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Morphological analysis of active microglia - rod and ramified microglia in human brains affected by some neruological diseases (SSPE Alzheimer's disease and Wilson's disease).
Folia Neuropathol. 2002: 40 (3) s.125-131, il., tab., bibliogr. 36 poz.
Hasła klasyfikacyjne GBL:
The activation of microglial cells in pathological conditions is manifested primarily by their proliferation, as well as by the occurrence of a new morphological form - rod microglia. In the present study immunohistochemical identification of rod microglial phenotype against ramified microglia was performed on segments of 17 brains derived from 7 cases of encephalitis of viral aetiology (including 5 SSPE cases), 6 cases of Wilson's disesase and 4 cases of Alzheimer's disease. Segments from frontal, temporal and occipital lobes, cerebellum and brainstem were subjected to histological, hostochemical and immunohistochemical reactions. The presence of activated rod and ramified microglia was observed in sections derived from al structures of the brains under study. Both morphological forms of acitivated microglia reacted to antibodies: HLA II, CD68, HAM56 and lectin RCA-1s. Expression of HLA II molecules was less intensive on the surface of microglial rod cells. A positive reaction to PCNA antibody was mainly observed in rod/elongated/cylinder-shaped nuclei, which is a characteristic feature of rod microglia. In the study material, the localisation of microglial processes seemed to depend rather on the structural topography of the cell in the brain than on the nuclear shape of the activated microglial cell. Our observations revealed a strong similarity between immunohistochemical phenotypes of both morphological forms of microglia with the indication that rod microglia is a first developmental form of activated microglia.
Ischemic preconditioning diminishes oxygen demand and increases coronary flow in the early phase of reperfusion in rat heart.
Med. Sci. Monitor 2002: 8 (9) s.BR362-BR368, il., tab., bibliogr. 45 poz.
Hasła klasyfikacyjne GBL:
Background: Ischemic preconditioning (IPC) can be defined as an adaptive mechanism induced by a brief period of reversible ischemia increasing the heart's resistance to a subsequent longer period of ischemia. The objective of our research was to describe the effects of IPC on the hemodynamic function and metabolism of the myocardium during postischemic reperfusion. Material/methods: 20 rat hearts were assigned to a preconditioning group (n = 10) or to a control group (n = 10). Preconditioning was achieved with 5 min. of global ischemia and 10 min. of reperfusion followed by 40 min. of ischemia. We investigated the postischemic recovery of aortic pressure, cardiac output, and coronary flow, as well as oxygen consumption, carbon dioxide release, and [H+] release. Results: No significant intergroup differences in aortic pressure and cardiac output were observed during reperfusion. In both groups, increased coronary flow (greater in the IPC group: 11.4 ń 0.6 ml/min. vs 9.1 ń 0.5 ml/min. in control group) was observed in the early phase of reperfusion. This was accompanied by a rise in CO2 and [H+] release, which was also greater in the IPC group. Oxygen consumption was significantly lower in the IPC group in the later phase of reperfusion (9.39 ń 0.53 vs 11.79 ń 0.54 ćmol/min/g dry weight), as were Co2 and [H+} release. Conclusions: IPC diminishes oxygen demand during reperfusion without changing the hemodynamic function considerably. IPC results in a transient increase of coronary flow accompanied by a rise in CO2 and [H+] release.
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