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Biomedical subjects

R A Fishman

Publications and source records attributed to R A Fishman.

At least 19 recordsLinked to original sources
PubMed1992

Spontaneous intracranial hypotension: report of two cases and review of the literature.

We report two patients with spontaneous intracranial hypotension. In addition to the cardinal features of a postural headache and a low CSF pressure, the patients also had subdural fluid collections demonstrated by head MRI. In both patients, radionuclide cisternography revealed a CSF leak along the spinal axis and rapid accumulation of radioisotope in the bladder. CSF leakage from spinal meningeal defects may be the most common cause of this syndrome. The headache is a consequence of the low CSF pressure producing displacement of pain-sensitive structures. Associated symptoms, including tinnitus and vertigo, and subdural fluid collections are presumably from hydrostatic changes among intracranial fluid compartments that occur at low CSF pressures. Methods of treatment are identical to those for post-dural puncture headaches. Epidural blood patches and epidural saline infusions have rapidly ameliorated the symptoms of spontaneous intracranial hypotension.

Adult↗
PubMed1990

Liposome-entrapped superoxide dismutase ameliorates infarct volume in focal cerebral ischaemia.

We studied the role of superoxide radicals in the pathogenesis of focal ischaemic brain injury using liposome-entrapped copper-zinc-superoxide dismutase which can penetrate the blood-brain barrier and cell membranes efficiently. Superoxide dismutase activities were significantly elevated in the blood and in the normal brain tissue 1, 2, 8, and 24 hours after a bolus intravenous administration of liposome-entrapped copper-zinc-superoxide dismutase. Copper-zinc-superoxide dismutase activities were also increased significantly in the ischaemic hemisphere and the contralateral cortex as well. The infarct sizes were reduced by 33%, 24% and 18%, respectively, for the anterior artery area, middle artery area, and posterior artery area by treatment at 24 hours following the injection of liposome-entrapped superoxide dismutase. These data demonstrate that superoxide radicals are important determinants of the size of an infarct following focal cerebral ischaemia, and that liposome-entrapped copper-zinc-superoxide dismutase may have pharmacological value for focal cerebral ischaemic injury.

Animals↗
PubMed1990

Liposome-entrapped superoxide dismutase reduces cerebral infarction in cerebral ischemia in rats.

We studied the role of superoxide radicals in the pathogenesis of ischemic brain injury using a model of focal cerebral ischemia in 102 rats and liposome-entrapped CuZn-superoxide dismutase, which can penetrate the blood-brain barrier and cell membranes efficiently. The bolus intravenous administration of 25,000 units of liposome-entrapped CuZn-superoxide dismutase elevated superoxide dismutase activities in the blood and brain 1, 2, 8, and 24 hours later as well as in the ischemic hemisphere and contralateral cortex. Determined 24 hours after right middle cerebral and bilateral common carotid artery occlusion by the lack of staining for mitochondrial dehydrogenase activity with 2,3,5-triphenyltetrazolium chloride, infarct sizes were reduced by 33%, 25%, and 18% in the anterior, middle, and posterior brain slices, respectively, by treatment with liposome-entrapped CuZn-superoxide dismutase. Our data demonstrate that superoxide radicals are important determinants of infarct size following focal cerebral ischemia and that liposome-entrapped CuZn-superoxide dismutase may have pharmacologic value for the treatment of focal cerebral ischemic injury.

Animals↗
PubMed1990

Pathogenesis of vasogenic edema in focal cerebral ischemia. Role of superoxide radicals.

Oxygen-derived free radicals have been postulated to be involved in brain edema and cell death secondary to ischemia and traumatic injury. Using a model of vasogenic brain edema produced by a permanent occlusion of the left MCA in rats, we have studied the role of superoxide radicals in pathogenesis of ischemic edema. The levels of NBF in ischemic brain were increased by 222%, 420%, and 614%, respectively, at 1, 4, and 24 hr after the MCAO. Topical application of superoxide dismutase to the injured cortex through a modified cranial window significantly reduced the NBF levels, indicating the involvement of superoxide radicals in ischemic brain. Liposome-entrapped SOD, when IV injected 5 min after the MCAO, significantly reduced the degree of edema at 24 hr. Our data indicate that superoxide radicals play an important role in the pathogenesis of vasogenic edema in cerebral ischemia.

Animals↗
PubMed1978

Brain edema: induction in cortical slices by polyunsaturated fatty acids.

The presence of polyunsaturated and saturated fatty acids in leukocytic membranes prompted study of their possible role in the induction of brain edema. Polyunsaturated fatty acids including sodium arachidonate, sodium linoleate, sodium linolenate, and docasahexaenoic acids induced edma in slices of rat brain cortex. This cellular edema was specific, since neither saturated fatty acids nor a fatty acid containing a single double bond had such effect.

Animals↗
PubMed1978

Neuropathy following abuse of nitrous oxide.

A disabling peripheral neuropathy, mainly sensory, developed in three health workers who habitually abused nitrous oxide. The distinctive clinical picture included patterns of numbness that were radicular rather than purely distal, and a "reverse" Lhermitte sign, in the absence of signs of spinal cord involvement. Nerve conduction studies suggested an axonal rather than demyelinative neuropathy. The neurologic disorder improved slowly when the patients abstained from further nitrous oxide abuse.

Adult↗