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Biomedical subjects

H M Shapiro

Publications and source records attributed to H M Shapiro.

At least 127 records · Page 7Linked to original sources
PubMed1979

High-dose barbiturate therapy in humans: a clinical review of 60 patients.

Over the past three years, high-dose barbiturate therapy has been used in the treatment of 60 patients with head injury (N = 45), encephalitis (N = 8), acute focal cerebral ischemia (stroke, N = 4), and global anoxia secondary to drowning (N = 3). High-dose barbiturates appear to be useful adjuncts in the control of intracranial hypertension refractory to other methods of therapy. Administration of barbiturates to patients with this problem will often reduce the requirement for osmotic agents, thereby facilitating medical management by avoiding hyperosmolality and fluid and electrolyte depletion. In a carefully controlled intensive care setting the risk of barbiturate therapy is low, though the costs and demands on personnel are great. Survival appeared to be improved in aptients with ,head injury and encephalitis. Although the ultimate outcome was not altered in patients with stroke or near-drowning, intracranial hypertension did not occur until barbiturate therapy was withdrawn. This experience provides an ethical basis to justify further randomized studies for determining whether or not barbiturates materially improve the neurological outcome following cerebral ischemic and traumatic insults.

Adolescent↗
PubMed1979

Local cerebral metabolism during enflurane anesthesia: identification of epileptogenic foci.

Electrocorticographic (ECoG) and depth recordings have previously demonstrated the epileptogenic nature of surgical concentrations of the volatile anesthetic enflurane. We contrasted ECoG activity with local cerebral glucose uptake [( 14C]2-deoxyglucose autoradiography) in 23 brain structures in order to identify the epileptogenic foci. Autoradiograms were obtained from sectioned rat brain following a 30 min period of steady-state anesthesia at 1, 1.5, or 2 MAC (minimum alveolar concentration) enflurane. Pseudo-epileptiform ECoGs were obtained at 1 MAC where bursts of slow waves and sharp waves were evoked by peripheral sensory stimulation. At 1.5 MAC, the ECoG displayed frank, spontaneous epileptiform activity with large amplitude spike-wave complexes; repetitive auditory stimulation occasionally precipitated grand-mal seizures. At 2 MAC, spike complexes were less frequent and could not be repetitively driven. At 1 MAC enflurane, regional cerebral metabolism was generally depressed approximately 14% from the awake controls. However, metabolism in the dentate gyrus of the hippocampus and other subcortical structures in the limbic brain was increased. At 1.5 MAC this dichotomy in local cerebral metabolic rate was maximal; we observed increased metabolism in the hippocampus, habenula, habenulo-interpeduncular tract and interpeduncular nucleus and pineal. Metabolism in all other structures was significantly depressed (P less than 0.05) compared to awake values. At 2 MAC, metabolism was decreased in all structures. We conclude that the low seizure threshold hippocampus and related structures associated with the limbic system and its pathways are the epileptogenic foci for seizures induced with enflurane in the rat. At 1.5 MAC, epileptiform activity spreads throughout the visceral brain when seizure threshold is at a minimum.

Anesthesia, General↗
PubMed1979

Estimation of membrane potentials of individual lymphocytes by flow cytometry.

The membrane potentials of individual cells can be estimated by flow cytometric quantitation of the cells' uptake of the fluorescent lipophilic cationic dye 3,3'-dihexyloxacarbocyanine iodide. Human lymphocytes separated from peripheral blood on Hypaque-Ficoll gradients are uniformly depolarized by gramicidin and hyperpolarized by valinomycin. Concanavalin A and phytohemagglutinin depolarize only a fraction of the lymphocytes. The flow cytometric technique allows precise detection of heterogeneous membrane potential responses to stimuli such as lectins; it could also provide a basis for sorting cells that respond differently to a given stimulus.

Cations↗
PubMed1979

Detection and discrimination of individual viruses by flow cytometry.

A new flow cytometer with a very small observation volume has been developed to detect individual viruses with good resolution, and has been used to discriminate between two types of viral particles based on differences in their light scattering. Measurements of light scattering and fluorescence made with such an instrument can provide a basis for quantitative analysis and sorting of viruses and other particles in the micron and submicron size range.

Capsid↗
PubMed1979

A system for storage and retrieval of individual cells following flow cytometry.

A system has been developed to deposit cells in indexed locations on a gelatin-coated film following flow cytometry, allowing the measurements made of individual cells to be correlated with observed morphology or with subsequent microspectrophotometric measurements. Samples are deposited in a continuous track on the film by a deposition nib attached to the flow system below the observation point; laminar flow is preserved by adjusting the tape speed and the flow velocity. Locations of individual cells are indicated by etching the film with a spark triggered by the detection of a cell in the flow cytometer. After deposition, the film is dried by forced warm air. Cells on gelatin may be washed and restained with Papanicolaou and other stains with reasonable preservation of morphology. The system may be used for validation of automated cytodiagnostic procedures based on flow cytometry and for biomedical research.

Cytological Techniques↗
PubMed1979

Acute therapeutic modalities for experimental vasogenic edema.

Experimental vasogenic cerebral edema was created in rabbits with a cold-induced left occipital cortical lesions. Intracranial pressure (ICP), intracranial elastance (Em), water content, hemispheric brain tissue volume, electrolytes, electroencephalograms, behavior, and gross pathology were studied. Various therapeutic modalities were employed alone or in combination to reduce ICP acutely: acetazolamide, furosemide, mannitol, pentobarbital, lorazepam, and dexamethasone. All therapies except dexamethasone were effective in reducing ICP. Peak ICP reduction occurred at 27 +/- 9.8 (SD) minutes with mannitol and at 71.4 +/- 15.5 minutes with acetazolamide, with the remaining agents and combinations falling between these two extreme values. Em improved by 31.7 +/- 17.02% in all therapuetic trials except those employing acetazolamide and lorazepam. With therapy, there was a reduction in the water content of the hemispheres, but the difference from that in the untreated, lesioned animals was not statistically significant. In the lesioned left hemisphere, sodium content was increased by acetazolamide (p less than 0.005), furosemide (p less than 0.025), pentobarbital (p less than 0.05), and the combination of dexamethasone, pentobarbital, and mannitol (p less than 0.005). Significant reduction was noted in the lesioned group for the potassium content of the left hemisphere in the dexamethasone (p less than 0.05), pentobarbital (p less than 0.025), and combination groups containing these agents (p less than 0.005 to 0.025). (Neurosurgery, 5: 656--665, 1979).

Acetazolamide↗
PubMed1978

Local cerebral glucose uptake in awake and halothane-anesthetized primates.

Local glucose consumption within specific brain structures in awake and halothane-anesthetized primates was studied using a quantitative autoradiographic technique for glucose (14C-deoxyglucose). In both awake and anesthetized animals, significant heterogeneity (one-way analysis of variance) in uptake of glucose was found in the cortex, subcortical grey matter, and brainstem nuclei. No significant variability was found for any of the white matter areas sampled under either experimental condition. Halothane produced significant decreases in glucose metabolic rates in the occipital cortex, brainstem nuclei, cerebellar cortex, cerebellar white matter, and anterior commissure, compared with the awake state. The greatest decrease in cerebral metabolic rate was found in the occipital lobes of halothaneanesthetized animals. Results of this study suggest that neurophysiologic and behavioral changes that occur with anesthetic agents can, for the first time, be correlated with alterations in local cerebral glucose metabolism.

Anesthesia, Inhalation↗
PubMed1978

Cerebral hypometabolism obtained with deep pentobarbital anesthesia and hypothermia (30 C).

Cerebral metabolic and vascular effects of hypothermia (30 C) and deep pentobarbital anesthesia, separately and combined, were evaluated in 15 mongrel dogs. External cardiovascular support was not used, and mean arterial blood pressures remained greater than 60 torr. Normothermic deep pentobarbital anesthesia, characterized by an electroencephalographic (EEG) frequency of less than 1 Hz, was associated with 30% decreases in cerebral metabolic rates for oxygen (CMRO2) and glucose (CMRG) from lightly anesthetized control values. Hypothermia (30 C) alone caused similar decreases in CMRO2 and CMRG in the presence of an active EEG. The use of pentobarbital anesthesia and hypothermia combined achieved significantly greater (P less than 0.05) decreases in CMRO2 (70%) and CMRG (72%) from the control state. Cerebral vascular resistance (CVR) increased by 70% (P less than 0.05) during hypothermia and about 20% when pentobarbital was administered to normothermic dogs. In hypothermic animals the addition of pentobarbital had a minimal effect on CVR. No alteration in the oxygen-glucose or lactate-glucose index indicative of cerebral hypoxia occurred in any experimental group. This study indicates that barbiturates combined with hypothermia decrease cerebral metabolism to a greater extent than hypothermia or barbiturate alone. When cerebral hypometabolism is therapeutically necessary, barbiturates may be indicated as an adjunct to moderate hypothermia.

Anesthesia↗
PubMed1978

Intracranial pressure responses to PEEP in head-injured patients.

PEEP (positive end-expiratory pressure) was required in 12 head-injured patients in whom intracranial pressure (ICP) monitoring had been previously established. In six, ICP increased by 10 mm Hg or more as 4-8 cm H2O of PEEP were administered. In 10 patients the mean arterial pressure decreased during PEEP. Before PEEP, the mean cerebral perfusion pressure (CPP = BP-ICP) was above 50 mm Hg in all patients. The CPP was less than 50 mm Hg in six patients given PEEP. Neurological deterioration occurred in two patients during PEEP therapy. In head-injured patients, optimal titration of PEEP therapy should include ICP measurement and/or continuous evaluation of neurologic status.

Brain Injuries↗
PubMed1978

Mannitol dose requirements in brain-injured patients.

There is little information as to the optimal use of mannitol. To determine the dose-response relationship, the osmotic gradient required, and the time course of intracranial pressure (ICP) reduction produced by mannitol, eight patients with acute head injury were studied in whom ICP was monitored with a ventriculostomy and found to be elevated. Ventilation was controlled to a pCO2 of 25 +/- 3 mm Hg and all were paralyzed with Pavulon. None had received barbiturates. Before mannitol administration the intracranial volume-pressure response was determined. Mannitol was administered as a bolus of 0.25 gm/kg, 0.5 gm/kg, and in six patients, 1 gm/kg, separated by at least 8 hours. In all patients the ICP reduction with 0.25 gm/kg (41.3 +/- 10.2 mm Hg leads to 16.4 +/- 5.6, p less than 0.01) was equivalent to that achieved with the larger doses. Serum osmolality rises of 10 mOsm or more were associated with a reduction in ICP. Much smaller doses than those previously recommended were effective in reducing the ICP acutely, although at 5 hours there was a trend toward persistent reduction when the larger dose is used. This trend was small and indicates that smaller and more frequent doses are as effective in reducing the ICP while avoiding the risk of osmotic disequilibrium and severe dehydration.

Brain Injuries↗