The effect of intracerebral ouabain administration on the composition of edema fluid isolated from cats with cold-induced brain edema

Gazendam, J.; Go, K.G.; Zanten, A. K. Van

doi:10.1016/0006-8993(79)91007-2

Cited by 14 publications

(5 citation statements)

References 6 publications

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“…Our hypothesis based on the observations in CSF of human beings is supported by recent findings by Gazedam et al [5].…”

Section: Discussionsupporting

confidence: 91%

“…They found that the ouabain injection was followed by an in crease of K+ content as well as by increased activities of creatine kinase and lactic acid dehydrogenase (both intracellular enzymes) in the edema fluid concomitant with a de crease in Na+ [5], They also concluded that improper functioning of the brain cellular Na+-and K+-dependent ATPase, as a result of ouabain administration or of an energy deficit in hypoxia, caused the inverted fluxes of compounds and also an uptake of Na+ and water by the cellular elements from the extra cellular space [5]. These results also agree with the well-established finding that local administration of ouabain to the brains of animals causes swelling of apical dendrites and of presynaptic terminals -the elements reported to contain high activities of the Na+-and K+-dependent ATPase system [8,14,17].…”

Section: Discussionmentioning

confidence: 99%

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Effect of Cardiac Glycosides on the Release of Adenylate Kinase into Cerebrospinal Fluid of Patients with Cerebral Arteriosclerosis

Ronquist

Frithz

1982

Eur Neurol

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48 patients with cerebral arteriosclerosis were found to have a manifest release of adenylate kinase (AK) into cerebrospinal fluid (CSF). This release was most probably due to an increased leak in the brain cells subsequent to a lowered adenylate charge potential followed by a diminished electrochemical potential in these cells suffering from disturbed oxygen supply. A further increase of AK release into CSF was noted for the 22 patients receiving cardiac glycosides compared to the 26 patients not treated with these drugs. The mean AK value of the former group was 0.119 ± 0.028 U/l compared to that of the latter group, being 0.089 ± 0.025 U/l, and this difference was significant (p < 0.001). The effect of cardiac glycosides is most probably explained by an additional lowering of the membrane electrochemical potential in brain cells of these patients due to the direct action of cardiac glycosides on the Na⁺- and K⁺-dependent ATPase system in these cells, resulting in an increased leak in the plasma membrane.

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“…Our hypothesis based on the observations in CSF of human beings is supported by recent findings by Gazedam et al [5].…”

Section: Discussionsupporting

confidence: 91%

Section: Discussionmentioning

confidence: 99%

Effect of Cardiac Glycosides on the Release of Adenylate Kinase into Cerebrospinal Fluid of Patients with Cerebral Arteriosclerosis

Ronquist

Frithz

1982

Eur Neurol

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“…As in the previous series, the tips of the needles measuring 4,5,8,9,10,11, and 12 mm were situated in the white matter underlying the lesion; the tips of those measuring 6 and 7 mm were in the uninjured wedge of cortex underneath the lesion and the needle 13 mm in length had its tip in the gray matter of the claustrum.…”

Section: Location Of Needlesmentioning

confidence: 55%

Influence of hypoxia on the composition of isolated edema fluid in cold-induced brain edema

Kito¹,

Vanzanten²

1979

Journal of Neurosurgery

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The isolation of edema fluid from cats with cold-induced cerebral edema allowed the study of changes of Na+ and K+ content, lactate dehydrogenase and creatine phosphokinase activity, colloid osmotic pressure and the level of intravenously administered 99mTc-albumin in the edema fluid during a period of hypoxia. The changes consisted of an increase of all mentioned parameters, except Na+; and could be interpreted as a concentration of solutes (but for Na+) in the extracellular edema fluid, concomitant to a reduction of the extracellular space, as the oxygen deficiency caused improper functioning of the cellular Na+-K+ pump, with a resulting shift of fluid (including Na+) into the cellular elements.

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“…46 -47 Capillary Na,K-ATPase might be involved in vasogenic brain edema induced by cold injury. 48 Gazendam et al 48 observed increases in K + concentration and decreases in Na + concentration in edema fluid caused by intracerebral ouabain administration within the edemic focus. Astrup et al 49 investigated to what extent Na,K-ATPaserelated energy consumption operated in the CNS using an isolated brain perfusion model.…”

Section: V--;•'mentioning

confidence: 99%

Effect of enhanced capillary activity on the blood-brain barrier during focal cerebral ischemia in cats.

Shigeno

Asano

Mima

et al. 1989

Stroke

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We hypothesize that enhanced activity of capillary Na,K-ATPase promotes Na + influx into the brain and causes early edema formation in focal cerebral ischemia. The pharmacologic suppression of brain capillary Na,K-ATPase as a means to ameliorate edema formation was examined using the middle cerebral artery occlusion model in 36 cats. With the help of a catheter inserted into the middle cerebral artery, the ischemic brain area was directly perfused with 10~5 M ouabain. Perfusion was maintained as intermittent 15-second pulse injections given every 5 (n=6) or 2 (w=6) minutes. By this method, the naturally occurring circulatory conditions during ischemia were not altered. Four hours after ischemia, the cortical specific gravity at each of six locations over the ischemic area was compared with the corresponding ischemic blood flow measured by the H 2 clearance technique. The results show that ouabain perfused every 2 minutes significantly ameliorated edema formation compared with six control cats perfused with Krebs-Ringer solution. In a separate series of experiments, the Na + flux across the blood-brain barrier was studied by injecting

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The effect of intracerebral ouabain administration on the composition of edema fluid isolated from cats with cold-induced brain edema

Cited by 14 publications

References 6 publications

Effect of Cardiac Glycosides on the Release of Adenylate Kinase into Cerebrospinal Fluid of Patients with Cerebral Arteriosclerosis

Effect of Cardiac Glycosides on the Release of Adenylate Kinase into Cerebrospinal Fluid of Patients with Cerebral Arteriosclerosis

Influence of hypoxia on the composition of isolated edema fluid in cold-induced brain edema

Effect of enhanced capillary activity on the blood-brain barrier during focal cerebral ischemia in cats.

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