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Biomedical subjects

D B Coursin

Publications and source records attributed to D B Coursin.

At least 55 records · Page 3Linked to original sources
PubMed1989

Exacerbation of tallysomycin toxicity in rats by concurrent exposure to sublethal hyperoxia.

Rats were given daily subcutaneous injections of tallysomycin S10b (TLM) or bleomycin (BLM) for 6 days (1.25 or 2.50 mg/day). One half of each group was exposed to 80% oxygen for the last 4 days of drug treatment and then returned to room air. TLM produced marked mortality in contrast to equal doses of BLM. Exposure to 80% oxygen increased the lethality of either TLM and BLM treatments. The cause of death appeared to be related to pulmonary changes. Two weeks following the end of treatment in the low dose experiment, the lungs of surviving BLM-hyperoxia, TLM, and TLM-hyperoxia rats demonstrated severe vascular damage consistent with both endothelial cell and smooth muscle proliferation in pulmonary blood vessels. BLM-hyperoxia rats also demonstrated a more typical diffuse interstitial disease. All treatments produced an increase in lung-to-body weight ratio and a decrease in vital capacity and total lung compliance, as compared to age-matched controls. TLM toxicity was exacerbated by short-term exposure to 80% oxygen. Morbidity and mortality appeared to be related to severe lung changes similar to the hyperoxic potentiation of BLM lung disease.

Animals↗
PubMed1988

Non-lethal hyperoxic potentiation of lung disease in the rat following subcutaneous administration of bleomycin.

Rats were treated with subcutaneous injections of either saline or 1, 3, or 5 units of bleomycin (BLM) each day for 5 days (5, 15, or 25 units total dose). One half of each group of animals was exposed to 80% oxygen for 4 days during BLM dosings. Rats treated with both 25 units BLM and hyperoxia died after being returned to room air. All remaining rats were sacrificed 6 weeks following the end of treatment. Of the BLM rats in room air, only the lungs of the 15-unit group exhibited histological change, a mild diffuse interstitial disease. Both lower dose groups demonstrated slight increases in hydroxy-proline (OHP) content, a marker of collagen deposition or lung injury. The lungs of BLM rats exposed to hyperoxia demonstrated greater increases in total lung OHP levels. The lungs of the 15-unit group demonstrated lesions consistent with diffuse interstitial pulmonary fibrosis. Short-term, sublethal hyperoxia clearly potentiated injury in the rat following subcutaneous BLM treatment as assessed by either lethality or markers of pulmonary pathology.

Animals↗
PubMed1988

Ranitidine produces minimal hemodynamic depression in stable intensive care unit patients: a double-blind, prospective study.

Ranitidine, a furan H2 receptor antagonist, is increasingly prescribed in the ICU setting. Before the availability of parenteral ranitidine, cimetidine had been the sole H2 blocker used to decrease gastric acidity in this setting. However, cimetidine has recently been shown to transiently, but significantly, reduce mean arterial pressure due to direct vasodilation in a critically ill population. Therefore, this double-blind prospective study was designed to examine the hemodynamic effects of iv ranitidine in an ICU population. Twenty-six critically ill hemodynamically stable patients were studied; all patients were already receiving ranitidine and had an arterial line and a pulmonary artery catheter in place. This study demonstrated that an iv infusion of ranitidine did not produce clinically significant hemodynamic effects in this patient population.

Adult↗
PubMed1988

The pulmonary effects of buthionine sulfoximine treatment and glutathione depletion in rats.

Buthionine sulfoximine (BSO), an inhibitor of de novo synthesis of glutathione (GSH), was used to deplete rats of GSH and determine the effect of treatment on antioxidant enzyme responses, lung injury, and the susceptibility to concurrent sublethal or lethal hyperoxia. In a preliminary experiment, total lung nonprotein sulfhydryl (NPSH) and GSH levels were measured at various times after single doses of BSO. The lowest concentrations were observed at 12 to 18 h. These experiments were used to establish a repeated dosing protocol for more prolonged GSH depletion. The lungs of rats treated with BSO for 4 days demonstrated markedly decreased GSH and NPSH levels (10 to 40% of control values) and glutathione peroxidase activity (45 to 60% of control values). Superoxide dismutase activities were elevated, glutathione reductase activity was slightly elevated, and catalase activity was unchanged. These changes were dose-responsive. The lungs of treated rats were grossly and microscopically normal. BSO treatment of additional rats did not increase susceptibility to lethal hyperoxia (greater than 98% oxygen). Combined treatment of rats with both BSO and sublethal hyperoxia (80% oxygen) for 4 days did not alter the biochemical responses demonstrated by rats treated solely with BSO. The marked increase in catalase activity obtained after hyperoxia alone was not observed in rats treated with both hyperoxia and BSO. The lungs of saline- and BSO-treated rats exposed to sublethal hyperoxia demonstrated a patchy distribution of slight perivascular and peribronchiolar edema.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

Adaptation to chronic hyperoxia. Biochemical effects and the response to subsequent lethal hyperoxia.

Adult rats were exposed to room air, 50%, 65%, or 80% oxygen for 6 wk. Subsets were sacrificed periodically in order to establish alterations in growth parameters and lung antioxidant responses. Prolonged exposure to 50% or 65% oxygen did not result in weight loss or changes in lung-to-body weight ratios relative to control values. Treatment with 50% oxygen produced delayed increases in nonprotein sulfhydryl (NPSH) content and catalase (CAT) activity, while treatment with 65% oxygen produced delayed increases in NPSH, CAT, and glutathione peroxidase (GPx) content. Rats treated for 6 wk with either 50% or 65% oxygen died significantly earlier than room-air control animals when these groups were subsequently exposed to 100% oxygen. Rats exposed to 80% oxygen had significantly decreased body weight, increased lung-to-body weight ratios, and increased levels of NPSH, CAT, GPx, total superoxide dismutase, and glutathione reductase by 11 days of treatment. At 6 wk they had significantly altered growth parameters and increased GPx catalase, and NPSH levels. Their final antioxidant profile was not significantly different from 65% oxygen-exposed rats. However, these animals survived significantly longer than any group when exposed to 100% oxygen. In summary, lower concentrations of sublethal hyperoxia (less than or equal to 65%) were capable of eliciting significant antioxidant enzyme responses. Levels of antioxidant enzymes in the lungs of rats chronically exposed to sublethal hyperoxia did not appear to be solely responsible for enhanced survival in subsequent lethal hyperoxia.

Adaptation, Physiological↗
PubMed1986

Pharmacological evidence that human intralobar airways do not contain different receptors that mediate contractions to leukotriene C4 and leukotriene D4.

Contractile responses to leukotriene (LT)C4, LTD4 and LTE4 were examined in intralobar airways from human lung obtained after surgical resection. In addition, the ability of the LT receptor antagonist FPL55712 to antagonize responses to LTC4 and LTD4 was quantified (by calculating -log molar KB values) under experimental conditions designed to minimize metabolic transformation of the LTs. In the absence of drug pretreatment, the three peptide LTs were approximately equipotent and produced similar maximum degrees of contraction. L-Serine borate complex, 45 mM, used as an inhibitor of the degradation of LTC4 to LTD4 by the enzyme gamma-glutamyl transpeptidase, in paired airway segments (adjacent segments from the same branch), produced a small degree (about 3-fold) of shift to the right of the dose-response curve and reduction of the maximum response to LTC4. L-Cysteine, 3 mM, used as an inhibitor of the degradation of LTD4 to LTE4 by the enzyme aminopeptidase, in paired segments, did not alter the dose-response effects of LTD4 or appear to further alter the dose-response effects of LTC4 when applied together with L-serine borate complex in unpaired (nonadjacent) segments. The -log molar KB value for FPL55712 (about 6) was similar for antagonism of responses to both LTC4 and LTD4 in the absence or presence of treatment with the metabolic inhibitors L-serine borate complex, L-cysteine or a combination of the two treatments. The results suggest that inhibition of the enzymes involved in the pathway from LTC4 to LTE4 has little consequence in human airways because the three peptide LTs are approximately equipotent.(ABSTRACT TRUNCATED AT 250 WORDS)

Arachidonic Acid↗
PubMed1979

A preliminary study of the effect of pyridoxine administration in a subgroup of hyperkinetic children: a double-blind crossover comparison with methylphenidate.

A small sample of six patients with the putative "hyperkinetic syndrome" participated in a research protocol comparing administration of pyridoxine, methylphenidate, and placeboes. The children had had low whole blood serotonin levels and a history of previous responsiveness to methylphenidate. The results of the double-blind clinical evaluation showed trends suggesting that both pyridoxine and methylphenidate were more effective than placebo in suppressing the symptoms of hyperkinesis. Pyridoxine elevated whole-blood serotonin levels, methylphenidate did not. Clinical and laboratory evidence indicated that the pyridoxine effects persisted after the 3-week period when the vitamin had been given in this experimental design.

Adolescent↗
PubMed1977

Longitudinal studies on the effects of malnutrition, nutritional supplementation, and behavioral stimulation.

Six major Western Hemisphere longitudinal studies of malnutrition and development are in their final stages. These studies are taking place in Columbia, Guatemala, Mexico, and the United States. As a step toward synthesis of the results, a conference was held at Cali, Colombia, with the aim of clarifying differences and similarities. The following features of each study were considered: The starting and completion dates; the research design (including scheduled periods of observation and the presence or absence of nutritional supplements and/or stimulation); the populations involved, their home diets, and the specific supplements and stimulation received; procedures and measurements used in the study; and any general conclusions reached. The conference also identified opportunities and needs for exchange of information between projects and for a collaborative approach to such specific problems and topics as birth-weight, physical growth, and behavioral development.

Adolescent↗
PubMed1976

Effect of postweanling pyridoxine deficiency on growth and concentration of the coenzyme pyridoxal-5'-phosphate in heart, kidneys, lungs, and adrenals in rats.

Dietary pyridoxine deficiency induced in postweanling rats to led to severe growth retardation and growth failure, with a sharp increase in the mortality rate after about 8 weeks on the diet. The absolute weights of heart, lungs, kidneys, and adrenals were all lower in the deficient animals than those of the controls. However, when the weights were expressed in terms of percentage of body weight, a 2-fold increase was observed indicative of marked hypertrophy. The depletion of the coenzyme pyridoxal-5'-phosphate from these tissues was extensive (heart 48%, lungs 85%, and kidneys and adrenals 88%.) The extent of loss of the coenzyme from the tissues suggests possible functional changes.

Adrenal Glands↗
PubMed1976

In vivo incorporation of glucose carbon into brain and liver proteins in biotin-deficient rats.

The in vivo utilization of D[U-14C]glucose with particular reference to its incorporation into brain and liver proteins was studied in biotin-deficient rats. The data show a significant reduction in the incorporation of glucose carbon into brain and liver proteins. A disturbance in the intermediary metabolism of glucose to be one of the factors responsible for the decreased incorporation of the label into proteins in biotin deficiency.

Animals↗
PubMed1976

Enzymatic microassay of pyridoxal-5'-phosphate using L-tyrosine apodecarboxylase and L-(1-14C) tyrosine.

A microassay for pyridoxal-5'-phosphate (PLP) is described, which incorporates both the enzymatic and radioisotopic techniques. The method is based upon the stoichiometric decarboxylation of L-(1-14C) tyrosine by L-tyrosine apodecarboxylase and PLP. This method is an extensive modification of the ones reported by us previously, the main features of this present method being the ease of preparation of the enzyme extract and the substrate, elimination of the preincubation period and shortening of the 14CO2-trapping step. The assay as described here is rapid, highly sensitive and specific.

Apoenzymes↗
PubMed1975

Avoidance behavior in vitamin B-6 deficient rats.

Pyridoxine deficiency was induced during the postweaning period in infant and young adult male rats and the effects on active avoidance and escape learning were studied. Five weeks of pyridoxine deficiency was sufficient to produce a deficit in active avoidance learning in the postweanling animals, whereas up to 10 weeks of deficient diet ingestion produced no effect on young adult animals. Mild motor impairment was produced in the young pyridoxine-deficient rats but the avoidance learning deficit could not be explained away on this basis, because a deficit in passive avoidance was also produced by the deficiency. Reversal of the deficiency by pyridoxine injection restored the active avoidance learning to normal within 1 week.

Age Factors↗
PubMed1975

The effect of pyridoxine hydrochloride on blood serotonin and pyridoxal phosphate contents in hyperactive children.

The contents of serotonin (hydroxytryptamine) and pyridoxal phosphate (PLP) in the blood of 11 hyperactive children and 11 controls were determined on an outpatient basis. A significant decrease in serotonin content was found in blood samples from hyperactive patients as compared with controls. There were no differences in PLP content of blood between the two groups. Four children were selected for a study of the effects of pyridoxine hydrochloride (vitamin B6) on low serotonin levels. Oral doses of pyridoxine resulted in an appreciable increase in the serotonin content and a very large increase in the PLP content of blood in these hyperactive patients.

Adolescent↗