Biomedical subjects

P Ostrow

Publications and source records attributed to P Ostrow.

11 recordsLinked to original sources

PubMed1995

Pontine ischemic rarefaction.

To investigate apparently asymptomatic, bilateral symmetrical predominantly pontine hyperintensities (PHI) on magnetic resonance imaging (MRI) scans in elderly patients, we examined the pons histopathologically in two brains of elderly hypertensives with PHI, and in three without PHI, on postmortem MRI scans. We also reviewed 85 serial in vivo MRI scans of patients over 60 and compared scan findings, vascular risk factors, and clinical symptoms between patients with PHI and a control group. A subcortical arteriosclerotic encephalopathy (SAE)-like pathology was present in the pons in only the two autopsy brains with PHI and corresponded with the location of PHI on the postmortem MRI scans and with the most frequent sites of PHI on in vivo scans. SAE also involved the hemispheric white matter in one of the autopsy brains. Five of 16 (31%) patients with, and 4 of 69 (6%) without, PHI on in vivo MRI scans had marked periventricular hyperintensity (PVHI) compatible with SAE (p = 0.01). We conclude that an SAE-like pathology may be seen in the pons in elderly hypertensives and this pathology is probably the cause of PHI seen on MRI scans of patients over 60 years of age.

Aged↗

PubMed1994

Motor performance, histologic damage, and calcium influx in rats treated with NBQX after focal ischemia.

2,3-Dihydroxy-6-nitro-7-sulfamoylbenzo(F)-quinoxaline (NBQX), an alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA) receptor antagonist, has been reported to provide neuronal protection after global ischemia. The objectives of this study were to evaluate the neuroprotective effects of NBQX initiated after focal cortical ischemia and to validate a method for measuring functional outcome in this model. Male spontaneously hypertensive rats (SHRs) were exposed to various durations of transient or permanent tandem middle cerebral artery (MCA) occlusion. Studies compared motor performance using balance beam and prehensile-traction tests, calcium-calmodulin (Ca-CaM) binding by immunohistochemistry, and infarct volume between NBQX-treated animals [intravenous (i.v.) 5 mg/kg/h x 6 h or intraperitoneal (i.p.) 30 mg/kg q 30 min x 3 begun postischemia] and controls. All ischemic groups performed less well than sham-operated controls on the motor performance tasks in proportion to the severity of ischemia. No significant improvement in motor performance was noted in the NBQX-treated versus the control animals after 1 h or permanent MCA/CCA occlusion. Treatment with NBQX (i.v. or i.p. dosing) did not reduce Ca-CaM binding after 1 h of occlusion with 1 h of reperfusion or after 2 h of occlusion. Similarly, there was no reduction in infarct size between NBQX-treated and control animals after 24 h of permanent MCA/CCA occlusion (74.6 +/- 7.1 vs. 80.1 +/- 6.0 ml; ns) or after 1 h of occlusion with 23 h of reperfusion (55.1 +/- 4.4 vs. 47.4 +/- 6.2 ml; ns).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1994

Graded bioassay for demonstration of brain rescue from experimental acute ischemia in rats.

BACKGROUND AND PURPOSE: This study explored the correlation between duration of focal ischemia and infarct volume in spontaneously hypertensive rats as a measure of outcome after neuroprotective intervention. METHODS: We used 2,3,5-triphenyltetrazolium chloride staining to discriminate infarcted tissue and calculate infarct volume 24 hours after temporary tandem common carotid/middle cerebral artery occlusion lasting 5 to 150 minutes. We used a graded bioassay described by logistic function and executed by computer program (ALLFIT) to evaluate changes in infarct volume after increasing durations of ischemia. The method allowed us to calculate the maximal infarct volume (Volmax) and the duration of ischemia before reperfusion producing half-maximal infarct size (T50). Hypothermia and the N-methyl-D-aspartate antagonist CNS-1102 begun after the onset of ischemia were tested for their ability to reduce Volmax and prolong T50 as analyzed by ALLFIT. RESULTS: Volmax was 180.6 +/- 22.4 mm3 and T50 was 45.9 +/- 5.8 minutes in control rats. Hypothermia (30 degrees C) applied during ischemia reduced Volmax by 66 mm3 and extended T50 by 50% (P < .05 for each comparison). CNS-1102, like hypothermia, extended T50 by 44% but did not have an effect on Volmax. CONCLUSIONS: Analysis of the changes of infarct size after increasing durations of ischemia indicates that although both were protective, the two treatments tested may exhibit different profiles of efficacy. This method of analyzing ischemia-induced damage may be very sensitive for studying the efficacy and possible clinical use of neuronal protective therapies for hyperacute stroke.

Acute Disease↗

PubMed1994

Calcium/calmodulin-dependent protein kinase II activity in focal ischemia with reperfusion in rats.

BACKGROUND AND PURPOSE: Evidence linking changes in calcium/calmodulin-dependent protein kinase II activity with ischemic cell death has been reported in animal models of global ischemia. The purpose of this study was to delineate the course of these changes after focal ischemia and to clarify the relation of changes in activity of calcium/calmodulin-dependent protein kinase II to the process of ischemic cell death. METHODS: Change in calcium/calmodulin-dependent protein kinase II activity was evaluated in a rat model of focal ischemia after 5 minutes, 30 minutes, and 1 hour of tandem middle cerebral artery and common carotid artery occlusion both with and without reperfusion. RESULTS: Calcium/calmodulin-dependent protein kinase II activity was significantly decreased after all three durations of ischemia followed by immediate decapitation compared with sham-operated animals, in both ischemic core and border-zone regions (P < .05 for all groups). Depression of activity occurred in a regionally graded fashion, with the most severe decrease in infarct core and progressively smaller decreases in samples moving out from the center, corresponding to the severity of histological injury later detected in infarct core and border-zone regions. There were only minor differences between the three durations of ischemia in the degree of enzyme depression noted in the more peripheral regions, indicating that the initial decrease in calcium/calmodulin-dependent protein kinase II activity is an early, sensitive marker for an ischemic insult. After reperfusion, the differences between the 5-minute group and longer periods of ischemia widened because of an increase toward baseline in the 5-minute group and a trend toward further decrease in the 30- and 60-minute groups. CONCLUSIONS: The extreme sensitivity of calcium/calmodulin-dependent protein kinase II to focal ischemia and the parallel temporal and regional changes in its activity to those of more delayed cell injury point to a potential role for this enzyme in the process of excitotoxic injury.

Amino Acid Sequence↗

PubMed1990

Baclofen does not protect against cerebral ischemia in rats.

Presynaptic release of glutamate into the extracellular compartment and activation of receptor-operated calcium channels may contribute to ischemic neuronal damage. We evaluated the effect of baclofen, a selective inhibitor of presynaptic glutamate release, on mortality, working memory, and light microscopic hippocampal and cortical damage in the four-vessel occlusion model of cerebral ischemia using 64 male Wistar rats. Baclofen (10 mg/kg i.p.) given 1 hour before and 30-60 minutes after 20 minutes of global ischemia did not lessen mortality, prevent ischemic cellular damage, or significantly improve working memory compared with no treatment. We conclude that preischemic and postischemic administration of baclofen does not protect neurons from ischemic injury.

Animals↗

PubMed1989

Functional outcomes and rehabilitation: an acute care field study.

The effectiveness of intervention including occupational therapy in combination with other rehabilitation services was investigated in 193 acute care patients with a variety of diagnostic conditions. The study was conducted in two phases. In both phases, patients who received occupational therapy in conjunction with other services were compared to patients who did not receive occupational therapy. In the first phase, patients (N = 77) were matched according to diagnostic category, age, sex, and severity of impairment. In both phases, outcome measures included length of hospital stay, Barthel Index change scores, and discharge destination. Results revealed statistically significant findings for the measure of discharge destination. Patients who received occupational therapy as part of their rehabilitation program were more likely to be discharged to home environments. This result occurred despite the fact that patients receiving occupational therapy were rated as more severely impaired than patients who did not receive occupational therapy as part of their rehabilitation program.

Aged↗

PubMed1987

Metastatic renal cell carcinoma simulating glomus jugulare tumor.

A 59-year-old man presented with jugular foramen syndrome caused by a mass with roentgenographic and histologic features highly suggestive of a glomus jugulare tumor. However, electron microscopic examination of the surgical specimen revealed features diagnostic of a previously unsuspected renal cell carcinoma. Because primary tumors of the glomus jugulare and metastatic renal cell carcinoma may present with the same clinical and roentgenographic findings and look similar histologically, careful electron microscopic examination of the tumor and urologic screening should be performed in suspected cases of glomus jugulare tumors.

Carcinoma, Renal Cell↗

PubMed1982

Familial cavernous angiomas: natural history and genetic study over a 5-year period.

In a kindred of 122 individuals we found 5 individuals with cerebral vascular malformation, 3 representing typical cavernous angiomas. The condition was inherited as an autosomal dominant trait with variable expressivity. Forty-three relatives were examined prospectively by cranial computed tomography (CCT) and lesions were found in 15; 7 were followed prospectively with CCT scans for 5 years. Angiography in 5 of these cases failed to demonstrate the lesion. In 3 patients with previously normal CCT scans a change in blood volume or membrane permeability allowed visualization of the lesion on contrast scans. In 2 individuals, both parents of affected children, a normal CCT scan was found. This emphasizes the limitations of CCT in detecting this disorder. Biochemical and red blood cell immunological genetic linkage studies were done in 36 persons. No linkage was found with any of the markers. The natural history of this disorder, characterized by marked clinical and radiographic variation in site of lesion, and the timing and severity of intracranial hemorrhage, make it a useful model for investigating contributing factors and consequences of intracranial hemorrhage in general. For at-risk and affected patients early and sequential CCTs are necessary. Familial cavernous angioma should be included in the differential diagnosis of all young persons presenting with cerebrovascular impairment, seizures, intracranial calcifications or hemorrhage.

Adolescent↗

PubMed1975

Clinical and pathological studies in a growth hormone-deficient dwarf.

Postmortem studies were performed in one of three closely related dwarfs. Repeated arginine infusions and insulin tolerance tests never resulted in plasma levels of human growth hormone (HGH) greater than 2.0 ng/ml in any of these three dwarfs. However, pituitary somatotropes in the autopsied subject were well granulated and were reduced in number to 20% of normal. In the absence of a second defect, there should have been substantially higher HGH levels in plasma after provocative stimulation. The clinical and pathological data appear most compatible with (a) deficiency of growth hormone releasing factor, or (b) insensitivity of somatotropes to this material. It seems reasonable to postulate that a major group of dwarfs clinically simulating HGH deficiency can be explained by one of these mechanisms rather than by an absolute deficiency of HGH.

Adult↗

PubMedDate not supplied

Fibrinogen, blood viscosity, and cerebral ischemia.

This study examines the effect of fibrinogen and consequent blood viscosity reduction on cerebral blood flow and cellular injury following severe cerebral ischemia for 30 minutes in 78 Wistar rats. In half of these rats 10 to 15 cc's of blood was removed and replaced with a mixture of 5% albumin and autologous red blood cells maintaining a constant hematocrit but resulting in a 30% decrease in fibrinogen and corresponding reduction in viscosity. Fibrinogen reduction in a slight increase in baseline CBF and the elimination of post-ischemic hyperemia at 24 hours. Both study and control animals showed a similar decrease in CBF at 30 minutes and 2 hours. There was no significant difference in the severity of ischemic cellular change between the fibrinogen reduction group and controls, although there was a significant inverse relationship between the amount of viscosity change and severity of cellular injury within the treatment group. Fibrinogen reduction alone cannot significantly ameliorate ischemic injury in this model. Viscosity reduction therapy should include reduction of hematocrit and alteration of red cell deformability.

Animals↗

PubMedDate not supplied

The effect of nicardipine on neuronal function following ischemia.

In cerebral ischemia, it has been proposed that calcium influx into neurons results in irreversible cellular injury during reperfusion. We administered nicardipine, a dihydropyridine calcium entry blocker, by continuous subcutaneous infusion to twenty five rats beginning before (PR) or following (PO) ischemia, and compared somatosensory evoked potentials (SEPs) to twenty eight ischemic control animals. Comparable ischemic cellular changes were seen in the hippocampi of all animals. SEP amplitude was higher in both the PR (p less than .005) and PO (p less than .0005) groups compared to controls. This effect was found in all three components (P1, N1, P2) of the evoked response. Plasma nicardipine levels of 6-10 ng/ml were associated with mild hypotension. We conclude that nicardipine improved neuronal function as measured by SEPs when administered before or after ischemia, most likely by interrupting the cytotoxic events occurring in cortical neurons during reperfusion.

Animals↗