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Biomedical subjects

A J Hansen

Publications and source records attributed to A J Hansen.

At least 73 records · Page 4Linked to original sources
PubMed1988

Calcium accumulation by glutamate receptor activation is involved in hippocampal cell damage after ischemia.

Rats exposed to 10 min of complete cerebral ischemia develop necrosis of the CA-1 region of the hippocampus after 2-3 days. We studied the involvement of synaptic transmission for this process by ablation of the afferent input (which is mainly glutamatergic) to CA1 by bilateral destruction of CA-3 neurons (Schafferotomi). The deafferentiation completely prevented the ischemic nerve cell destruction as revealed by histological studies after 6 days. The role of intracellular Ca++ overload was assessed by measurement of the interstitial Ca++ concentration. In control animals the interstitial Ca++ concentration decreases abruptly to 10% of the initial value 1.6 min after the onset of ischemia. The denervated hippocampi, however, showed no decrease during the 10 min of ischemia and hippocampi injected with 2-amino-5-phosphovalerate (APV), a competitive antagonist of the glutamate N-methyl-D-aspartate (NMDA) receptors, displayed a significantly reduced decrease (45% of the initial value) during ischemia. It is concluded that calcium influx via the glutamate-operated channels during the ischemic period is an important link in the development of ischemic brain cell damage.

2-Amino-5-phosphonovalerate↗
PubMed1987

Late results after meniscectomy in children.

Seventy-five children undergoing 77 meniscectomies have been reviewed from 1 to 30 years (mean 15) after operation in order to determine the late results of meniscectomy. Arthroscopy of the patients with a poor result was performed at the follow-up. In 30 per cent osteoarthrosis was diagnosed, all with follow-up times from 19 to 25 years. Delay in operation resulted in worse results. The younger the patient the worse the result. The benefit of operation was less in girls than in boys. Bucket-handle lesions and peripheral tears produced the best results after meniscectomy. Fifty-eight per cent of men and 26 per cent of women had symptom-free knees at follow-up. Removing a meniscus is not a benign procedure. Only 44 per cent of patients in whom a damaged meniscus and 17 per cent in whom a normal meniscus had been removed were without symptoms. These results stress the need for making an accurate diagnosis by careful examination and arthroscopy before embarking on meniscectomy in children. Efforts to preserve the meniscus in children must be made whenever possible.

Adolescent↗
PubMed1987

Temporal relationship between neurotransmitter release and ion flux during spreading depression and anoxia.

Brain ion homeostasis is severely perturbed during spreading depression of Leao and during anoxia. The ionic composition of the extracellular space changes abruptly and approaches the intracellular concentrations owing to an increase in cell permeability. In spreading depression, synchronous transmitter efflux caused by a depolarization of the presynaptic terminals has been implicated as a possible mechanism that would explain the concomitant movement of ions. Anoxia, having many features in common with spreading depression, may follow the same mechanism. We have measured the concentrations of extracellular potassium with ion-selective microelectrodes and dopamine by in vivo voltammetry with carbon fiber microelectrodes during spreading depression and anoxia to compare the temporal relationship between the release of dopamine and ion movements in the striatum. There is a pronounced release of dopamine during both spreading depression and anoxia. In spreading depression, the sharp increase of potassium concentration that follows an initial smaller and slower increase of potassium is accompanied by the release of dopamine. In anoxia, the dopamine release clearly precedes the fast rise of extracellular potassium concentration. We conclude that in striatum, there is a pronounced dopamine release during spreading depression and anoxia, but that the relationships between ionic changes and transmitter release for these two phenomena are different and probably reflect different mechanisms.

Animals↗
PubMed1985

Nonpulsatile cardiopulmonary bypass disrupts the flow-metabolism couple in the brain.

The effect of cardiopulmonary bypass on the relationship between brain glucose consumption and regional blood flow is unknown. We measured this relationship in pigs subjected to 3 hours of pulsatile or nonpulsatile cardiopulmonary bypass at normothermia and compared the results to the relationship established in a control group of pigs. A total of 10 regions were sampled in both hemispheres of the porcine brain. In control pigs, cerebral blood flow averaged 46 ml/100 gm and the glucose consumption, 21 mumol/100 gm/min. The ratio between blood flow and glucose consumption was close to 2 ml/mumol in all regions. In pulsatile cardiopulmonary bypass both the whole-brain average and the regional values declined, so that the ratio remained the same, about 2 ml/mumol. In nonpulsatile cardiopulmonary bypass regional blood flow remained normal; the average was 49 ml/100 gm/min, whereas the average glucose consumption declined to 16 mumol/100 gm. In regions with high blood flow rates, the ratio between blood flow and glucose consumption increased to about 3 ml/mumol, indicating perfusion in excess of metabolic demand. We conclude that nonpulsatile cardiopulmonary bypass at normothermia affects the metabolic flow regulation in the brain by interfering with the myogenic contractility of cerebral arterioles.

Blood Flow Velocity↗
PubMed1984

Ion and membrane changes in the brain during anoxia.

Anoxia has two main effects on the brain, a rapid, reversible loss of function and permanent damage when the period of anoxia exceeds a critical length of time. The initial loss of function is related to a K+-conductance increase of the nerve membrane, leading to reduction of membrane resistance and hyperpolarization. After a few minutes, a non-selective increase of membrane permeability mediates rapid transfer of ions between the intra- and extracellular spaces. The subsequent rise of intracellular Ca2+ concentration may be responsible for the nerve cell death.

Acid-Base Equilibrium↗
PubMed1984

Extracellular pH changes during spreading depression and cerebral ischemia: mechanisms of brain pH regulation.

We have examined the extracellular pH (pHe) during spreading depression and complete cerebral ischemia in rat parietal cortex utilizing double-barrelled H+ liquid ion exchanger microelectrodes. The baseline pHe of the parietal cortex was 7.33 at a mean arterial PCO2 of 38 mm Hg. Following spreading depression and cerebral ischemia, highly reproducible triphasic changes in pHe occurred, which were intimately related to the negative deflection in tissue potential (Ve). The changes in pHe for spreading depression (n = 23) were a small initial acidic shift, beginning before the rapid change in Ve, followed by a rapid transient alkaline shift of 0.16 pH units, the onset of which coincided with the negative deflection in Ve. A prolonged acidic shift of 0.42 pH units then occurred. The maximal decrease in pHe was to 6.97 and the mean duration of the triphasic pHe change was 7.8 min. The lactate concentration in brain cortex increased from baseline 1.2 mM to 7.0 mM (n = 6) during the maximal acidic change in spreading depression. In addition, lactate levels correlated well with resolution of the pHe changes during spreading depression. The triphasic pHe changes following complete cerebral ischemia were an initial acidic shift of 0.43 pH units which developed over 2 min, then an alkaline shift of 0.10 pH units coincident with the negative deflection in Ve, and a final acidic shift of 0.26 pH units. The terminal pHe was 6.75. Superfusion of the cortex with inhibitors of carbonic anhydrase (acetazolamide), Na+/H+ counter transport (amiloride), and Cl-/HCO-3 countertransport (4,4'-diisothiocyanostilbene-2,2'-disulfonic acid) altered the triphasic pHe changes in a similar fashion for both spreading depression and cerebral ischemia, providing insights into the pHe regulatory mechanisms in mammalian brain.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗