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Biomedical subjects

C Carlsson

Publications and source records attributed to C Carlsson.

At least 127 records · Page 7Linked to original sources
PubMed1978

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↗
PubMed1978

A double blind study with melperone and placebo in the treatment of chronic alcoholics.

In a 2-wk randomized double blind study 60 chronic alcoholics were treated with either melperone (Buronil) or placebo. The patients were assessed daily using a scale including 4 items: tension, depression, craving and sleep. Statistically significant improvement was achieved in the placebo group only for "tension" and "sleep"; whereas, in the melperone group all four items improved significantly. Comparison between the groups revealed statistically significant superiority of melperone over placebo for the item "craving".

Adult↗
PubMed1977

A catecholamine-mediated increase in cerebral oxygen uptake during immobilisation stress in rats.

Anxiety and grave apprehension have been supposed to increase cerebral metabolism, and it has earlier been suggested that intravenous infusion of adrenaline may increase cerebral blood flow (CBF) and cerebral oxygen consumption (CMR02). In an experimental model on rats, it could be shown that immobilisation stress increased CBF and CMR02 after 5 min (about 150% of control values) and 30 min (about 190% of control values). By previous adrenalectomy or by administration of a beta-receptor blocker (propranolol, 1.4 mg/kg) the changes in CBF and CMR02 could be prevented. It is concluded that the excessive increase in CBF and CMR02 was mediated via release of catecholamines from the adrenal glands.

Adrenalectomy↗
PubMed1976

Protective effect of hypothermia in cerebral oxygen deficiency caused by arterial hypoxia.

To study the cerebral protective effects of hypothermia in arterial hypoxia, anesthetized (70% N2O), mechanically ventilated rats were cooled to a body temperature of 27 C. Hypoxia was induced by decreasing the oxygen content in the inspired gas mixture either to 6-7 per cent or to 2.5-3 per cent. This reduced mean PaO2 to about 25 and 11-12 torr, respectively. At PaO2 torr, there was no change in cerebral blood flow (CBF), cerebrla oxygen consumption (CMRO2), or labile tissue metabolites. The absence of signs of cerebral hypoxia could be attributed to an effect of temperature and pH on the hemoglobin-oxygen dissociation curve. Thus, at 27 C with a PaO2 of 25 torr the total oxygen content (TO2) of arterial blood remained greater than 15 ml (100 ml)-1, about three times the value obtained at this PO2 in normothermic rats. At PaO2 11-12 torr, arterial TO2 was reduced to about 5 ml (100 ml) (-1). The hypoxia induced no change in CMRO2, a threefold increase in CBF, a moderate lactacidosis in the tissue, and a small decrease in phosphocreatine content, but no change in ATP, ADP, or AMP. These changes are less marked than those occurring at the same arterial TO2 in normothermic rats. It is concluded that hypothermia exerts a pronounced protective effect on the brain in hypoxic hypoxia, and that two mechanisms are involved. First, since hypothermia shifts the oxyhemoglobin-dissociation curve towards the left, and prevents or minimizes a rightward shift due to acidosis, it maintains a high TO2 in arterial blood at a given PaO2. Second, by reducing CMRO2, and thereby presumably also cellular energy requirements, hypothermia exerts a protective effect at the cellular level.

Adenosine Diphosphate↗
PubMed1976

The effects of diazepam on cerebral blood flow and oxygen consumption in rats and its synergistic interaction with nitrous oxide.

The effects of diazepam on cerebral blood flow (CBF) and cerebral oxygen uptake (CMRO2) was studied using a 133xenon modification of the Kety-Schmidt (1948) technique in paralyzed, artifically ventilated rats with and without simultaneous administration of 70 per cent nitrous oxide. Diazepam was given iv in doses that induced light to heavy sedation or general anesthesia. When given with 70 per cent nitrous oxide, diazepam in sedative and anesthetic doses lowered CBF and CMRO2 to about 60 per cent of control. In the absence of nitrous oxide all doses of diazepam caused moderate (20-30 per cent) decreases in CBF, but CMRO2 remained unchanged or was only slightly lowered. It is concluded that diazepam interacts with nitrous oxide to produce a reduction in CMRO2 similar to that seen in barbiturate anesthesia, but that alone the drug produces sedation and anesthesia without a comparable decrease in CMRO2.

Acidosis↗
PubMed1976

The effect of nitrous oxide on oxygen consumption and blood flow in the cerebral cortex of the rat.

The effect of 70% nitrous oxide upon cerebral oxygen consumption (CMRo2) and cerebral blood flow (CBF) was studied in artificially ventilated rats. The control groups consisted of unanaesthetized animals in which a stress-induced increase in CMRo2 and CBF was prevented by previous adrenalectomy, or by administration of a beta blocker (propranolol). There were no significant differences in CMRo2 between animals ventilated with either N2O or N2. It is concluded that if nitrous oxide depresses cerebral metabolism the depression cannot exceed 10%.

Adrenalectomy↗
PubMed1976

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↗
PubMed1976

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.

Adenine Nucleotides↗