Biomedical subjects
Publications and source records attributed to L Lollini.
An incidental finding of unilateral ovarian adenocarcinoma in a bonnet monkey (Macaca radiata) was examined histologically and ultrastructurally. The tumor was somewhat confusing histologically, but had many of the ultrastructural characteristics of endometrioid carcinoma of man.
The effects on renal morphology of exchange transfusion with stroma-free hemoglobin solutions (SFHS) were compared in rats to the results obtained using an asanguineous resuscitative fluid containing albumin. Animals underwent 75 per cent blood volume replacement, and tissue collected at intervals after the exchange transfusion was examined by light and electron microscopy. Urine volumes, osmolarity, and pH also were determined, and serum creatinine and blood urea nitrogen were measured both before and after exchange transfusion. Hemoglobin was filtered through the renal glomerular basement membrane, and a portion was reabsorbed into the proximal tubular cells in the form of absorption droplets. Unabsorbed hemoglobin was excreted in the urine. Despite a distention of proximal and distal tubules 5 hours after exchange transfusion with SFHS, there was no ultrastructural evidence of renal parenchymal damage. Proximal tubular cells of albumin-exchanged animals contained fewer protein absorption droplets and no intraluminal material. The apparent higher rate of glomerular filtration of hemoglobin over albumin probably reflected the dissociation of hemoglobin into dimers, resulting in a diuresis. Urine volumes were 3 times greater in SFHS-exchanged animals than in albumin-treated rats, and the urine was relatively hypoosmolar in the former. The greater urine volumes in SFHS-treated animals also were associated with a large reduction in intravascular fluid volume. There was no alteration of serum creatinine or blood urea nitrogen after exchange transfusion with albumin and only a mild elevation in blood urea nitrogen in SFHS-treated rats. The latter most likely was a result of prerenal hypovolemia. SFHS, even when exchange-transfused in massive quantities, does not appear to affect renal function or ultrastructural morphology adversely. However, the rapid disappearance of hemoglobin from the intravascular space, the consequent loss of intravascular fluid volume, and the diuresis induced by its administration are complications which must be overcome before the product can be a useful adjunct in the treatment of hemorrhagic shock.
Hepatic morphology was studied in rats that were exchange transfused with either a stroma-free hemoglobin solution (SFHS) or with various asanguineous resuscitative fluids. The animals under-went 75 per cent blood volume replacement and tissues were collected and fixed at timed intervals after the exchange transfusion. In addition, blood volumes were determined, using chromium labeled red blood cells, in both albumin and SFHS-treated rats at varying time periods after exchange transfusion. One hour following exchange transfusion, livers of animals infused with asanguineous fluids demonstrated marked centrolobular hepatocellular vacuolization and mitochondrial shape alterations consistent with the effects of hypoxia. SFHS appeared to protect the liver from these early abnormalities. However, at later time intervals livers of albumin-treated animals appeared normal, whereas those of SFHS-transfused rats exhibited centrolobular necrosis. Blood volume was reduced approximately 10 per cent during the first 18 hours after exchange transfusion with albumin, while SFHS-treated rats experienced a 42 per cent blood volume decrement in only 6 hours. Blood volumes were near normal in all animals by 48 hours. These findings suggest that SFHS protects the liver from hypoxia immediately after exchange transfusion, presumably by its ability to transport and release oxygen. However, the eventual disappearance of hemoglobin from the intravascular space is associated with a marked reduction in blood volume which is accompanied by hepatic ischemia and centrolobular necrosis.
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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.