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Biomedical subjects

J Astrup

Publications and source records attributed to J Astrup.

At least 73 records · Page 4Linked to original sources
PubMed1984

Minimum cerebral blood flow and metabolism during craniotomy. Effect of thiopental loading.

Cerebral blood flow and metabolism were measured repeatedly during surgery for cerebral tumours by a modification of the classical Kety & Schmidt method using 133Xe infusion intravenously. Our standard procedure for neuroanaesthesia (pentobarbitone-fentanyl induction, halothane-nitrous oxide maintenance) reduced blood flow from 47.1 to 24.2 ml X 100 g X ml-1 and metabolism from 3.30 to 1.83 ml O2 X 100 g-1 X ml-1. PaCO2 was reduced by hyperventilation from 5.3 to 3.6 kPa. Additional thiopental loading and maintenance using 4 + 4 mg X kg-1 (n = 5) or 8 + 8 mg X kg-1 (n = 5) reduced cerebral metabolism by an additional 15% (P less than 0.01) and blood flow by 16.5% (P less than 0.01), while mean arterial blood pressure fell from 11.0 to 9.9 kPa (P less than 0.05). PaCO2 remained unchanged. This additional reduction in cerebral metabolism and blood flow is small, but we nevertheless conclude that it may well be of clinical interest to the problem of protecting the brain in case of episodes of focal cerebral ischaemia which may arise peroperatively during intracranial surgery.

Adult↗
PubMed1981

Increase in extracellular potassium in the brain during circulatory arrest: effects of hypothermia, lidocaine, and thiopental.

The effect of temperature (37 degrees C, 28 degrees C, and 18 degrees C), 160 mg/kg lidocaine, and 40 mg/kg thiopental on the efflux of cellular potassium in the cerebral cortex during complete global ischemia was examined. Cerebral ischemia was induced in dogs on cardiopulmonary bypass circulation by stopping the pump. Potassium concentration was measured on the brain surface by a valino-mycine-membrane electrode, which in its response corresponded well to an inserted microelectrode. Hypothermia reduced the ischemic potassium efflux rate to about 50 per cent at 28 degrees C, and about 25 per cent at 18 degrees C. At all temperature levels lidocaine caused an additional reduction in the potassium efflux rate of about 50 per cent, probably by reducing membrane ion permeability in accordance with its local anesthetic action. Thiopental had no effect on the potassium efflux during ischemia. This study opens the possibility that lidocaine, like hypothermia, may provide protection of the ischemic brain.

Animals↗
PubMed1981

Inhibition of cerebral oxygen and glucose consumption in the dog by hypothermia, pentobarbital, and lidocaine.

The effect of lidocaine, 160 mg/kg, and pentobarbital, 40 mg/kg, on cerebral oxygen and glucose consumption was examined at brain temperatures of 37 degrees C, 28 degrees C, and 18 degrees C. Cerebral metabolic rate was measured in dogs on cardiopulmonary bypass circulation by using the sagittal sinus outflow technique. When studied separately, both drugs suppressed synaptic transmission and inhibited metabolism, and a maximum effect was obtained when the EEG became flat. Using halothane 1-1.5 per cent as the control condition, this function-metabolism coupled inhibition was about 30 per cent. When the drugs were studied in combination, it was found that when lidocaine was given after pentobarbital, it caused an additional metabolic inhibition of 15-20 per cent, while pentobarbital given after lidocaine had no effect. It is concluded that pentobarbital has no inhibitory effect on cerebral metabolism in the absence of synaptic activity, while lidocaine--in addition to the effect related to suppression of synaptic transmission--has a specific "membrane stabilizing" effect. In analogy to its local anesthetic action, lidocaine blocks the Na+ channels and restricts the Na+-K+ leak fluxes. The load on the ion pump is reduced and metabolism is decreased accordingly. This specific effect on lidocaine was evident also at brain temperatures of 28 degrees C and 18 degrees C. The study supports the possibility that lidocaine, like hypothermia, may provide protection for the ischemic brain.

Animals↗
PubMed1981

Inhibition of cerebral metabolism by lidocaine.

The effects of lidocaine in high doses, i.e. higher than seizure doses, on cerebral function and metabolism are reviewed. Evidence is presented that lidocaine (160 mg/kg) reduces membrane NA+-K+ permeability, restricts leak fluxes of these ions, and decreases the load on the associated ion transport. In the ischemic brain (circulatory arrest in dogs on cardiopulmonary bypass circulation), lidocaine delays K+ efflux, indicating reduced membrane permeability. In the nonischemic brain lidocaine has two effects. One is to abolish electrocortical activity and reduce oxygen and glucose consumption accordingly ("barbiturate-like" effect). The other is a specific membrane sealing effect by which Na+-K+ leak fluxes are restricted and associated demand for active transport according reduced. By this effect lidocaine is able to reduce cerebral metabolism by an additional 15-20% below the barbiturate minimum at flat EEG. These effects of lidocaine resemble those of hypothermia and may enhance the hypothermic protection of the ischemic brain.

Animals↗
PubMed1980

The increase in extracellular potassium concentration in the ischemic brain in relation to the preischemic functional activity and cerebral metabolic rate.

The course of ischemic increase of extracellular potassium concentration ([K+]e) was studied in rat cerebral cortex with potassium selective microelectrodes and correlated to the preischemic functional and metabolic state. Complete cerebral ischemia was induced in artificially ventilated rats by cardiac arrest. Seven different functional states including conditions with cerebral hypermetabolism (seizures, amphetamine intoxication, hyperthermia) and hypometabolism (barbiturate anesthesia, hypothermia) were chosen in order to cover a wide range of cerebral metabolic rates (CMRO2 : 28.7--2.4 ml O2/(100 g)/min). The ischemic increase of [K+]e was delayed in conditions with low CMRO2 and accelerated in conditions with high CMRO2; the time interval to the terminal steep rise in extracellular potassium concentration varied within the extremes of 35 +/- 5 and 365 +/- 12 sec (means +/- S.E.M.), the control state (N2O-analgesia) being 116 +/- 5 sec. In groups with high CMRO2 electrocortical activity ceased within 15 sec and in groups with low CMRO2 within 22 sec. The rates of the ischemic [K+]e increase, measured as rate of change in the potassium electrode potential (mV/sec), remained high in conditions with high preischemic CMRO2 and low in conditions with low CMRO2, indicating a remaining influence of the preischemic metabolism on membrane ion permeability. These results support previous metabolic data indicating that the rate of consumption of high energy phosphates during ischemia mirrors the preischemic cerebral metabolic rate. Phenobarbital anesthesia did not change the initial rate of [K+]e increase but reduced the rate of [K+]e increase later during ischemia, suggesting a special effect of barbiturates on partly depolarized membranes.

Adenosine Triphosphate↗
PubMed1980

Red cell sodium and potassium contents in liver cirrhosis.

Red cell sodium and potassium contents were investigated in 57 patients with histologically proven liver cirrhosis and were compared with 13 controls without clinical evidence of liver disease. Patients with normal serum electrolytes (and without digoxin treatment) had normal red cell sodium content indicating no influence of the cirrhosis per se on the sodium-potassium pump or membrane permeability for sodium. Red cell potassium content was elevated, possibly as a consequence of subclinical hemolysis and a relatively young cell population. Hypokalemia was correlated to increased red cell sodium. Hyponatremia was correlated to low red cell sodium indicating reduced influx due to a decreased concentration gradient. According to the concept of the "sick cell syndrome," membrane failure and cellular gain of sodium and loss of potassium can lead to hyponatremia. Our findings of normal or low red cell sodium contents provide evidence against this mechanism as explanation for the often sever hyponatremia in terminal liver failure. The abnormalities found in the red cells could be attributed to secondary complications to the cirrhosis.

Acid-Base Equilibrium↗
PubMed1979

Effects of reduced cerebral blood flow upon EEG pattern, cerebral extracellular potassium, and energy metabolism in the rat cortex during bicuculline-induced seizures.

Progressive cerebral ischemia was induced by blood pressure (BP) reduction in rats during status epilepticus, and the sequence of cerebral functional (EEG, extracellular K+ activity) and metabolic (levels of high energy phosphates, glucose, glucose-6-phosphate, lactate, pyruvate, alpha-ketoglutarate) changes were determined. Very moderate reductions of BP were accompanied by tissue lactate accumulation and a decrease of the rate of re-uptake of K+ extruded during discharges. These changes were pronounced at BP about 50 mm Hg, when also the energy state showed some deterioration, and the EEG activity changed from one of bursts and suppressions into single spikes. At BP about 30 mm Hg EEG activity was abolished, but not until a slightly lower BP level was there a severe energy depletion and a massive K+ release, indicating generalized membrane depolarization. The results show an increased susceptibility to ischemia during seizures with changes of membrane pump function, and energy metabolism appearing at moderate reductions of BP. Concomitant decrease of seizure activity delayed to some extent the development of massive energy failure and membrane depolarization.

Animals↗
PubMed1977

Presence of anti-c in the serum of 42 women giving birth to c positive babies: serological and clinical findings.

During routine ante-natal testing during the period 1953-73 anti-c was found in the serum of 63 women. Twenty-four of them had received blood transfusion previously and of these 22 were multigravidae. In 39 women pregnancies alone were responsible for the immunization. The anti-c titres of the 42 women giving birth to c positive babies showed that the probability of developing haemolytic disease increases with higher titres. But low titres by no means exclude the existence of such disease. Among the 42 c positive babies 32 had a positive direct antiglobulin test. Some of the affected infants had a serious degree of haemolytic disease.

Blood Transfusion↗
PubMed1977

Complement C1-inactivator in the serum of patients with malignant disease.

Complement C1-inactivator (C1-IA) in serum was determined in 423 individuals. The normal range for the concentration of C1-IA in serum was calculated from values in 94 blood donors and the concentrations in the sera of 329 patients were determined in relation to this range. A significant correlation was found between widespread malignant neoplastic disease and increased quantity of C1-IA in serum. Determination of C1-IA may be used to evaluate the extent to which a malignant disease is disseminated.

Complement C1 Inactivator Proteins↗