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Biomedical subjects

T F Zuck

Publications and source records attributed to T F Zuck.

At least 37 records · Page 2Linked to original sources
PubMed1979

Morphologic effects following massive exchange transfusions with a stroma-free hemoglobin solution. II. Kidney.

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.

Animals↗
PubMed1978

Morphologic effects following massive exchange transfusions with a stroma-free hemoglobin solution. I. Liver.

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.

Animals↗
PubMed1977

Characteristics of stroma-free hemoglobin prepared by crystallization.

Stroma-free hemoglobin was prepared from outdated human red cells by crystallization. After hemolysis with water and toluene and low speed centrifugation, the solution was dialyzed against 2.8M phosphate buffer. Hemoglobin crystals formed within the dialysis casing and were washed with phosphate buffer. After being dissolved in water, dialyzed against kidney dialysis fluid, and sterilized by Millipore filtration, the hemoglobin solution obtained had normal serum potassium, sodium, and osmolality. Spectral maxima and minima were characteristic for oxyhemoglobin, and cellulose acetate electrophoresis showed a sharp, well-defined hemoglobin band and slight contamination with carbonic anhydrase. The crystallized hemoglobin solution showed no coagulant activity, and preparation from group A cells showed no blood group A activity by hemagglutination inhibition. Methemoglobin was less than 0.28 gm./dl. and did not increase with storage at refrigerated temperature for a period up to 6 months. The P50 ranged between 15 and 18 mm. Hg at pH 7.4 and n values were normal.

Crystallization↗
PubMed1976

Newborn platelet dysfunction: a storage pool and release defect.

Per cent aggregation, release and content of adenine nucleotides, and specific radioactivity were evaluated in citrated platelet-rich plasma (PRP) prepared from paired samples of maternal and cord blood. Platelets of newborn infants aggregated normally in response to highdose ADP (20 muM), strong collagen suspensions, and thrombin; however, when compared with PRP from the mothers or from normal adults, per cent aggregation in response to lower concentrations of ADP (2 muM), weak collagen, and part particularly epinephrine was markedly reduced. Nucleotide release after stimulation of the newborns' PRP with the latter two inducers was also impaired. ATP and ADP content of the newborns' platelets was also significantly less than that of their mothers or of normal adults, but specific activity was normal. The data suggest that the impairment of ADP release in the platelets of newborn infants is due to decreased sensitivity to external stimuli. Since metabolic ATP is necessary for the platelet release reaction, it is postulated that the platelet dysfunction results from a lack of metabolic ATP.

Adenine Nucleotides↗