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Biomedical subjects

E G Fischer

Publications and source records attributed to E G Fischer.

63 records · Page 4Linked to original sources
PubMedDate not supplied

In vitro studies on PMN-independent endothelial cell damage in trauma: decrease of PMN-endothelial cell adherence by fibrinogen degradation products and disturbance of endothelial cell membrane integrity by trauma serum.

Trauma favors the development of adult respiratory distress syndrome (ARDS). Adherence of polymorphonuclear leukocytes (PMN) to endothelial cells (EC) with subsequent EC damage by the respiratory burst products and proteases of the PMN is thought to be one of the basic mechanisms in the pathogenesis of ARDS. Recent studies have shown that there might also be PMN-independent mechanisms of EC damage. It would speak for PMN-independent EC damage if in the state of risk for this damage factors were found which decrease PMN activity or if EC damage appeared without PMN. Because in trauma and sepsis pathologic coagulation with high levels of fibrinogen degradation products (FDP) is often diagnosed, we investigated whether FDP-D and FDP-E might influence PMN adherence to EC. We also investigated whether serum of traumatized patients might provoke EC damage in a PMN-independent system in vitro. To achieve this we evaluated the viability of EC using a fluorescence staining method. We found that both FDP-D and FDP-E decreased PMN adherence to human EC significantly (p < 0.01) at a concentration of 50 micrograms/ml. Furthermore we found that EC membrane integrity can be disturbed by serum of trauma patients. These results suggest that in trauma also PMN-independent mechanisms are important for EC damage.

Cell Adhesion↗
PubMedDate not supplied

A simplified method for measuring regional blood flow.

A method of measuring regional blood flow (RBF) that is simple in procedure and calculations is described. By arresting flow promptly after a short pulse of diffusible tracer, it is feasible to equate the tracer retained in the tissue (Cfi) with that delivered by the blood. If the arterial pulse is characterized by its mean concentration (Ca) over a known duration (delta t), RBF can be estimated from Cif/Ca delta t). The error involved is relatively small and can be corrected for. If the amount of tracer injected is known, this procedure also provides an estimate of cardiac output and its fractional distribution to the regions sampled. The values obtained for RBF in 4 regions of brain were similar to those previously reported.

Animals↗
PubMedDate not supplied

Cerebral blood flow immediately following brief circulatory stasis.

Cerebral blood flow was studied in rabbits immediately following complete circulatory stasis of varying duration. Systemic arterial pressure was measured continuously. The postischemic circulation was examined both by an infusion of carbon black and, in separate experiments, by injection of 14C-antipyrine into the blood. We examined the relationship between the duration of stasis, the postischemic arterial pressure, and the amount of cerebral reperfusion. As stasis increased from 5 to 30 min the pressure required to achieve reperfusion of the entire brain rose from 20 to 100 torr. Following even temporary exposure to arterial pressures above 110 torr all areas of the brain were generally reperfused. Blood flow in reperfused brain varied directly with arterial pressure, indicating failure of autoregulation. At normal (preischemic) arterial pressure, postischemic cortical flow was twice the normal rate. The data indicate that the pressure required to initiate flow in ischemic brain increases as the duration of stasis is lengthened and that once flow occurs there will be a significant hyperperfusion unless systemic arterial pressure is lowered to the low normal or hypotensive range.

Animals↗
PubMedDate not supplied

Reassessment of cerebral capillary changes in acute global ischemia and their relationship to the "no-reflow phenomenon".

Electron and light microscopic studies were performed on rabbit brain to re-examine the structural changes of endothelial cells and perivascular glia following ischemia. Although swelling of perivascular glia occurred, earlier findings of extreme perivascular glial swelling and bleb formation leading to luminal collapse and plugging could not be confirmed. Ischemic brains, however, had a higher proportion of small-diameter capillaries than controls. It is felt that structural changes in ischemic capillary walls in themselves are not sufficient to explain failed cerebral reperfusion, or the no-reflow phenomenon.

Animals↗
PubMedDate not supplied

Treatable extramedullary cord compression. Meningioma as a cause of the Brown-Séquard syndrome.

The Brown-Séquard syndrome is infrequently reported. Though widely considered indicative of intramedullary spinal cord disease, in the absence of penetrating spinal cord trauma, the syndrome is frequently an early stage of extramedullary spinal cord compression, as an extensive analysis of diverse literatures reveals. We describe two cases resulting from compression of the spinal cord by a meningioma. While previous reviews emphasize that radicular or vertebral pain is a prominent feature of spinal cord compression by intradural tumors, our patients had no pain referable to tumor. Awareness that painless extramedullary spinal cord compression can produce the Brown-Séquard syndrome, early myelography, and surgical intervention are necessary to prevent progressive deficit. Even when encountered in a patient who has previously well-documented demyelinating disease, the syndrome should not be written off as a relatively untreatable intramedullary process.

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