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Biomedical subjects

M Hägerdal

Publications and source records attributed to M Hägerdal.

At least 19 recordsLinked to original sources
PubMed1979

Additive effects of hypothermia and phenobarbitol upon cerebral oxygen consumption in the rat.

The quantitative effects of a combination of hypothermia and phenobarbital on cerebral oxygen uptake (CMRo2) was studied in rats, curarized and artificially ventilated with 70% nitrous oxide in oxygen. Cerebral blood flow (CBF) was measured with a modification of the KETY & SCHMIDT (1948) technique, using 133xenon as a tracer. Arteriovenous difference in oxygen content over the brain was measured and CMRo2 was calculated. Four groups were studied. Group 1 was a control group. The three experimental groups were injected with phenobarbital intraperitoneally: Group 2 with 50 mg/kg body weight; Group 3 with 150 mg/kg; and Group 4 with 50 mg/kg of phenobarbital, and, in addition, body temperature was lowered to 32 degrees C in this group. CMRo2 in groups 2, 3 and 4 was reduced by 22, 37 and 43%, respectively, compared to Group 1. The changes in CBF were of the same magnitude. In a previous study we have found that CMRo2 decreases by 5% per 1 degree C decrease in body temperature. The value for CMRo2 in Group 4 is close to the value obtained if the effect of 50 mg/kg body weight of phenobarbital on CMRo2 is added to the effect of a temperature reduction of 5 degrees C. It is concluded that the effects of barbiturates and hypothermia on CMRo2 are additive.

Animals↗
PubMed1979

Myocardial protection during heart surgery. An experimental evaluation of normothermic and hypothermic cardioplegia.

Heart surgery with hypothermic cardioplegia during normothermic bypass is sometimes complicated by rewarming of the myocardium caused by collateral flow of arterial blood. This problem is particularly evident in surgery of congenital malformations. The present work is a comparative study in dogs on 3 methods of avoiding the rewarming problem. In the first group, the heart was kept cold and the warm blood was drained off from the left atrium. In the second group, total body hypothermia to the level desired was used and in the third group, normothermic cardioplegia was induced (Cardioplegin) in normothermic animals. In the two latter groups, the undesired temperature gradient between heart and body was eliminated. Evaluation of the differences was made by means of ventricular function determinations. Local, hypothermic cardioplegia showed the best postoperative function (69%) followed by the total body cooling which was fully acceptable (41%). Normothermic cardioplegia after the same duration of arrest showed a too low myocardial performance (20%).

Anesthesia↗
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↗
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

Electroencephalographic study of children during ketamine anesthesia.

EEG was recorded on nine occasions of ketamine anesthesia in eight children. Two of the patients were neurologically normal and six were under investigation for various neurological disorders. The EEG during the catatonic phase of ketamine anesthesia is characterized by alternating high amplitude delta complexes and periods of fast activity. The two cases which in the routine EEG showed focal paroxysmal activity did not show any electroencephalographic aggravation or clinical seizure during ketamine influence. One case exhibiting a subcortical type of epileptiform activity showed a marked potentiation of this activity with ketamine. On routine neurological examination during the catatonic phase of ketamine anesthesia the pharyngeal reflex was generally weak and failed altogether in two cases and corneal reflexes were absent in three cases.

Action Potentials↗
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

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↗
PubMed1975

Influence of changes in arterial PCO2 on cerebral blood flow and cerebral energy state during hypothermia in the rat.

In order to study the relationship between arterial PCO2 and cerebral blood flow (CBF) in hypothermia, the body temperature of artifically ventilated rats was decreased to 22 degreesC, and changes in CBF were evaluated from arteriovenous differences in oxygen content (AVDO2) at PaCO2 values of 15, 30, 40 and 60 mm Hg. The results were compared to those obtained at normal body temperature (37 degrees C) over the PaCO2 range 15-60 mm Hg. Separate experiments were performed to evaluate CBF and CMRO2 at 22 degrees C and a PaCO2 of 15 mm Hg, using an inert gas technique for CBF. The tissue contents of phosphocreatine, ATP, ADP, AMP and lactate were measured in hypothermic animals at PaCO2 values of 15, 30 and 60 mm Hg. The results showed that changes in CBF were of the same relative magnitude in hypothermia and normothermia when PaCO2 was increased from about 35 to about 60 mm Hg. However, with a decrease in PaCO2 the reduction in CBF was much more pronounced in hypothermia, and at PaCO2 15 Mm Hg CBF was less then 20% of the value measured in normothermic and normocapnic animals. The results of the metabolite measurements gave no evidence of tissue hypoxia in spite of the pronounced reduction in CBF. Although the results demonstrate that the brain of a hypothermic animal is protected against the harmful effects of a lowered CBF, it may not warrant recommending hyperventilation in clinical cases of hypothermia, especially not in patients with arteriosclerosis or cerebrovascular diseases.

Adenosine Diphosphate↗