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Biomedical subjects

D M Turner

Publications and source records attributed to D M Turner.

86 records · Page 5Linked to original sources
PubMed1971

Metabolism of small multiple doses of (14C) nicotine in the cat.

1. The distribution and metabolism of (2'-(14)C) nicotine given as a series of small intravenous injections (4 mug/kg every 60 s for 20 min) have been studied in the cat.2. Blood concentrations of ((14)C) nicotine reached a maximum of 100 ng/ml at 20 min whereas blood concentrations of cotinine were maximal shortly afterwards.3. The maximum concentration of nicotine in the blood was greater than that obtained by giving the same total dose as a continuous infusion ((4 mug/kg)/min for 20 min).4. Urinary excretion accounted for 90% of the total multiple dose in 72 hours. After 24 h, however, only 2.5% of the radioactivity as ((14)C) nicotine and 0.05% as ((14)C) cotinine was excreted.5. Gastric juice after 2 h contained significant amounts of activity which was almost entirely composed of ((14)C) nicotine and ((14)C) cotinine.6. There were significant regional differences in the concentration of ((14)C) nicotine in the brain; amounts were greatest in cerebral hemispheres and smallest in the spinal cord. The hypothalamus and thalamus contained significantly higher concentrations of ((14)C) nicotine than the whole mid brain. ((14)C) Cotinine concentrations were highest in the cerebellum.

Animals↗
PubMed1970

Enzyme and isoenzyme alterations in Friend disease.

The activities of certain enzymes in the tissus of mice infected with Friend virus have been studied. Progressive increases in LDH, G6PDH and 6PGDH have been observed in the spleen and liver concomitant with malignant transformation. Plasma LDH activity was also observed to increase over the period of study, but changes in the isoenzyme distribution probably resulted from contamination of the Friend virus preparation with lactic dehydrogenase virus. The tissue enzyme changes are similar to those observed in human malignancies.

Animals↗
PubMed1969

The metabolism of [14C] nicotine in the cat.

The metabolism of [2'-(14)C]nicotine given as an intravenous injection in small doses to anaesthetized and unanaesthetized cats has been studied. A method is described for the quantitative determination of [(14)C]nicotine and [(14)C]cotinine in tissues and body fluids. Nanogram amounts of these compounds have been detected. After a single dose of 40mug. of [(14)C]nicotine/kg., 55% of the injected radioactivity was excreted in the urine within 24hr., but only 1% of this radioactivity was unchanged nicotine. [(14)C]Nicotine is metabolized extremely rapidly, [(14)C]cotinine appearing in the blood within 2.5min. of intravenous injection. [(14)C]Nicotine accumulates rapidly in the brain and 15min. after injection 90% of the radioactivity still represents [(14)C]nicotine. Metabolites of [(14)C]nicotine have been identified in liver and urine extracts. [(14)C]Nicotine-1'-oxide has been detected in both liver and urine.

Animals↗
PubMedDate not supplied

Comparison of the effect of naloxone on cerebral versus mesenteric arterial smooth muscle in feline and primate species.

This study was conducted in order to investigate naloxone's in vitro action on both epinephrine-induced constriction of mesenteric artery and norephinephrine-induced constriction of cerebral arteries in different species (cat and monkey). Naloxone (3 X 10(-5)M) augmented the epinephrine-induced constriction of both feline and monkey mesenteric artery at epinephrine concentrations of 10(-7) to 10(-5) M. Naloxone (3 X 10(-5)M) suppressed the constriction of feline basilar artery induced by high concentrations (10(-4), 10(-3) and 3 X 10(-3)M) of norepinephrine, while it failed to alter the constriction induced by lower concentrations (10(-7) to 10(-5)M) of norepinephrine. The constrictor response of monkey basilar artery to norepinephrine (10(-8) to 10(-5) M) was not altered by treatment with naloxone (3 X 10(-6) and 3 X 10(-5)M). Such varying effects of naloxone in different tissues and species may have to be taken into account when evaluating the cerebral blood flow changes following naloxone administration.

Animals↗
PubMedDate not supplied

Pharmacological comparison of isolated monkey and dog cerebral arteries.

Pharmacological differences between canine and monkey basilar arteries were studied in vitro. The constrictor response of canine basilar artery to either norepinephrine or an alpha 1-adrenoceptor agonist phenylephrine was partly inhibited by an alpha 2-adrenoceptor antagonist yohimbine but not by an alpha 1-adrenoceptor antagonist prazosin. The contraction elicited by an alpha 2-adrenoceptor agonist clonidine was inhibited by neither prazosin nor yohimbine. These results suggest that the receptors in canine basilar artery which mediate norepinephrine-induced contraction are different from classical alpha 1 or alpha 2-adrenoceptors, although they more closely resemble the alpha 2- rather than the alpha 1-subtype. Using monkey basilar artery, phenylephrine produced the same amplitude of maximum contractile response as norepinephrine, though a much higher concentration of phenylephrine than norepinephrine was needed in order to elicit that maximum response. Clonidine did not elicit contractions. The contraction induced by norepinephrine was markedly suppressed by both prazosin and yohimbine in a noncompetitive fashion. The constrictor response of monkey basilar artery to norepinephrine, therefore, appears to be mediated by alpha 1-like adrenoceptors. Comparison of ED50 values for thromboxane A2 revealed that the monkey basilar artery was more sensitive to thromboxane A2 than that of the canine. Prostaglandin F2 alpha produced a larger maximum contraction in monkey basilar arteries than in canine basilar arteries, although the ED50 values for monkey basilar arteries were larger than those for canine basilar arteries. The ED50 values for serotonin in canine basilar arteries were a little less than those for monkey basilar arteries, although both arteries produced nearly identical maximum contractions.

Adrenergic alpha-Agonists↗
PubMedDate not supplied

Time-dependent effects of prolonged hypercapnia on cerebrovascular parameters in dogs: acid-base chemistry.

Prolonged normoxic hypercapnia initially caused an increase in canine cerebral blood flow, as measured by the radioactive microsphere technique, accompanied by a decrease in cerebrovascular resistance. These effects persisted for 3 hours. An adaptive decrease in cerebral blood flow and increase in cerebrovascular resistance were seen when hypercapnia was maintained for an additional 3 hours. Regional variations occurred; those areas with the greatest initial hypercapnic blood flow (cortex, caudate nucleus) showed a greater rate of decay of flow over time. Cerebrospinal fluid pH, initially acidotic during hypercapnia, increased over the subsequent 5 hours from 6.99 +/- 0.02 to 7.13 +/- 0.02. This was accompanied by an increase in the cerebrospinal fluid bicarbonate ion concentration from a normocapnic baseline of 19.6 +/- 0.6 to 26.2 +/- 4 mEq/l. Total and regional cerebral blood flow were linearly related to cerebrospinal fluid pH (R2 = 0.97). Extrapolation of a full adaptive return of flow to baseline indicated a shift in the cerebrovascular sensitivity to extracellular hydrogen ion concentration during prolonged hypercapnia.

Acid-Base Equilibrium↗