Histologic and ultrastructural effects of stroma-free hemoglobin solutions on rat liver, kidney, and brain.
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Biomedical subjects
Publications and source records attributed to H I Friedman.
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This report provides information on the morphology of rat intestinal epithelial cells during fat absorption. In addition, the role of protein metabolism in this process has been evaluated by blocking its synthesis with puromycin and studying the fine structure of mucosal cells from rats at various times after fat intubation. The results indicate that SER-derived vesicles, containing fat droplets, migrate from the apical cytoplasm of the absorptive cell and fuse with saccules or vacuoles of the Golgi complex. Arguments are made that the Golgi complex is important in completing chylomicron formation and in providing appropriate enveloping membranes for the chylomicron. Such membranes may be necessary for Golgi vacuoles to fuse with the lateral cell membranes and release chylomicra. Puromycin treatment causes the absorptive cell to accumulate increased quantities of lipid that are devoid of membrane during fat absorption. In addition, puromycin-treated cells contain much less RER and Golgi membranes are strikingly decreased in number. In this paper we discuss the consequences of these abnormalities and suggest that continued protein synthesis by the RER is required in order to generate Golgi membranes. If such membranes are absent the cell's ability to discarge chylomicra is impaired and lipid accumulates.
Plasma DEHP concentrations were measured weekly in whole blood and red cell concentrates (RCC) during 21 days of storage in standard CPD within PL-130 blood bags. In addition, DEHP and MEHP accumulation patterns were investigated in blood stored for 42 days in modified CPD with adenine within PL-146 and BB-69 storage containers. Total per-unit plasma DEHP of RCC units was 49 to 71 per cent of the total in plasma of whole blood units (PL-130). From 28 to 42 days, mean DEHP levels were 12 to 19 per cent higher in whole blood stored in PL-146 than in BB-69. Although MEHP was not found in any blood bag plastic, MEHP accumulated in plasma during whole blood storage. MEHP concentrations were 2.8 to 3.8 times higher in plasma stored in BB-69 than in PL-146. It is postulated that MEHP arises from hydrolysis of DEHP by plasma lipase, even in frozen plasma sample, and that the rate of this reaction is influenced by blood bag plastic surface characteristics.
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The essential fatty acids, particularly arachidonic, are important components of intracellular membrane systems. Their absence during dietary manipulation has been postulated to cause alterations in both composition and function of membranes and associated enzyme systems. In the current investigation, the effect of essential fatty acid deficiency on the induction of hepatic microsomal membranes my phenobarbital was studied. Control rats were fed a standard chow diet and either injected daily for 4 days with phenobarbital or with a placebo. Experimental animals were given an essential fatty acid-deficient (EFAD) diet and similarly injected with either phenobarbital or placebo. Following the above regimens, liver tissue was obtained for electron microscopy and biochemical membrane analysis. Control animals given phenobarbital displayed a marked proliferation of smooth endoplasmic reticulum in comparison to placebo controls. In contrast, EFAD rats did not exhibit an endoplasmic reticulum response to phenobarbital injection and appeared to recover from the drug administration injection more slowly than control animals. The alterations in fatty acid composition characteristic of an EFAD diet were observed in the microsomal membranes of the deficient animals. The concentrations of palmitic, palmitoleic, oleic, and 5,8,11-eicosatrienoic acids were significantly increased above that found in control animals. Concentrations of linoleic and arachidonic acids were reduced. Phenobarbital administration significantly increased the concentrations of palmitic, linoleic, and arachidonic acids in microsomal fractions of chow-fed animals but not in EFAD animals. Conversely, eicosatrienoic acid concentrations increased in phenobarbital-treated EFAD animals but not in chow-fed, drug-injected rats. The triene/tetraene ratio reflected these alterations. Essential fatty acid deficiency causes biochemical alterations of the hepatic microsomal membranes which are exaggerated by the administration of phenobarbital. These compositional changes appear to alter the functional ability of the membranes to proliferate in response to phenobarbital and, thereby, inhibit the efficaceous metabolism of this drug.
The breast implant crisis has been widely publicized. Beyond its immediate problems for the patients, the crisis has also discredited the use of silicone rubber as one of the most widely used biomaterials. Silicone elastomer or gel, the primary material in mammary prostheses, may be exposed to the body's tissues via envelope rupture, gel bleed, or elastomer fragmentation. Local responses to silicone include granulomatous inflammation, capsular contraction, and infection, all in varying degrees depending on ill-defined factors, which may include patient condition, peri- and postoperative complications, and hereditary predisposition, as well as material properties such as surface texture. The theory that silicone breast implants cause immunological disorders has not been proven. However, further study is necessary because some patients report autoimmune-like disorders (human adjuvant disease) following implant placement. Like autoimmune disease, human adjuvant disease is characterized by abnormalities of the immune response, autoantibody formation, and chronic inflammation. Silicone has been shown to play the role of an adjuvant, providing constant nonspecific stimulation of the immune system. Some researchers have hypothesized the role of silicone in specific immune reactions, including immunoglobulin formation and T-cell activation. This report examines the role of silicone as an agent of disease, focusing on material surface-tissue interactions.
A rabbit animal model of tissue edema was created to determine its effect on transcutaneous oximetry (T-com). Measurements of T-coms were performed before and at 5-minute intervals after the injection of body temperature saline into the skin and subcutaneous tissues of 5 rabbits. Photomicrographs were obtained to document the morphological appearance of edema. The injection of saline had no effect on relative T-com values. This investigation suggests that edema alone does not influence T-com measurements.