Paul D. Altland

Life Span of the Duck and Chicken Erythrocyte as Determined with C14

Summary Measurements of the life span of the erythrocyte with glycine-2-C14 give a value of 20 days for mean survival time for the chicken and 39 days for the duck. The uptake of the a-carbon of glycine into the cell proteins in the chicken was similar to that observed in the mammals. The shape of the decay curve was typical of that observed when a homogeneous group of red cells are labeled in the marrow, and gave little evidence of re-utilization of the labeled carbon. The utilization of glycine a-carbon by the duck cells was similar to that observed in the chicken except for the rapid uptake which gave some evidence of uptake by the cells in the peripheral circulation.

Some Factors Affecting Blood Formation in Turtles

Summary Sex differences in control blood values of box turtles are presented. Mild to toxic doses of cobalt, including mineral supplement and injections of crude liver extract failed to stimulate erythropoiesis. Marked reticulocytosis was induced by repeated bleeding. High reticulocyte counts persisted for 3 weeks following the last bleeding and 4 months were required for restoration of normal erythrocyte values. Blood formation was altered by injections of folic acid antagonist, aminopterin. Arrested maturation of blood cells was detected in form of enlarged marrow blast cells as early as 5 weeks and anemia and leucopenia followed after 6 weeks treatment.

Effects of dimethyl sulfoxide on serum enzymes and tissues in exercised rats

Abstract Five hours exercise of rats increased as much as four-fold serum levels of glutamic oxalacetic transaminase (SGOT), glutamic pyruvic transaminase (SGPT), aldolase (SAld), lactic dehydrogenase (SLDH), malic dehydrogenase (SMDH) and urea nitrogen (SUN). Exercise also caused virtually complete depletion of liver glycogen, and a moderate intensification of the 5 isoenzyme bands of SLDH. Nineteen hours after exercise was terminated, approximately half of the rats showed slight to moderate fatty changes in the liver and thigh muscles. Administration of 4.5 mg/kg dimethyl sulfoxide (DMSO) i.p., without exercise increased slightly serum transaminase levels within 24 hours. DMSO combined with exercise (5 hours) increased serum enzymes as much as nine-fold and intensified all 5 isoenzyme bands of SLDH. In addition the isoenzyme band of malic dehydrogenases associated with the mitochondria was found in the serum. Nineteen hours after terminating exercise, fatty changes in the liver and thigh muscles occured in all 6 rats given DMSO and in only 3 of 6 untreated rats. These results suggest that DMSO in exercised rats enhances the permeability of cellular and mitochodrial membrane, facilities the release of tissue enzymes into the circulation, and may increase the incidence of fatty changes in the liver and in thigh muscles.

Alterations in serum enzymes and isoenzymes in various species induced by epinephrine

Abstract 1. 1. The administration of epinephrine to rats, rabbits, guinea pigs and dogs leads to an elevation of several serum enzyme levels. 2. 2. Serum lactic dehydrogenase isoenzyme patterns and histological examination indicate that several tissues may contribute to this increase, but that there is a relatively greater contribution from cardiac tissue and/or erythrocytes. 3. 3. Adrenergic blocking agents prevent the serum enzyme alterations, the tissue changes and the abnormal isoenzyme patterns induced by epinephrine. 4. 4. A likely cause of the serum elevations is an increase in cellular permeability.

Induction of Hypothermia by Dimethyl Sulfoxide in Rats Exposed to Gold Tissue and Enzyme Changes.

Summary Topical and intraperitoneal treatment of rats with DMSO produced a 1 to 2°C drop in body temperature in 5 hours at 23°C; however, those treated topically showed an early transient rise of as much as 0.7°C. No serum enzyme, urea nitrogen, or sugar changes were produced by DMSO at 23°C. The only serum enzyme changes noted during a 5-hour exposure to 1.7°C was a fall in SAkP levels, but 19 hours later a rise in serum transaminases became evident. DMSO given intraperitoneally prior to cold exposure caused a marked decrease in body temperature and a marked increase within 5 hours in all serum enzymes studied, including SGOT, SGPT, SAld, SLDH, and SMDH. DMSO did not influence SAkP values. Also, the DMSO-treated rats exposed to cold showed intensification of all 5 SLDH iso-enzyme bands and the isoenzyme band of SMDH associated with mitochondria and an increased elevation in SUN, serum glucose and hematocrit. At 5 hours, all rats exposed to cold showed marked depletion of hepatic glycogen, but repletion was delayed in the DMSO-treated group. Nineteen hours after exposure to cold, only depletion of liver glyco-gen and fatty changes in the liver, heart, or muscle persisted. Topicaly DMSO before exposure to cold did not alter the serum enzyme values or tissue changes produced by cold exposure alone. These findings show that intraperitoneal injection of DMSO in rats exposed to cold induces marked hyper-glycemia, a severe hypothermia accompanied by a marked rise in serum enzyme values and glycogen depletion, and an increased incidence of fatty changes in the liver and muscle.

Serum Alkaline Phosphatase in Dogs with Experimental Splenic and Renal Infarcts and with Endocarditis

Summary and Conclusions Infarcts of spleen and kidney were produced by vascular ligation in 13 dogs. The level of serum alkaline phosphatase increased significantly in 3 of 6 dogs with splenic infarcts and in 6 of 7 with renal infarcts. The level reached a maximum in about 24 hours and gradually returned to normal in about a week. An increase in serum alkaline phosphatase level was noted also in dogs with experimental endocarditis. This increase correlated well with the occurrence of infarcts in spleen and kidneys and proved to be of great diagnostic and prognostic value.

Effect of Altitude and Cobalt Polycythemia, Hypoxia, and Cortisone on Susceptibility of Rats to Endocarditis

Rats with polycythemia induced by exposures to simulated high altitudes developed a significantly higher incidence of endocarditis following intravenous bacterial injections than rats with cobalt polycythemia or ground level controls. No increase occurred in altitude rats when polycythemia was prevented by repeated bleedings. These findings suggest that both polycythemia and hypoxia are necessary to explain increased susceptibility of altitude rats. Cortisone increased susceptibility of ground level rats injected with Streptococcus faecalis. Unlike altitude exposures, however, cortisone did not render rats susceptible to endocarditis due to Hemophilus parainfluenza.

Effects of graded concentrations of cigarette smoke on plasma enzyme, corticosterone, and body temperature in rats

Abstract Male rats were exposed to cigarette smoke concentrations from 2.4 mg/m3 of suspended particulate matter (SPM) and 8 ppm of CO to 199 mg/m3 of SPM and 220 ppm of CO for 4 hours at rest or after light intermittent exercise. Hypothermia (37.3°C) was produced after exercise in smoke containing 15 mg/m3 of SPM and 13 ppm of CO and its severity increased at higher smoke concentrations. Plasma lactic dehydrogenase increased significantly after exercise in smoke containing 34 mg/m3 of SPM and 51 ppm of CO. An increase in the concentration of plasma creatine kinase and of blood glucose and in the density of PLDH isoenzyme Band 5 were found only at the highest smoke level (199 mg/m3 of SPM and 220 ppm of CO). Plasma corticosterone concentrations were elevated after exercise in the two highest smoke concentrations. No tissue changes were found, so elevations in plasma enzymes were attributed to increased cellular permeability. Some changes induced by smoke were more severe following light exercise and were attributed to SPM at levels exceeding 34 mg/m3 and to tissue hypoxia (COHb 11.7%) induced by Co concentrations above 51 ppm. The amount of cigarette smoke needed to induce significant systemic changes in rats greatly exceeded acceptable national air quality standards and threshold limits for SPM and CO established for man.

Streptococcal and Staphylococcal Endocarditis and Renal Lesions in Rats After Epinephrine in Oil and Dibenamine

Summary and Conclusions Five series of rats were given either 1 or 2, intravenous injections of a broth culture of S. mitis or 2 injections of a culture of Staph, aureus. Each series was divided into a control group given bacteria alone, a group given 2 daily doses of 5 mg/kg epinephrine in oil subcutaneously beginning the day before the first bacterial injection, and a third group receiving, in addition, 2 doses of 50 mg/kg Dibenamine hydrochloride 1 and 2 days before the first dose of epinephrine in oil. The animals receiving bacteria and epinephrine in oil developed a significantly higher incidence of bacterial endocarditis than either controls or rats given Dibenamine prior to epinephrine in oil. The incidence of bacterial lesions involving the renal papilla was also higher in rats given epinephrine in oil than in controls. All groups had a high incidence of focal interstitial nephritis. It is suggested that a relative and localized hypoxia induced by epinephrine in oil may be a major factor contributing to the increased susceptibility of epinephrine-treated rats to bacterial endocarditis and renal bacterial papillitis.

Effect of Exposure and Acclimatization to Gold on Susceptibility of Rats To Bacterial Endocarditis

Summary Groups of rats were exposed in a cold room maintained at 1.7°C for periods ranging from 0 to 36 days and showed little or no reduction in body temperature during this period. These groups, along with appropriate controls maintained in a normal temperature environment, were then given either 1 or 4 intravenous injections of a broth culture of Streptococcus mitis JH 26. Survivors were killed for pathologic study 7 days after the first bacterial inoculation. In control groups and in the one group of cold rats returned to a normal temperature environment after the bacterial inoculation, the incidence of severe bacterial endocarditis was 16-19% and mortality rate was 0-9%. In the groups kept in the cold room 1-36 days before and 7 days after the first inoculation, the incidence of severe bacterial endocarditis was 82-100% and the mortality rate 41-73%. The corresponding figures for rats kept in the cold room after but not before inoculation were 50 and 43% respectively. In rats acclimatized to cold for 35-36 days, the mortality rate was lower and length of survival was longer than in rats placed in the cold room only one day before bacterial inoculation.