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M Hägerdal

Publications and source records attributed to M Hägerdal.

33 records · Page 2Linked to original sources
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↗
PubMedDate not supplied

Brain metabolism in the critically ill.

A large number of clinical conditions are associated with a transient or permanent disturbance of brain function. Common to all of them is that, in some way, brain metabolism is changed from the normal. These changes cover a vast spectrum, ranging from the subtle alterations of metabolism encountered in mental disease to those underlying death and dissolution of cells in conditions of oxygen lack. This communication is concerned with brain metabolism in the critically ill with emphasis on conditions of hypoglycemia, hypoxia, and ischemia. We begin by briefly recalling the salient features of brain metabolism in the healthy individual. Since clinicians caring for critically ill patients take an interest in factors that may aggravate the primary disease and in measures that may prevent or minimize its final effect on the brain, we will also briefly consider how brain metabolism is influenced by potentially harmful factors (hyperthermia, anxiety and stress, and tissue acidosis due to CO2 retention) as well as by measures that are often instituted to ameliorate the effects of hypoxia and ischemia (hypothermia, administration of anesthetics and sedatives). We refer the reader to selected references with preference to recent articles reviewing previous literature.

Brain↗