in patients who have developed a pulmonary embolus and in whom anticoagulation is either contraindicated or in whom anticoagulation must be discontinued because of the development of bleeding complications. At the present time, either the Greenfield filter placed through a jugular, femoral, or axillary venotomy or the bird's nest filter are appropriate and appear to be the most effective and least fraught with complications. The use of venous thrombectomy has waxed and waned over the last several decades. At the present time, the procedure is advocated mainly for lower limb venous thrombosis which is extensive enough to threaten limb viability. On occasion, it may be appropriate to extend the indications for venous thrombectomy to include femoral thrombosis of less than 10 days duration or iliac thrombosis of less than 3 weeks duration with floating thrombi at the level. Technical modifications which improve the patency of the obliterated veins which are predisposed to rethrombosis include the creation of a temporary arteriovenous fistula and meticulous care in removing the entire clot. The patient should be treated with anticoagulants postoperatively to prevent a recurrence of the problem. The main theoretical advantage of venous thrombectomy is a reduced incidence of postthrombotic syndrome. Objective data to support this contention do not exist.

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The use of minimally invasive techniques of removing gallstones, and the gall‐bladder, is an attractive option for patients who may be severely ill with pancreatitis. We describe here a patient with gallstone pancreatitis who was managed completely by endoscopic techniques consisting of endoscopic retrograde cholangiopan‐creatography (ERCP) followed by laparoscopic cholecystectomy.