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Biomedical subjects

S Rehncrona

Publications and source records attributed to S Rehncrona.

70 records · Page 4Linked to original sources
PubMed1978

Coupling of cerebral metabolism and blood flow in epileptic seizures, hypoxia and hypoglycaemia.

This study examines the possibility that changes of cerebral extracellular pH (PH e) or adenosine concentration may provide coupling mechanisms of a general nautre, adjusting cerebral blood flow (CBF) to metabolic demands. Although there is considerable indirect evidence that CBF varies inversely with pHe, results obtained during the last few years indicate that large increases in flow may occur in the absence of a fall in pHe. Thus, induction of hypoxia or epileptic seizures leads to maximal increase in CBF before pHe falls or even when there is initial alkalosis due to concomitant hypocapnia. Furthermore, CBF increases in hypoglycaemia and after administration of amphetamine, two conditions unassociated with tissue acidosis. The possibility that adenosine may be a coupling factor was examined in hypoxia and during epileptic seizures in rats. In both conditions a four- to fivefold increase in CBF occurs in spite of the fact that tissue adenosine concentrations remain at or below 1 mumolkg-u. It is concluded that adenosine accumulates first when there is a perturbation of cerebral energy state with a rise in AMP concentration. It seems unlikely that adenosine, formed by breakdown of AMP, acts as a general coupling factor.

Adenosine↗
PubMed1978

Reduction of cerebral blood flow and oxygen consumption with a combination of barbiturate anaesthesia and induced hypothermia in the rat.

The influence of phenobarbitone anaesthesia on cerebral blood flow (CBF) and cerebral metabolic rate for oxygen (CMRo2) during hypothermia (23 degrees C & 27 degrees C) was studied in the rat, using a modification of the Kety & Schmidt (1948) technique and arterio-venous differences for oxygen. Phenobarbitone (150 mg/kg) was found to decrease CMRo2 by 40-60% during hypothermia, when compared to N2O anaesthesia. At a body temperature of 23 degrees C, and during phenobarbitone anaesthesia, CMRo2 was reduced to about 15% of normal control value (about 10.3 ml.100g-1). CBF was reduced to about 50% of the phenobarbitone control value but was similar to the value obtained with N2O anaesthesia at 22 degrees C. It is concluded that the combination of phenobarbitone anaesthesia and hypothermia results in a more pronounced reduction in cerebral metablic rate for oxygen than can be achieved by administration of barbiturates to normothermic animals, or by reducing body temperature by 15 degrees C during superficial anaesthesia.

Anesthesia, General↗
PubMed1978

Adenosine and cyclic AMP in cerebral cortex of rats in hypoxia, status epilepticus and hypercapnia.

The influence of hypercapnia, hypoxia and status epilepticus on cerebral cortex concentrations of adenosine, adenine nucleotides and cyclic AMP was studied on lightly anaesthetized (70% N2O) and artificially ventilated rats. Neither hypercapnia (arterial PCO2 about 80 and about 300 mmHg) nor hypoxia (minimal values of 19 mmHg) altered tissue concentrations of AMP, cyclic AMP or adenosine. Bicuculline-induced status epilepticus was accompanied by increased concentrations of cyclic AMP but adenosine concentration did not change. Experiments with ischemia, and those in which tissue hypoxia was exaggerated by unilateral carotid artery ligation, showed that tissue adenosine concentrations were elevated only when AMP concentration rose. It is concluded that the marked increase in cerebral blood flow which occurs in hypoxia and status epilepticus is unrelated to changes in tissue adenosine concentration and that the increase in cyclic AMP during neuronal hyperactivity is triggered by other mechanisms than adenosine accumulation.

Adenine Nucleotides↗
PubMed1977

Adenosine in rat cerebral cortex: its determination, normal values, and correlation to AMP and cyclic AMP during shortlasting ischemia.

It has recently been suggested that adenosine is a metabolic coupling factor responsible for an increased cerebral blood flow during hypoxia or increased functional activity. However, tissue adenosine concentrations have been reported to increase in situations previously shown to be unassociated with changes in tissue AMP concentrations. The present experiments were undertaken to assess cerebral cortex concentrations of adenosine under normal circumstances, and to relate changes in adenosine, AMP and cyclic AMP during shortlasting ischemia. Following freezing and extraction of tissue, adenosine was measured using high pressure liquid chromatography. In paralyzed and anaesthetized (70% N2O) rats, freezing of tissue through intact skull bone gave an adenosine concentration of 0.9 +/- 0.1 mumol-kg-1 (mean +/- S.E.M.). With freezing through the exposed dura the concentration was 3 times as high with a large scatter. When special precautions were taken to avoid tissue trauma during craniotomy, the adenosine concentration was 1.1 +/- 0.1 mumol-kg-1. It is concluded that previously reported values are erroneously high. During the first 60 s of total ischemia there was a linear correlation between increase in AMP and in adenosine concentration (as well as between adenosine and cyclic AMP concentrations). It is concluded that increases in tissue adenosine concentration only occur if AMP accumulates. However, since (relative) changes in adenosine concentrations are at least twice those of AMP, analyses of adenosine may provide sensitive measures of a change in phosphorylation state.

Adenosine↗
PubMed1977

Postischemic cerebral blood flow and oxygen utilization rate in rats anesthetized with nitrous oxide or phenobarbital.

The present experiments were undertaken to measure postischemic regional cerebral blood flow (rCBF) and oxygen utilization rate (CMRo2) in rats anesthetized with either 70% N2O or phenobarbital (150 mg x kg-1). In previous studies we have found that extensive restitution of cerbral energy metabolites occurs after 30 min of complete cerebral ischemia irrespective of the type of anesthesia used. Following 30 min of pronounced, incomplete ischemia, however, a comparable restitution of cerebral energy state was obtained in deeply anesthetized (phenobarbital 150 mg x kg-1) but not in superfically anesthetized (70% N2O) rats. The objectives of the present investigation were (1) to study whether postischemic cerebral blood flow was higher in barbiturate-anesthetized animals during the initial recirculation period, and (2) to investigate if the protective effects of phenobarbital previously observed could be attributed to a decrease in CMRo2. In both groups of animals a considerable variability in postischemic rCBF was observed between different animals. However, no signs of gross inhomogeneity in blood flow were found and no consistent differences in flow values between the two groups of animals were observed. Since the measured postischemic CMRo2 were identical in both groups of animals and since cerebral venous oxygen contents were above normal the results leave little support to the assumption that, in the present model of transient, incomplete cerebral ischemia, failure of recovery of cerebral metabolism (N2O group) is primarily due to impaired recirculation, nor do they indicate that the protective effects of barbiturates is due to their ability to reduce rate of cerebral energy utilization.

Anesthesia, General↗
PubMedDate not supplied

Cerebral hemodynamic changes and electroencephalography during carotid endarterectomy.

Some patients undergoing endarterectomy for occlusive carotid artery disease run a risk of brain ischemia during cross-clamping of the artery. The present study of 15 patients was undertaken to evaluate changes in cerebral blood flow (CBF), as measured with an intravenous (IV) tracer (133Xenon) technique, and to relate CBF changes to changes in the electroencephalogram (EEG). CBF was measured before and after induction of anesthesia, during cross-clamping of the carotid artery, after release of the clamps, and at 24 hours after the operation. All the patients were anesthetized with methohexitone, fentanyl, and nitrous oxide and oxygen. EEG was continuously recorded during the operation. Carotid artery shunts were not used. In 8 patients, cross-clamping of the carotid artery did not influence the EEG. In this group of patients, induction of anesthesia caused a 38% decrease in CBF, which presumably reflects the normal reaction to the anesthetic agent given. There were no further changes in CBF during cross-clamping. In 7 patients, the EEG showed signs of deterioration during the intraoperative vascular occlusion. In these patients, anesthesia did not cause any CBF change, whereas cross-clamping the artery induced a 33% decrease in CBF. In individual patients, the severity of EEG changes correlated with the decrease in CBF. The absence of a change in CBF by anesthesia and a decrease due to cross-clamping of the carotid artery may be explained by the presence of a more advanced cerebrovascular disease and an insufficiency to maintain CBF during cross-clamping.(ABSTRACT TRUNCATED AT 250 WORDS)

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