Search PubMed⌕ Search

Biomedical subjects

A J Hansen

Publications and source records attributed to A J Hansen.

At least 91 records · Page 5Linked to original sources
PubMed1982

Hyperglycemic ischemia of rat brain: the effect of post-ischemic insulin on metabolic rate.

To identify the mechanism by which hyperglycemia impairs recovery after cerebral ischemia, cortical blood flow (CBF), cortical metabolic rate for oxygen (CMRO2), and the cortical phosphorylation rate for glucose (CPRg1c) were measured in rats 1 h after a global ischemic insult of the brain. A control group remained hyperglycemic after ischemia. The experimental group received insulin which reduced plasma glucose during the period of recirculation after ischemia. Thus, the brains of both groups were hyperglycemic before and during ischemia. The CMRO2 after ischemia was higher in insulin-treated rats than in hyperglycemic rats (250 vs 168 mumol . 100 g-1 . min-1) while the CPRg1c was lower (22 vs 58 mumol . 100 g-1 . min-1). We conclude that glucose-induced inhibition of oxygen consumption in brain contributes to the impaired recovery after ischemia.

Animals↗
PubMed1982

Persistent oligemia of rat cerebral cortex in the wake of spreading depression.

Cerebral blood flow during and after spreading depression (SD) was studied in rat brain by quantitative autoradiography. The rise of cortical blood flow during SD was followed by 20 to 25% reduction below normal after SD, lasting at least an hour. Blood flow in th putamen, thalamus, and hippocampus did not change at any time during or after SD. Previous measurements of cerebral blood flow in humans showed that migraine attacks may be accompanied by wavelike spreading oligemia (Olesen et al, 1981). We speculate that the spreading oligemia of migraine may be a phenomenon physiologically related to the present finding of an oligemia after SD.

Animals↗
PubMed1982

Anoxia increases potassium conductance in hippocampal nerve cells.

The effect of anoxia on nerve cell function was studied by intra- and extracellular microelectrode recordings from the CA1 and CA3 region in guinea pig hippocampal slices. Hyperpolarization and concomitant reduction of the nerve cell input resistance was observed early during anoxia. During this period the spontaneous activity first disappeared, then the evoked activity gradually disappeared. The hyperpolarization was followed by depolarization and an absence of a measurable input resistance. All the induced changes were reversed when the slice was reoxygenated. Reversal of the electro-chemical gradient for Cl- across the nerve cell membrane did not affect the course of events during anoxia. Aminopyridines blocked the anoxic hyperpolarization and attenuated the decrease of membrane resistance, but had no effect on the later depolarization. Blockers of synaptic transmission. Mn++, Mg++ and of Na+-channels (TTX) were without effect on the nerve cell changes during anoxia. It is suggested that the reduction of nerve cell excitability in anoxia is primarily due to increased K+-conductance. Thus, the nerve cells are hyperpolarized and the input resistance reduced, causing higher threshold and reduction of synaptic potentials. The mechanism of the K+-conductance activation is unknown at present.

Animals↗
PubMed1982

[Simultaneous diffusion of inositol and mannitol in the rat brain].

The diffusion of both inositol and mannitol has been determined simultaneously by the integral bolus method in rat brain. The permeability constant (Kin) of inositol averaged 0.27 +/- 0.02 ml X (100 g)-1 X min-1 or 4 X 10(-7) cm X s-1 at a cerebral capillary surface area of 100 cm2 x g-1. The permeability of mannitol was 0.08 +/- 0.01 ml X (100 g)-1. min-1 or 1 X 10(-7) cm X s-1. Neither glucose nor galactose affected the inositol permeability. Hypoglycemia increased somewhat the Km value for mannitol. The basal ganglia showed an increase Km for both substrates as compared with those obtained for cortex, temporal and parietal tissues.

Animals↗
PubMed1981

Blood-brain glucose transfer in spreading depression.

Spreading depression in rat brain cortex is associated with a twofold increase of cerebral blood flow. It is not known whether this increase is coupled to increases of cerebral metabolic rate and glucose transport from blood to brain. During the passage of a single spreading depression, we measured blood-brain glucose transport and glucose metabolism in rat cerebral cortex by single intravenous injection of tracer glucose. Blood flow and tissue content of glucose were measure as well. Reduction of tissue glucose and the consequent increase of net transfer of glucose from blood to brain were consistent with a threefold increase of the consumption of glucose before the increase of blood flow. There was no increase of unidirectional blood-brain transfer.

Animals↗
PubMed1981

Extracellular ion concentrations during spreading depression and ischemia in the rat brain cortex.

We compared interstitial ion concentrations in rat brain cortex during two conditions where pronounced changes are observed: spreading depression and ischemia. Initially, during the two phenomena, an increase of [K+]e from 3 to approximately 10 mM were observed, but only small changes of the other ion concentrations. Hereafter, [K+]e exhibited a rapid increase (2-3 s) to 55 mM, whereas [Na+]e rapidly decreased to 60 mM, [Cl-]e to 75 mM, and [Ca++]e to 0.08 mM. The changes were accompanied by a rapid negative shift in the local electrical potential. However, there were differences in the ionic events during the two phenomena. In spreading depression, the initial [K+]e increase took place in 5-10 s, but in ischemia it lasted 1-2 min. The ionic perturbations were spontaneously reverted in SD, but in ischemia they proceeded further and reached after 5 min (mM): [K+]e 75, [Na+]e 50, [Cl-]e 72, and [Ca++]e 0.06. The similar chain of ionic events during spreading depression and ischemia suggests a common mechanism for the ionic changes, probably involving changes of ionic permeability of brain cells.

Animals↗
PubMed1980

Extracellular potassium and blood flow in the post-ischemic rat brain.

The concentration of extracellular potassium, [K+]e, was measured in parietal cortex and basal ganglia of rats during and after ten minutes of complete cerebral ischemia. The post-ischemic normalization of [K+]e was considerably delayed in parietal cortex compared to basal ganglia, but in both regions, [K+]e reached its normal concentration within 4 min of the end of the ischemia. Also, in both regions blood flow was elevated at the time of maximal [K+]e decrease. Our findings suggest that the normalization of [K+]e and cerebrovascular resistance after ischemia are related by positive feed-back, possibly via the stimulation of Na+-K+-ATPase.

Animals↗
PubMed1980

Rapid simultaneous determination of regional blood flow and blood-brain glucose transfer in brain of rat.

A new method was developed and used in rat to measure regional and whole-brain blood flow and blood-brain glucose transfer simultaneously and in 20 s. This simple method consisted of i.v. bolus injection of labeled butanol and tracer glucose, determination of the average arterial tracer concentration and subsequent assay of cerebral tissue activity 20 s after bolus injection. The whole-brain blood flow rate averaged 129 ml (100 g)-1 min-1. The unidirectional blood-brain glucose transfer was twice as high as previously estimated in similar studies on rat, or 144 mumol (100 g)-1 min-1 at 10 mM glucose in plasma. The magnitude is sufficient to explain the high cerebral glucose consumption rates recently determined by means of autoradiographic 2-deoxy-D-glucose method of Sokoloff et al. (1977).

Animals↗
PubMed1980

Brain extracellular space during spreading depression and ischemia.

The change of extracellular space volume of rat brain cortex during ischemia and cortical spreading depression, CSD (Leão 1944) was evaluated by a new method. The cortical surface was irrigated with isotonic CSF containing the extracellular markers 50 mM cholin or 50 mM trimethyltris(hydroxymethyl)methyl ammonium ion (N-TRIS), and their extracellular concentrations were monitored by ion-selective microelectrodes. When steady-state for the concentration of these markers was attained, CSD evoked a reversible increase of the concentration of the markers, indicating shrinkage of the interstitial volume of distribution. During ischemia an initial slow rate of concentration increase was observed, followed a few minutes later by a rapid increase concomitant with the sharp rise in extracellular potassium concentration. During CSD and ischemia, the maximal increases of choline and N-TRIS concentration reflected a shrinkage of the extracellular space amounting to about 50% of the initial volume.

Animals↗
PubMed1980

Relationship between local changes in cortical blood flow and extracellular K+ during spreading depression.

Change of local cerebral blood flow in response to a single cortical spreading depression of Leão was studied in the brain. During a spreading depression, potassium briefly accumulates in the brain extracellular space. The cortical blood flow was normal during the maximal rate of increase of the extracellular potassium concentration. The blood flow doubled during the subsequent period of normalization of potassium and remained high for one minute thereafter. Thus, potassium cannot be the immediate mediator of the blood flow increase.

Animals↗
PubMed1978

The extracellular potassium concentration in brain cortex following ischemia in hypo- and hyperglycemic rats.

The extracellular potassium concentration, [K+]e, was measured in the brain cortex of hypo-, normo- and hyperglycemic rats following brain ischemia. The increase in [K+]e in control rats could be characterized by 3 phases: an initial slow rate of rise where the [K+]e rose in 2 min from 3 to 9 mM followed by an abrupt, steep increase to 60 mM within 10 s and finally a slow rise to 80 mM. In the hyper- and hypoglycemic rats the same pattern appeared, but there were significant differences in the time course. The duration of the initial phase was approximately doubled in the hyperglycemic and halved in the hypoglycemic group. The [K+]e at which the steep increase was elicited was 8--10 mM in all groups. It is concluded that the duration of the initial phase is dependent upon available stores of glucose in the brain.

Animals↗
PubMed1978

Clinical restitution following cerebral ischemia in hypo-, normo- and hyperglycemic rats.

Rats with different levels of blood glucose concentration were exposed to 10 min of complete brain ischemia achieved by compression of neck vessels by a pneumatic cuff. All normoglycemic rats survived the ischemic period and made the best clinical recovery. Hyperglycemic rats died within 12 h. Seizure activity was observed in all animals in this group. Three of eight hypoglycemic rats died between 3 and 16 days. The clinical recovery was less complete than in the control group. Thus, recovery from cerebral ischemia depends upon preischemic blood glucose concentration. Hyper- and hypoglycemia hamper the clinical recovery after transient cerebral ischemia.

Animals↗
PubMed1977

K+-permeability of the blood-brain barrier, investigated by aid of a K+-sensitive microelectrode.

The K+-permeability of the blood-brain barrier at the capillary level was estimated from determinations of brain extracellular K+-concentration in response to an isotonic bolus containing KCl injected into the carotid artery. A very low permeability appeared from the fact that the extracellular K+-concentration--measured by aid of K+-sensitive microelectrodes--remained unchanged during the passage of the bolus. An upper limit for the blood-brain barrier K+-permeability in the rat was estimated to be 2.8 X 10(-7) cm. with s-1.

Animals↗
PubMed1977

Extracellular potassium concentration in juvenile and adult rat brain cortex during anoxia.

The extracellular K+ concentration, ([K]e), in the brain cortex of rats at different ages was measured by means of K+-sensitive microelectrodes. [K]e was between 3 and 5 mM at all ages. Following nitrogen inhalation there was an increase in [K]e which exhibited a sigmoid pattern in every age group: Firstly, there was a slow rate of rise which was followed by a sudden, steep increase where the [K]e rose to about 70 mM. During the subsequent 5-10 min a plateau value of about 90 mM was reached. The prominent difference between the age groups was the time until the steep rise began. The time to the steep increase in [K]e and the [K]e at the start of the steep was inversely related to the age of the animal. A close relation was found between the time to the start of the steep increase and the time to the last gasp during nitrogen breathing (r = 0.98). It is suggested that the different resistence to anoxia in young and adult animals is related to differences in the ability to keep near normal potassium gradients across the cells in the brain.

Age Factors↗
PubMed1976

The potassium concentration in cerebrospinal fluid in young and adult rats following complete brain ischemia. Effects of pretreatment with hypoxia.

The potassium concentration in the cisternal cerebrospinal fluid (CSF) was measured following brain ischemia in rats of different ages which has been kept at normoxia or pretreated with hypoxia (PIO2 = 70 mmHg) for 24 h. In all age groups the potassium concentration rose following ischemia. The rate of rise was relatively slow in the 4-day rat and faster in 16- and 24-day rats; beyond this age the rate of rise became slower. Pretreatment with hypoxia significantly diminished the rate of rise in CSF potassium in 4- and 8-day rats, while no effect was observed in the older age groups. It is suggested that the rate of rise in CSF potassium is inversely correlated with the capacity of surviving a period of oxygen deprivation.

Age Factors↗