Biomedical subjects
Publications and source records attributed to S S Iyer.
Profound circulatory failure developed in a 45-year-old man after an acute myocardial infarction. A left ventricular assist device was used successfully to bridge the patient to transplantation despite recurrent and medically refractory ventricular arrhythmias that lasted from the second through the 12th day of circulatory support.
The brachial approach for recanalizing an abdominal aortic occlusion utilizing a combination of thrombolysis and balloon angioplasty is described. The patient was deemed too ill to permit any surgical intervention. The unique aspects of the procedure are described including angioplasty of the unmasked (by lytic therapy) aortoiliac bifurcation stenoses utilizing double wires and double balloons through a single arteriotomy site. The advantages of the brachial approach in managing this unusual entity are outlined.
Rotational coronary ablation was utilized in two cases in which balloon angioplasty initially failed. In both cases, the balloon could not be fully expanded despite using high (18 Bar) inflation pressure. Rotational coronary ablation debulked the lesion, in each instance, and permitted successful balloon angioplasty to be accomplished without difficulty. These cases illustrate the point that complementary deployment of devices may not only improve the primary success of percutaneous coronary interventions, but also may widen its scope.
Thrombolysis of two occluded above-knee femoropopliteal Gortex bypass grafts utilizing the popliteal approach for catheter placement was successfully performed without complication. In both cases, the proximal anastomoses of the graft could not be identified. A percutaneous popliteal approach was used for catheter placement and delivery of urokinase. Angioplasty was performed on the unveiled stenoses that, presumptively, led to graft closure. Selective thrombolysis via catheter placed from popliteal approach is a new technique for recanalization of occluded femoropopliteal bypass grafts and warrants further investigation.
The neutrophil serine proteinases elastase and cathepsin G produce connective tissue injury, the extent of which depends on the balance between these enzymes and their inhibitors. The most important of these inhibitors is alpha 1-proteinase inhibitor, a member of a superfamily of homologous proteins known as serpins. Neutrophil cytosol inhibited the activities of human neutrophil elastase and cathepsin G in a dose-dependent fashion. To demonstrate formation of an enzyme-inhibitor complex, we combined 125I-elastase or 125I-cathepsin G with neutrophil cytosol or alpha 1-proteinase inhibitor and analyzed the products by polyacrylamide gel electrophoresis. Unbound elastase and cathepsin G each migrated to an apparent molecular weight of 25 kDa. In the presence of cytosol from neutrophils both radiolabeled enzymes migrated with a relative size of 68 kDa, whereas in the presence of alpha 1-proteinase inhibitor the relative size was 85 kDa. Enzyme-inhibitor complexes were stable in sodium dodecyl sulfate at 100 degrees C but were dissociated by hydrolysis in ammonium hydroxide (1.5 mol/L) at 37 degrees C. Formation of each complex was prevented by pretreatment of elastase or cathepsin G with diisopropylfluorophosphate, indicating that the inhibitor binds to the active site of the enzyme. Exposure of either alpha 1-proteinase inhibitor or neutrophil cytosol to the myeloperoxidase-H2O2-halide system prevented complex formation, suggesting the presence of an oxidizable amino acid at the binding site of the inhibitor. By electrophoretic analysis, the molecular weight of the cytosolic inhibitor was 43 kDa and neutrophils contained approximately 1 attomol of inhibitor per cell. The isoelectric points of the elastase and cathepsin G inhibitor were 5.5-5.9 and inhibitors of the two proteinases coeluted using size exclusion chromatography. These data demonstrate that human neutrophil cytosol contains a single serpinlike protein that inhibits elastase and cathepsin G. The inhibitor may be important in protecting the intracellular environment from proteolytic injury during degranulation.
Recanalization of two occluded posterior tibial arteries was successfully achieved by utilizing a retrograde approach via a posterior tibial artery cutdown at the level of the ankle. Both cases were previously unsuccessfully attempted by using an antegrade approach. Thus, the choice of access vessel (arterial entry site) becomes a crucial determinant of angioplasty success.
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Angioplasty using the percutaneous popliteal approach was utilized in 50 patients (PTS) to recanalize 59 occluded superficial femoral arteries which had been unsuccessfully canalized by using the antegrade approach because of either a flush origin occlusion or inability to maintain the guide wire in the true lumen. All PTS had claudication; 8 had rest pain; 3 had non-healing ulcers. The laser Probe was used in 17 cases and the Rotablator in 3 cases. Occlusion length varied between 1 and 40 cm: 7 lesions were less than 10 cm (group 1); 9 were between 10 and 20 cm (group 2); and 43 were greater than 20 cm (group 3). An angiographic success was obtained in 48/59 lesions (81%): 14/16 (87%) in groups 1 and 2 and 34/43 (79%) in group 3. Three PTS needed complementary common femoral endarterectomy and one required percutaneous aspiration of a thromboembolus. Complications included: arterial perforation and/or dissection (without clinical sequelae) in 11 and a popliteal hematoma in 1 PT. One patient with a severely ischemic leg underwent successful emergency vascular surgery, while another limb salvage patient required below-knee amputation. There was no worsening of limb ischemia from any popliteal approach attempt. At discharge, 39 patients (78%) whose outcome would have been unsuccessful with the traditional antegrade approach were clinically improved after utilizing the popliteal approach to achieve a successful angioplasty procedure.
A not well-appreciated but clinically important aspect of malignant tumours is their effects on distantly located host cells. The effects, termed paraneoplastic syndromes, also pose an intriguing mechanistic problem: how do malignant cells influence properties of host cells not in contact with them? Erythrocytes from the circulation of rats bearing intraperitoneal Yoshida ascites sarcoma exhibit higher agglutinability with concanavalin A (Con A) than the cells from normal animals. Since the tumour and the red cells are not in contact, the enhanced agglutinability of the latter is a paraneoplastic effect. The mechanism by which the tumour brings about this effect is investigated as a model for paraneoplastic syndromes. The cell-free ascites fluid is able to impart high agglutinability on cells from normal animals in vitro. Also, when injected intraperitoneally in normal animals, the ascites fluid is able to enhance the agglutinability of erythrocytes in circulation. Apparently the tumour produces a substance(s) that appears in the ascites fluid and is able to diffuse into circulation, explaining the mechanism by which it can reach distant sites. From the cell-free ascites fluid three fractions have been isolated that are active in vitro. Of these, only one showed activity in vivo. From this fraction, a glycoprotein has been purified to homogeneity that confers maximal Con A-agglutinability on normal erythrocytes at 8 x 10(-7)M, at which concentration 6,400 molecules bind per cell. The protein has a molecular weight of 600 kDa in the native state and a pI of 5.35. It is made up of 4 identical subunits of Mr 170,000. It is detected in the plasma of tumour-bearing but not normal rats.(ABSTRACT TRUNCATED AT 250 WORDS)
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A family of beta-glucosidase-stimulating proteins (called cohydrolase SPH-I here) was isolated from bovine, Gaucher human and control human spleens. All preparations exhibited a similar pattern of four major electrophoretic bands in polyacrylamide when stained with the cationic dye, Stains-All. The bovine bands migrated more rapidly, while the two types of human cohydrolase migrated very similarly. The two human preparations differed in several respects: the concentration was much higher in Gaucher spleen; the Gaucher factors eluted a little earlier from gel permeation and decyl agarose columns; much more of the cohydrolase was bound by a concanavalin A column; the control bands stained less intensely in gels than the Gaucher bands. Antibodies raised in rabbits to bovine cohydrolase reacted with all three preparations. All four bands from Gaucher cohydrolase showed similar ability to stimulate glucosidase and to bind the antibodies. It is evident that the cohydrolases from control and Gaucher spleens are similar in many respects, yet differ in some secondary fashion, possibly in carbohydrate content. It is suggested that Gaucher cohydrolase is formed from normal cohydrolase by the nonenzymatic action of cellular glucose over a period of many years, due to slowed catabolism of the cofactor.
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Inactivation of (Na+ + K+)-ATPase of Yoshida sarcoma cells and beef brain microsomes by phospholipase A2 and a cytotoxin P6 from snake venom has been examined in relation to their activity to degrade phospholipids. Cytotoxin P6 which was most basic and devoid of phospholipase activity was most effective in inhibiting the (Na+ + K+)-ATPase of Yoshida sarcoma cells. Phospholipase A2 from Naja naja which was most active in degrading phospholipids was least effective in inhibiting (Na+ + K+)-ATPase in Yoshida sarcoma cells or in beef brain microsomes. Addition of trace amounts of cytotoxin P6 to the phospholipase considerably enhanced the inactivation of (Na+ + K+)-ATPase. The evidence suggests that the charge of the inhibitor protein and its specific structure play an important role in the inactivation of (Na+ + K+)-ATPase.
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