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Biomedical subjects

L Berntman

Publications and source records attributed to L Berntman.

13 recordsLinked to original sources

Influence of "lytic cocktail" on blood flow and oxygen consumption in the rat brain.

The influence of a sedative dose of "lytic cocktail" (chlorpromazine, promethazine and pethidine) on cerebral blood flow (CBF) and oxygen consumjtion (CMRO2) was tested in artificially ventilated rats, maintained on either 70% N2 or 70% N2O. When given alone, the lytic cocktail had no significant effect on CBF or CMRO2. However, in the presence of nitrous oxide there was a 25% reduction in blood flow and oxygen consumption.

Animals

Circulatory and metabolic effects in the brain induced by amphetamine sulphate.

Cerebral circulatory and metabolic effects of amphetamine sulphate (0.25-25 mg.kg-1 i.v. or 5-10 mg.kg-1 i.p.) were studied in anesthetized, paralyzed and artifically ventilated rats. Cerebral blood flow (CBF) was measured with a modification of the Kety and Schmidt (1948) technique, and oxygen consumption (CMRO2) was calculated from CBF and arteriovenous differences in oxygen content. Regional CBF was evaluated from the uptake of 14C-ethanol. Cortical metabolites were analysed following freezing of tissue in situ. Amphetamine administration gave rise to a marked increase in CBF that was doubled following 0.25 mg.kg-1 and increased 4-fold following 15 mg.kg-1. However, such excessive increases in flow were confined to frontoparietal cortical regions, while other cortical or subcortical areas showed more moderate hyperemia. The increase in CBF was unrelated to changes in arterial PCO2, blood pressure, or tissue lactate content. CMRO2 increased by 30% to 95% depending on dose and rat strain used. At all doses employed, amphetamine gave rise to glycogenolysis in cerebral cortex but, in animals studied within the first 30 min after 5 mg.kg-1, or less, the only other changes were increases in glucose-6-phosphate and alpha-ketoglutarate concentrations. When the dose was increased to 15 mg.kg-1, there were moderate increased in lactate concentration and lactate/pyruvate ratio. Sixty min after 5 mg.kg-1 there were increases in tissue concentrations of pyruvate, citric acid cycle intermediates and alanine, as well.

Amphetamine

Influence of intravenously administered catecholamines on cerebral oxygen consumption and blood flow in the rat.

In order to study effects of catecholamines on cerebral oxygen consumption (CMRo2) and blood flow (CBF), rats maintained on 75% N2O and 25% O2 were infused i.v. with noradrenaline (2, 5, or 8 microgram.kg-1.min-1) or adrenaline (2 or 8 microgram.kg-1.min-1) for 10 min before CBF and CMRo2 were measured. In about 50% of animals infused with 2--8 microgram.kg-1.min-1 of noradrenaline, CMRo2 (and CBF) rose. However, there was no dose-dependent response, and CMRo2 did not exceed 150% of control. The effects of noradrenaline in a dose of 5 microgram.kg-1.min-1 on CMRo2 and CBF were blocked by propranolol (2.5 mg.kg-1). In animals infused with adrenaline (8 microgram.kg-1.min-1) CMRo2 was doubled and, in many, CBF rose 4- to 6-fold. It is concluded that, when given in sufficient amounts, catecholamines have pronounced effects on cerebral metabolism and blood flow, the effects of adrenaline on CMRo2 and CBF resembling those observed in status epilepticus.

Animals

Restoration of oxygen uptake and blood flow in the rat cerebral cortex after halothane anaesthesia.

Halothane decreases both the cerebral blood flow (CBF) and the cerebral metabolic rate for oxygen (CMRO2) when given in anaesthetic doses. A recent report (GJEDDE & HINDFELT 1975) suggests that when halothane is administered to rats for 1 hour, CBF and CMRO2 are depressed by about 30 and 40%, respectively, for as long as 4 hours after discontinuation of the halothane anaesthesia. In the present study rats were anaesthetized with 1% halothane for 1 hour, and CBF and CMRO2 were measured at the end of a 30 min recovery period, during which 70% N2O was administered. Comparison with animals maintained on 70% N2O throughout the entire 90 min period showed that previous halothane anaesthesia had no effects on CBF or CMRO2.

Anesthesia, General

Cerebral metabolic state after discontinuation of nitrous oxide supply in artificially ventilated rats.

Previous results from this laboratory have shown that when administration of 70% nitrous oxide is discontinued in artificially ventilated rats, cerebral oxygen uptake increases by about 40% at 5 min and by about 80-90% at 30 min, and that this increase is blocked by previous adrenalectomy. In the present experiments, nitrous oxide was withdrawn for 45 s, 2 min 45 s, or 15 min, in non-adrenalectomized animals, and for 5 min in adrenalectomized animals, and the tissue was frozen in situ for subsequent measurements of labile phosphates, glycolytic metabolites, citric acid cycle intermediates and associated amino acids and ammonia. The results allow the conclusion that upon withdrawal of nitrous oxide in non-adrenalectomized animals, there is an increase in metabolic rate at an essentially unchanged metabolic state. In adrenalectomized animals, discontinuation of nitrous oxide supply did not induce changes in any of the tissue metabolites measured. We conclude that 70% N2O neither influences the metabolic rate of the tissue, nor its metabolic state.

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