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Objective: Oxygen radical mediated endothelial injury plays an important role in cardiovascular disease. Carvedilol, a new β blocker and antihypertensive agent, has been shown to have antioxidant activity. The aim of this study was to determine whether carvedilol protects oxygen radical induced endothelial injury. Methods: Cultured bovine pulmonary artery (BPAEC) and human umbilical vein endothelial cells (HUVEC) were used and oxygen radicals were generated by xanthine-xanthine oxidase or phorbol myristate acetate (PMA) activated human neutrophils. Cell injury was assessed by lactate dehydrogenase (LDH) release and cell death, or 51Cr release from prelabelled BPAEC. The electron paramagnetic resonance (EPR) spin trapping technique was used to detect the amount of radical spin adducts formed in cell lipids. Results: Carvedilol dose dependently inhibited xanthine-xanthine oxidase induced LDH release from BPAEC and HUVEC, with IC50 values of 3.8 μM and 2.6 μM, respectively, and significantly reduced cell death by xanthine-xanthine oxidase. Other β blockers tested (propranolol, labetalol, pindolol, and celiprolol) showed a mild effect or no effect at all. Increasing the time of pretreatment with carvedilol enhanced its cell protective effect against oxidative stress. Carvedilol also protected BPAEC dose dependently from PMA activated, neutrophil induced cell injury. Carvedilol had no effect on xanthine oxidase activity. EPR study confirmed that xanthine-xanthine oxidase induced the formation of lipid derived radicals in cell lipids and carvedilol scavenged free radicals, as indicated by the decreased EPR signal. Conclusions: Carvedilol protects endothelial cells against oxygen radical mediated cell injury and death by scavenging free radicals. The prevention of oxidative injury to endothelial cells might potentially contribute to the clinical beneficial effects of carvedilol as an antihypertensive agent.Cardiovascular Research 1994;28:400-406 [ABSTRACT FROM PUBLISHER]

The clinical course of a patient with subarachnoid hemorrhage and increased systemic fibrinolysis is presented. Mechanisms to explain the fibrinolytic activity in this particular case are discussed in detail. Evidence is presented to show that systemic fibrinolysis was increased during the procedure of angiography. The complications of both the subarachnoid hemorrhage and angiography in this patient suggest that patients with subarachnoid hemorrhage should be evaluated for increased systemic fibrinolytic activity as part of a routine hemostatic workup. [ABSTRACT FROM AUTHOR]

A pregnant patient with Australia antigen-positive hepatitis developed fulminant hepatic failure with coma shortly after her delivery. Plasmapheresis with plasma exchange was instituted. Her blood became negative for Australia antigen and she emerged from coma on the fifth day of treatment and plasmapheresis was terminated. Within 48 hours, she developed pulmonary infiltrates, leucocytosis and fever and her blood was again positive for Australia antigen. Resumption of plasmapheresis was contraindicated by thrombocytopenia. Hyperimmune Australia-antibody-rich plasma (220-350 ml. per day) was given slowly intravenously for three days. A dramatic clinical response ensued, the patient's blood became negative for Australia antigen and she proceeded to make a steady and ultimately complete recovery. [ABSTRACT FROM AUTHOR]

Presents a study which examined patients with hypersplenic hemolyic anemia before and after splenectomy. Findings obtained from the laboratory examinations performed on the patients; Effect of splenectomy on red cell production; Discussion.

Presents a discussion on the developmental rehabilitative approach for the treatment of schizophrenia in the United States. Reduction of functional deficits through the use of therapeutic activity; Emphasis on the approach on the intrapsychic maturation; Stages of treatment.