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B A Brockway

Publications and source records attributed to B A Brockway.

8 recordsLinked to original sources

Forearm and finger hemodynamics, blood pressure control, and lipid changes in diabetic hypertensive patients treated with atenolol and prazosin. A brief report.

Hypertension and diabetes mellitus frequently coexist and are independent risk factors for reduced peripheral perfusion. Antihypertensive medications that reduce blood pressure and improve peripheral perfusion would have advantages in diabetic hypertensive patients. In a randomized, two-placebo-period, single-blind, two-way, crossover study, finger and forearm blood flow, lipid levels, and blood pressure control were determined in 19 diabetic hypertensive patients given prazosin and atenolol, with each drug and placebo period lasting four weeks. Both drugs reduced blood pressure (sitting, 157/95 to 142/84 mm Hg for atenolol and 155/95 to 138/82 mm Hg for prazosin; standing, 154/94 to 144/84 mm Hg for atenolol and 154/94 to 133/81 mm Hg for prazosin). Lipid levels did not change, except that low-density lipoprotein levels decreased from 148 to 127 mg/dl with prazosin. Atenolol did not change forearm or finger blood flow or vascular resistance. Prazosin increased blood flow and reduced vascular resistance in both finger and forearm. In conclusion, prazosin demonstrated a potentially more appropriate hemodynamic profile than atenolol in diabetic hypertensive patients in this study.

Adult↗

Thrombus imaging in a primate model with antibodies specific for an external membrane protein of activated platelets.

The activated platelet is a potential target for the localization of thrombi in vivo since, after stimulation and secretion of granule contents, activated platelets are concentrated at sites of blood clot formation. In this study, we used antibodies specific for a membrane protein of activated platelets to detect experimental thrombi in an animal model. PADGEM (platelet activation-dependent granule-external membrane protein), a platelet alpha-granule membrane protein, is translocated to the plasma membrane during platelet activation and granule secretion. Since PADGEM is internal in unstimulated platelets, polyclonal anti-PADGEM and monoclonal KC4 antibodies do not bind to circulating resting platelets but do interact with activated platelets. Dacron graft material incubated with radiolabeled KC4 or anti-PADGEM antibodies in the presence of thrombin-activated platelet-rich plasma bound most of the antibody. Imaging experiments with 123I-labeled anti-PADGEM in baboons with an external arterial-venous Dacron shunt revealed rapid uptake in the thrombus induced by the Dacron graft; control experiments with 123I-labeled nonimmune IgG exhibited minimal uptake. Deep venous thrombi, formed by using percutaneous balloon catheters to stop blood flow in the femoral vein of baboons, were visualized with 123I-labeled anti-PADGEM. Thrombi were discernible against blood pool background activity without subtraction techniques within 1 hr. No target enhancement was seen with 123I-labeled nonimmune IgG. 123I-labeled anti-PADGEM cleared the blood pool with an initial half-disappearance time of 6 min and did not interfere with hemostasis. These results indicate that radioimmunoscintigraphy with anti-PADGEM antibodies can visualize thrombi in baboon models and is a promising technique for clinical thrombus detection in humans.

Animals↗

Kinetics of pulmonary platelet deposition and clearance during thrombin-induced microembolism in rabbits.

Using 111In-labeled autologous platelets, we studied the kinetics of pulmonary platelet deposition and clearance in relation to hemodynamic and structural events during thrombin-induced pulmonary microembolism in rabbits. Autologous platelets were radiolabeled and returned to animals prior to infusion of thrombin (100 units/kg over 15 min) (n = 20) or saline (n = 6). All animals were pretreated with tranexamic acid, an inhibitor of fibrinolysis. Thrombin-treated animals manifested progressive increases in mean pulmonary platelet activity, reaching a maximum of 38% above baseline (p less than .0001), whereas no change was observed in saline-treated controls. Animals that died during, or immediately following, thrombin infusion manifested significantly greater increases in pulmonary platelet uptake (mean 1.55 +/- 0.47 times baseline), compared to surviving animals (1.14 +/- 0.16; p less than .05 survivors vs. nonsurvivors). In surviving animals, following cessation of thrombin, pulmonary platelet activity cleared gradually, with a half-time of approximately 12 min. Thrombin reduced circulating platelet counts (p less than .001), increased mean pulmonary artery pressure (13 +/- 3 mm Hg to 18 +/- 6 mm Hg; p less than .0001), and reduced mean systemic arterial pressure (55 +/- 10 mm Hg to 44 +/- 7 mm Hg; p less than .001). The time courses of these events approximated that of thrombin-induced pulmonary platelet uptake. Furthermore, the increase in pulmonary artery pressure occurred predominantly in the group of animals in which the increase in pulmonary radiolabeled platelet activity exceeded the median value of 20%. Postmortem histology showed extensive pulmonary thrombus extending from small arterial to capillary levels in animals that died during, or immediately following, thrombin infusion, but not in surviving animals. Our findings suggest that platelet aggregation plays an important role in the pathogenesis of hemodynamic change following thrombin-induced pulmonary embolization.

Animals↗

Magnetic resonance imaging with gadolinium-DTPA for detecting cardiac transplant rejection in rats.

To date, no noninvasive tool has gained widespread acceptance as an adequate substitute for endomyocardial biopsy for the diagnosis and grading of cardiac transplant rejection. We examined the potential role of magnetic resonance imaging with gadolinium (Gd)-diethylenetriamine penta-acetic acid (DTPA) image enhancement for the diagnosis of cardiac graft rejection. We studied 15 rats with heterotopic cardiac transplants, nine of which received no immunosuppression, and six of which received cyclosporine, azathioprine, and methylprednisolone. The animals underwent magnetic resonance imaging, which was immediately followed by sacrifice (2-12 days after transplant). Myocardial image enhancement was assessed on T1-weighted images performed before and after administration of Gd-DTPA, 0.5 mmol/kg. Histological specimens were graded I, II, or III to indicate increasing severity of rejection. In the absence of rejection, Gd-DTPA induced mild homogeneous myocardial enhancement. Ten of 11 cases with Grade II or III rejection manifested one or more areas of intense myocardial enhancement. The extent and distribution of intense myocardial enhancement corresponded to the severity and distribution of histological rejection. Quantitative myocardial enhancement, expressed as the ratio of maximal signal intensity after Gd-DTPA to signal intensity before Gd-DTPA administration, separated Grade I animals (1.61 +/- 0.27; mean +/- SD) from Grades II (2.89 +/- 0.58) and III (3.10 +/- 0.77; p less than 0.01) animals. In conclusion, cardiac transplant rejection is characterized by intense T1-weighted image enhancement after administration of Gd-DTPA. Magnetic resonance imaging with Gd-DTPA thus has potential application in the clinical diagnosis of cardiac transplant rejection.

Animals↗

Effect of amrinone on right ventricular function: predominance of afterload reduction.

Although the bipyridine agent amrinone is reported to have a positive inotropic effect on the left ventricle, the effect of this drug on right ventricular contractility in the clinical setting is unknown. We studied the effect of short-term intravenous administration of amrinone on right ventricular systolic function in nine patients with severe congestive heart failure and, using radionuclide ventriculography, examined the right ventricular end-systolic pressure-volume relationship to determine whether reduced right ventricular afterload or increased contractility predominantly accounted for the observed improvement in right ventricular systolic function. In each patient the right ventricular end-systolic pressure-volume relationship was derived with use of varying doses of nitroprusside. After nitroprusside was stopped, intravenous amrinone (3 mg/kg) caused decreases from baseline in pulmonary arterial end-systolic pressure in eight of nine patients (23 +/- 11% [overall mean +/- SE], p less than .05), and in pulmonary vascular resistance in all patients (38 +/- 6%, p less than .001). Right ventricular end-systolic volume decreased (23 +/- 8%, p less than .01) and right ventricular ejection fraction increased (31 +/- 10%, p = .01). The amrinone-induced decrease in right ventricular end-systolic volume was compared with that predicted for right ventricular afterload reduction alone based on the effect of amrinone on pulmonary arterial end-systolic pressure and the pressure-volume relationship observed during infusion of nitroprusside.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Echocardiography and cardiac transplantation: a literature review and practical approach.

This article reviews the utility of noninvasive echocardiography in the detection of early cardiac transplant rejection before and after the use of cyclosporine. It addresses the use of Doppler and two-dimensional echocardiography in the routine cardiac evaluation of the heart-transplant patient, including the use of two-dimensional echocardiography in guiding the endomyocardial biopsy procedure.

Cyclosporins↗