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J Majkowska

Publications and source records attributed to J Majkowska.

3 recordsLinked to original sources

Ultrastructural features of the neurohypophysis of reanimated rat in connection with experimentally induced clinical death lasting 15 min. A case report.

Neurohypophysial pituicytes and axons of the rat 48 h after reanimation in connection with experimentally induced clinical death lasting 15 min were examined electron microscopically. In most of pituicytes there appeared ultrastructural alterations indicating a high sensitivity of the cells to the ischaemic conditions associated with clinical death and the postreanimation period. Hyperactive forms of pituicytes rich in subcellular organelles, including lysosomes, as well as hypoactive forms of the cells scarce in organelles but containing numerous electron-lucent vacuoles were seen in the neurohypophysis. Intermediate forms of pituicytes were also perceived. Close appositions of pituicytes and neurosecretory axons (axons enclosed by pituicytes) were frequently observed, and several phases of axon degeneration due to pituicytes were noted. These findings are indicative of an enhanced neuronal-glial interaction in the neurohypophysis during the postreanimation period. Except for degenerated axon profiles enclosed by pituicytes, other altered profiles were occasionally found throughout the neurohypophysis. Thus, in the neurohypophysis unchanged axons predominated rich in neurosecretory granules. Post-embedding PAP-immunolabelling for vasopressin visualised an abundance of vasopressin-positive axon profiles filled with labelled neurosecretory granules. The results of immunocytochemical studies, therefore, suggest a restriction of the release of neurohypophysial hormones in the reanimated rat examined here. At the same time, the results of conventional electron microscopy may indicate an enhanced involvement of pituicytes in the mechanisms regulating the neurohypophysial hormone release.

Animals

Rapid decrease of high affinity ouabain binding sites in hippocampal CA1 region following short-term global cerebral ischemia in rat.

High affinity [3H]ouabain binding was examined in the hippocampal CA1 region and frontal cortex of rats subjected to 5 min complete cerebral ischemia in a clinical death model, and to subsequent resuscitation. A decrease of Bmax directly after ischemia and its further gradual decrease during 120 min of reperfusion were noted in the ischemia-vulnerable CA1 region, whereas no change of Bmax was observed in frontal cortex. The apparent Kd constant showed insignificant fluctuations in either of the two brain regions. Since ouabain binds with high affinity to the neuronal (alpha +)-form of Na+/K+-ATPase, the results indicate a rapid enzyme loss in CA1 neurons. The high affinity ouabain binding test proved to be a sensitive detector of premorphological changes in nerve cell membranes in ischemia.

Animals