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D F Gruber

Publications and source records attributed to D F Gruber.

23 records · Page 2Linked to original sources
PubMed1977

Temporal transition in the site of rat erythropoietin production.

Plasma erythropoietin levels have been determined in nephrectomized, hepatectomized, nephrectomized and hepatectomized, and intact hypoxic rats--1, 2, 3 and 8 weeks of age. The liver appears to be the primary site of erythropoietin production during the first 2 weeks of life. By the third week, the kidneys began producing erythropoietin and by 8 weeks, they were the major organs of erythropoietin production. Indirect immunofluorescent staining for erythropoietin of renal and hepatic tissue correlated with the results of the erythropoietin bioassay. Fluorescent staining of glomerular cells in the kidney and macrophages or Kupffer cells in the liver implicate these areas as possible specific sites of erythropoietin production.

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PubMedDate not supplied

Alteration of rat polymorphonuclear leukocyte function after thermal injury.

One portion of host defense to bacterial challenge(s) involves the activation and infiltration of endogenous polymorphonuclear leukocytes. Thermal injuries are frequently associated with immunologic abnormalities including alterations of polymorphonuclear leukocyte-associated nonspecific resistance. We examined isolated peripheral rat polymorphonuclear leukocytes for alterations in membrane potential, oxidative capability, and locomotor function after the experimental application of 20% full-thickness body surface area thermal injury. Thermal injury resulted in significant reductions of peripheral red blood cell concentration(s) and increases in leukocyte and platelet concentrations for 42 days after injury. In addition to the quantitative changes, polymorphonuclear leukocytes also demonstrated altered qualitative functions. Compared with phorbol myristate acetate-induced activation of normal cells, polymorphonuclear leukocyte membranes from thermal-injured animals were electrophysiologically less responsive for 3 weeks after injury. The ability of polymorphonuclear leukocytes to produce intracellular H2O2, a measure of oxidative function, was also significantly decreased for 7 days after injury. The paradox in this paradigm of thermal injury was the demonstration of peripheral polymorphonuclear leukocyte quantitative increases with concurrent significant qualitative impairment. Qualitative lesions included altered states of membrane depolarization and depressed oxidative capability that may individually, or collectively, reduce nonspecific immune capabilities of the host to levels that are inadequate to combat infection.

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PubMedDate not supplied

Bone marrow myelopoiesis in rats after 10%, 20%, or 30% thermal injury.

The high incidence of serious opportunistic infections that follow thermal injuries is well documented. Normal levels of functioning leukocytes are essential to the host's ability to resist infection. This study examined alterations in murine granulopoiesis after the inducement of a standardized, sublethal, third-degree burn covering 10%, 20%, or 30% of the dorsal body surface area. Significant alterations arose in peripheral leukocyte concentrations after inducement of uncomplicated thermal injury. In general, within the first day of injury, all three trauma levels produced a peripheral leukocytosis that lasted for 35 days or more. The leukocytoses that followed 20% and 30% injuries were similar and in numerous respects paralleled previously reported human peripheral responses after similar levels of thermal trauma. Differential examinations of peripheral blood demonstrated the peripheral leukocytosis to be due primarily to the influx of morphologically mature-appearing polymorphonuclear neutrophils. Premature bone marrow release did not appear to be a factor as immature polymorphonuclear neutrophils were seldom greater than 2% of polymorphonuclear neutrophil totals. Bone marrow granulopoietic activity was examined by in vitro clonal cell culture techniques and assessed over a period of 35 days after injury. Granulocyte-macrophage colony forming cells (GM-CFC), indicative of marrow progenitor cell concentrations, were significantly increased for 28 to 35 days after 10% injury and 11 to 14 days after 20% or 30% injury. Normal or increased progenitor cell concentrations and a lack of morphologically appearing premature forms suggest that the leukocytosis is the result of injury-induced alteration(s) in polymorphonuclear neutrophil margination or release mechanisms.(ABSTRACT TRUNCATED AT 250 WORDS)

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PubMedDate not supplied

Quantitative and functional alterations of peripheral blood neutrophils after 10% and 30% thermal injury.

Polymorphonuclear leukocytes (PMNs) comprise the majority of early nonspecific inflammatory responses to infection or trauma and, as such, must be of sufficient number and qualitative function to properly limit and combat inflammation. Peripheral PMNs isolated from rats that received 10% or 30% body surface area full-thickness thermal injuries were quantitated and examined for functional alterations in membrane potential and cytosolic hydrogen peroxide production for 35 days after thermal injury. With 10% thermal injury, leukocytes increased quantitatively to experimental maximums that were 70% above normal on day 7 before a return to normal by day 28. Platelet levels showed a nonsignificant decrease for 2 days after thermal injury before increasing to levels 20% to 40% above normal through day 28. Phorbol myristate acetate-induced PMN membrane depolarization was inhibited as much as 30% for 21 days after 10% thermal injury. No changes in oxidative activity were apparent except for day 14, when hydrogen peroxide production was 40% above normal. With 30% thermal injury, leukocyte quantities were three to five times normal, with increased relative numbers of PMNs and decreased lymphocytes through day 28. Platelet levels decreased for 4 days before increasing to levels 30% to 47% above normal through day 21. Compared with 10% thermal injury, 30% thermal injury further reduced the ability of PMN membranes to depolarize through day 35. In addition, PMN hydrogen peroxide production was 30% lower on day 1 and increased thereafter to levels that were 40% above normal on day 21.

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