Biomedical subjects

D G Corby

Publications and source records attributed to D G Corby.

At least 19 recordsLinked to original sources

PubMed1989

Effect of minoxidil on platelet function and the synthesis of prostaglandins in platelets.

At the 12.5 micrograms level, minoxidil prevents the irreversible aggregation of platelets by 2 x 10(-6) mol/L adenosine diphosphate (ADP). Levels of minoxidil greater than 12.5 micrograms cause a reversal of primary aggregation by 2 x 10(-6) mol/L ADP. Aggregation of platelets in response to 125 micrograms of arachidonic acid is measurably reduced by 12.5 micrograms of minoxidil and totally suppressed by 30 micrograms. Concurrent with the inhibition of platelet aggregation, increasing concentrations of minoxidil cause a gradual reduction in the synthesis of prostaglandin E2 (PGE2) and thromboxane B2 (TxB2). In the presence of 100 micrograms of minoxidil, PGE2 is reduced from a control value of 87.7 +/- 2.2 pg/ml to 23.9 +/- 3.2 pg/ml. At this level of minoxidil, TxB2 drops from 105 +/- 3.3 ng/ml to 10.5 +/- 2.6 ng/ml. The effect of minoxidil on platelet aggregation is not associated with increased cyclic adenosine monophosphate synthesis. All data support the conclusion that minoxidil functions (in platelet metabolism) primarily as a cyclooxygenase inhibitor.

Adenosine Diphosphate↗

PubMed1987

Effects of hypothyroidism and short-term aging on whole blood thromboxane and arterial prostacyclin synthesis.

Hypothyroidism results in decreased platelet aggregation and has unique effects on the development of atherosclerosis and angina pectoris. Because prostacyclin and thromboxane A2 profoundly influence platelet function and vascular tone and are thought to be important in the development of atherosclerosis and angina pectoris, we studied the effects of hypothyroidism in rats on the in vitro elaboration of prostacyclin passively by aortic tissue and of thromboxane A2 by thrombin-stimulated whole blood. Hypothyroidism induced by iodine 131 (given at age 7 weeks) persistently caused a mild decrease in platelet count (P less than 0.01) and 30% decrease in immunoreactive thromboxane B2 (the hydrolysis product of thromboxane A2) generation per platelet (P less than 0.01) compared with age-matched euthyroid rats. Between 20 and 23 weeks of age immunoreactive 6-ketoprostaglandin F1 alpha (the hydrolysis product of prostacyclin) generation decreased by 30% in euthyroid rats. In hypothyroid rats less than 23 weeks of age, 6-ketoprostaglandin F1 alpha production was the same as that of age-matched euthyroid rats. With further aging, 6-ketoprostaglandin F1 alpha production did not decrease as it did in euthyroid rats. Hypothyroid rats more than 20 weeks old had, therefore, significantly greater 6-ketoprostaglandin F1 alpha production than age-matched euthyroid rats (P less than 0.005). L-Thyroxine given daily for 28 days to 23-week-old hypothyroid rats caused a rapid increase in platelet count and a delayed normalization of the thromboxane synthetic abnormality. 6-Ketoprostaglandin F1 alpha production transiently increased in response to L-thyroxine, but decreased to the euthyroid level after 28 days of therapy.(ABSTRACT TRUNCATED AT 250 WORDS)

6-Ketoprostaglandin F1 alpha↗

PubMed1985

Hemoperfusion of phencyclidine in the dog.

Experiments were conducted to determine whether charcoal hemoperfusion (HP) would be useful in severe phencyclidine (PCP) overdose. Dogs were given a single 5 mg/kg injection of PCP. In 6 experiments HP for 2.5 hours was done; and in 6 control experiments, the extracorporeal circuit contained no HP cartridge. The number of seizures, symptoms, duration of coma, and PCP concentrations in the tissues of HP dogs were not different from control. PCP clearance by HP was 67 +/- 16.5 ml/min. PCP recovery by HP was 2.25 +/- 0.25 mg (2.0% of the administered dose). Urinary excretion of PCP was 1.33 +/- 0.46 mg (1.2% of the dose). Volume of distribution of PCP was 21.8 +/- 1.7 L/kg. Due to the high volume of distribution, high lipid solubility and low plasma levels of PCP, HP was not effective in managing PCP overdose in the dog.

Animals↗

PubMed1978

Aspirin in pregnancy: maternal and fetal effects.

Recent surveys of prenatal drug consumption indicate that aspirin is the most frequently consumed drug in pregnancy. Over the past several years, numerous reports have suggested a possible association between prenatal aspirin ingestion and adverse effects in the pregnant woman and her developing fetus. This review summarizes the available experimental animal and human epidemiological data on the possible teratogenicity of aspirin, its effects on fetal lethality, its effects on the duration of pregnancy and parturition, and its ability to alter hemostatic mechanisms in both the mother and newborn. From an analysis of the data, it appears that, although direct conclusive evidence of adverse effects in humans is lacking, a potential hazard does exist and thus "the indiscriminate use of aspirin during pregnancy is contraindicated."

Abnormalities, Drug-Induced↗

PubMed1977

IgE-IgM kappa gammopathy associated with lymphocytic lymphoma: immunological evaluation.

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Aged↗

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↗

PubMed1974