Enhanced streptokinase-induced thrombolysis using heparin in a rabbit model.

Heparin potentiation of clot lysis by streptokinase was studied in a rabbit model. Clot was initiated in the rabbit aorta with stasis and thrombin and allowed to naturally propagate proximally until stasis met flow. The clot was allowed to age for 1 h before assigning treatment. Fifteen rabbits (group I) were given streptokinase (10,000 IU/h) and 11 rabbits (group II) were given streptokinase (10,000 IU/h) plus sodium-heparin (120 IU/h). Thrombolytic therapy was continued for 5 h. Clot lysis averaged 30% in group I and 70% in group II. Ten of 11 rabbits in group II had more than 50% clot lysis, whereas only 4 of 15 in group I had this degree of lysis. One group II rabbit and four group I rabbits died prematurely; each was noted to have clot propagation at the time of death. While a trend for amelioration of hypofibrinogenemia was observed in the group receiving both streptokinase and heparin, this difference was not statistically significant. We conclude, in the animal model, that thrombolysis by a combination of heparin and streptokinase is more effective than streptokinase alone. Systemic effects are apparently no worse with the combination.

Etiology and prevention of thromboembolic disease. Taming a complex circulatory malfunction.

Deep venous thrombosis is a complex process involving many factors in the circulatory system, an important one apparently being the intrinsic fibrinolytic system. Specific activators of the process include venous trauma and hypercoagulability states. In spite of efforts at prophylaxis, venous thrombosis will occur, a dangerous condition in itself and also a precursor of pulmonary embolism. Several schemes for prophylaxis, including drug regimens and mechanical means, have been tried, and future research will surely identify others. A patient's best protection against thrombosis at present, however, is a vigilant physician with a high index of suspicion who will expedite diagnosis and treatment if necessary.

Clinical experience with preoperative myocardial nutrition management.

Three hundred and twelve elective adult coronary artery surgery patients were divided into five groups differing as to preoperative glucose or fat loading. The control group (n = 54) had a mean myocardial glycogen level of 880 mg/100 gram heart weight, a 18.5% incidence of serious ventricular arrhythmias, 24.2% dependence on vasopressors, a mean peak postoperative SGOT level of 100 IU, and a 3.7% perioperative transmural myocardial infarction rate. The 10% glucose loading group (n = 67) had elevated myocardial glycogen of 1180 mg/100 gram heart, 14.9% serious ventricular arrhythmias but a lessened dependence on vasopressors (17.9%), a peak post bypass SGOT of 74 IU, and 2.9% transmural infarction rate. A 20% glucose overnight loading group (n = 65) had myocardial glycogen level of 1270 mg/100 gram heart, a 23.0% incidence of serious ventricular arrhythmias, a significant reduction in vasopressor dependence (3.1%), no transmural myocardial infarctions, and peak post bypass SGOT of 53 IU. The intravenous fats (10% Intralipid) group (n = 57) had the highest glycogen level of 1509 mg/100 gram heart, the lowest peak SGOT of 51 IU, no infarctions, a low vasopressor dependence (5.2%), but high rate of serious ventricular arrhythmias (22.8%). The oral fat and 20% glucose loading group (n = 69) had a myocardial glycogen of 1486 mg/100 gram heart, a low vasopressor dependence rate of 4.3%, no infarctions, a peak SGOT of 66 IU, and the lowest serious ventricular arrhythmia rate of 4.3%. These results suggest that it is possible to alter prebypass myocardial substrate levels against the stresses of cardiac surgery with fat and/or glucose loading and that myocardial protection is evident.(ABSTRACT TRUNCATED AT 250 WORDS)