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Biomedical subjects

I Klatzo

Publications and source records attributed to I Klatzo.

106 records · Page 6Linked to original sources
PubMedDate not supplied

Role of circulatory disturbances in the development of post-ischemic brain edema.

Two post-ischemic circulatory disturbances that play a significant role in pathophysiology of an ischemic lesion are: (1) reactive hyperemia or hyperperfusion and (2) hypoperfusion. The reactive hyperemia promptly follows release of major cerebral artery occlusion, and it is associated with the opening of the blood-brain barrier to serum proteins and ensuing edema. Prevention or reduction of reactive hyperemia results in significant amelioration of edema and the resulting ischemic brain tissue injury. The post-ischemic hypoperfusion, studied in gerbils, develops soon after recirculation and usually lasts up to 6 h. Its relationship to post-ischemic edema is evident in repeated ischemic insults. In these studies, three ischemic insults of 5 min duration when applied at 1 h intervals, i.e., during the period of hypoperfusion, resulted in a cumulative effect, post-ischemic edema and tissue injury becoming considerably more pronounced that those following a single 15 min ischemia. There was no cumulative effect when the ischemic insults were spaced 3 min or longer than 6 h apart. These observations indicate that repeated ischemic insults taking place during the phase of post-ischemic hypoperfusion may significantly increase the development of edema and brain tissue injury.

Animals↗
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Arterial air embolism: structural effects on the gerbil brain.

Air injection into the carotid artery of adult mongolian gerbils caused, within 10 minutes, multifocal brain lesions. The extracellular spaces were widened and neurons, oligodendrocytes and myelin sheaths remained unchanged. The "delayed" effects of air embolism (first seen after 3 h) were similar to those observed in gerbils after unilateral carotid ligation. The histologic alterations after 3 h consisted of astrocytic swelling and shrinkage/necrosis of neuronal soma. The observations reported here illustrate the temporal and spatial separations that exist between a) brain water retention, and b) intraparenchymal entry of horseradish peroxidase. Both alterations can be a consequence of either decreased blood flow or arterial air embolism. Edema and protein leakage in each situation may be initiated by different mechanisms.

Animals↗
PubMedDate not supplied

Effects of oxygen saturation and pCO2 on brain uptake of glucose analogues in rabbits.

The effect of oxygen saturation and PCO2 on brain uptake of glucose analogues was studied in rabbits. Using a modified Oldendorf technique, 14C-labeled glucose analogues with a 3H2O reference standard were introduced into the cerebral circulation via the common carotid artery, and the radioactivity of the ipsilateral cerebral cortex was counted and expressed in terms of a brain uptake index (BUI). Severe hypoxia (oxygen saturation less than or equal to 18%) resulted in approximately a 40% decrease in the BUI of 2-deoxy-D-glucose and a 45% decrease in the BUI of 3-0-methyl-D-glucose. Severe hypercapnia (PCO2 = 100 mm Hg) caused a 45% decrease in the BUI of both of these glucose analogues. Hypercapnia superimposed on severe hypoxia had no additional effect. Hypocapnia (PCO2 = 15 mm Hg) increased the BUI of 3-0-methyl-D-glucose by 35% of the control value, and this increase was extremely sensitive to competitive inhibition. When BUI values were plotted against pH rather than PCO2 for the same experiments, there was a good correlation with the calculated linear regression. These results are compared with previous findings on pathologically induced changes in brain uptake of glucose analogues, and the possible role of blood flow is considered in detail.

Animals↗
PubMedDate not supplied

Report of Joint Committee for Stroke Resources. IV. Brain edema in stroke.

A classification of brain edema is provided as well as an extensive review of the animal models from which we have derived most of the basic information we have about the formation and resolution of edema. The clinical aspects of cerebral edema in stroke are discussed and also modern methods for identifying cerebral edema in the human. Attention is given to computed tomography and enhanced CT and advances in their application to this condition. Treatment of cerebral edema in the stroke patient using glycerol, dextran 40, mannitol, steroids, and other drugs is discussed and the need pointed out for controlled clinical trials of the therapeutic effectiveness of these agents.

Adrenal Cortex Hormones↗