Biomedical subjects

J A Feilbach

Publications and source records attributed to J A Feilbach.

4 recordsLinked to original sources

PubMed1988

Erythrocytes are essential for development of cerebral vasculopathy resulting from subarachnoid hemorrhage in cats.

In an effort to determine which blood elements play a critical role in the development of cerebral vasospasm, adult cats were subjected to prepontine injection of either autogenous whole blood or erythrocyte-free blood containing latex beads as a substitute morphologic marker. Seven or 10 days later the cats were anesthetized and perfused with fixative, and the basilar arteries were prepared for light and electron microscopy. Successful clot deposition was confirmed by the presence of numerous erythrocytes or latex beads within the adventitia of vessels. In agreement with previous studies, instillation of whole blood produced luminal narrowing associated with profound ultrastructural changes in all layers of the vascular wall. No significant alterations, however, occurred in arteries bathed in erythrocyte-free blood. These findings suggest first, that erythrocytes are essential for the development of the vasculopathy associated with chronic cerebral vasospasm, and second, that the role, if any, of other blood elements is not autonomous.

Animals↗

PubMed1988

Bilirubin and the induction of intracranial arterial spasm.

Although a number of substances which participate in the physiological control of vascular caliber have been proposed to play a causative role in cerebral vasospasm, none of these has been shown to induce the profound, sustained degree of constriction or the vasculopathy that characterize this disorder. The present study was undertaken to determine whether bilirubin, a hemoglobin breakdown product with detergent-like activity, accrued in incubated blood or in intracranial hematoma and whether topical application of bilirubin altered the caliber or morphology of cerebral arteries. As a model of blood residing in the subarachnoid space, sterile vials of cat blood and of human blood were incubated in vitro at 37 degrees C. The concentration of bilirubin in the supernatant of cat blood increased from a value of 0.27 +/- 0.3 mg% (mean +/- standard error of the mean) on Day 0 to a value of 9.57 +/- 2.4 mg% on Day 10; the respective values for human blood were 0.53 +/- 0.02 mg% and 13.4 +/- 5.4 mg%. Samples of intracranial hematoma that had been surgically removed from three patients between 4 and 11 days after hemorrhage yielded bilirubin levels from 2.1 to 15.2 mg%. Application of a bilirubin suspension of 5, 10, or 20 mg% in buffered Ringer's solution to cat basilar artery in vivo led to progressive and sustained constriction; at 4 hours the mean decrease in the width of the blood column was 34% +/- 2.1%. Ultrastructural analysis of these vessels showed widespread pathological changes similar to those associated with cerebral vasospasm. Application of a 10-mg% bilirubin suspension to the basilar artery of two baboons produced similar alterations. Minimal changes in diameter or morphology were observed in cat arteries bathed in buffer solution alone. These findings in animal models indicate that bilirubin may play a central role in the development of cerebral vasospasm.

Animals↗

PubMed1986

Ultrastructural evidence of arterial denervation following experimental subarachnoid hemorrhage.

Loss of catecholamine histofluorescence, increased sensitivity to norepinephrine, and changes in alpha1 receptor binding have led to the proposal that denervation hypersensitivity may play a role in cerebrovascular spasm. Because the significance of these alterations has remained unclear, the present study was undertaken to determine whether there was direct ultrastructural evidence of arterial denervation following experimental subarachnoid hemorrhage. Under general anesthesia, adult cats were subjected to pre-pontine injection of blood or serum (5 to 7 ml) via a transclival approach. The animals were sacrificed 4, 7, or 10 days later and basilar artery segments were prepared for electron microscopy. Control vessels appeared normal, whereas those bathed in blood revealed unequivocal changes in neural and supporting elements, including: 1) disintegration of both clear- and dense-core vesicles; 2) fragmentation of varicosities; 3) loss of Schwann cell cytoplasm; and 4) axonal degeneration. These changes were most pronounced 7 days after instillation of blood, and correlated in time with maximal injury of the media and endothelium. Although the development of smooth-muscle hypersensitivity remains unsettled, this study indicates that prolonged exposure to blood can cause extensive denervation of cerebral arteries.

Animals↗

PubMedDate not supplied

Does cerebral vasospasm result from denervation supersensitivity?

This study examined the role of denervation supersensitivity in the development of cerebral vasospasm. Adrenergic denervation of cat basilar artery was accomplished by resection of the superior cervical ganglia or by injection of 6-hydroxydopamine into the cisterna magna. In vivo dose-response characteristics were determined for normal and for denervated arteries, and no significant differences were found between topical applications of serotonin, norepinephrine, epinephrine, fresh blood, or incubated blood. In addition, analysis of cat blood incubated in vitro revealed that the levels of serotonin, norepinephrine, and epinephrine diminished over time, whereas levels of hemoglobin and methemoglobin increased up to Day 14. The results of this study indicate that adrenergic denervation is not the cause of cerebral vasospasm and that, whatever the mechanism, hemoglobin is far more likely to play a role than are the other agents.

Animals↗