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Biomedical subjects

P Scheinberg

Publications and source records attributed to P Scheinberg.

At least 19 recordsLinked to original sources
PubMed1991

Transient ischemic attacks: an update.

This is a review of extant concepts of transient ischemic attacks (TIAs), their definitions, prognostic significance, pathogenesis, physiology, and management. The natural history of TIAs depends upon the risk factors of the population group studied, so that therapeutic trials should be controlled and randomized and not dependent upon published natural history data. A strong association between TIAs and coronary artery disease has now been established. It may be difficult to establish the cause or pathogenesis of TIAs in any given patient in view of the relatively poor correlation between the patient's symptoms and location of arterial plaques. Recent studies have suggested mechanisms aside from impaired perfusion or embolization from carotid plaques or vertebral basilar disease. There are no proven indications for carotid endarterectomy, a procedure which has been excessively used in the United States, but presently ongoing prospective, randomized, controlled multi-center studies will likely resolve this important issue. Neither is there scientific validation for the use of long-term anticoagulants, but data support the efficacy of ASA in reducing the incidence of stroke and myocardial infarction in patients with TIAs.

Anticoagulants↗
PubMed1991

The biologic basis for the treatment of acute stroke.

This is a review of therapeutic modalities that have been utilized in the treatment of stroke. Each is based upon data obtained from the study of the biologic events that occur during experimentally induced cerebral ischemia in animals. The type of information obtained from these studies could not have been obtained in any other manner. Despite the apparent effectiveness of some of these modalities in modifying stroke in animals, their application to humans with stroke has been disappointingly ineffectual. The delay between onset of stroke symptoms and initiation of treatment is usually several hours or more, which may be too late to rescue ischemic neurons. In order to be effective, treatment will have to be initiated as early as possible (preferably within 1 hour) to take advantage of the biologic window of opportunity. There is evidence that this can be accomplished by proper planning and training of personnel.

Acidosis, Lactic↗
PubMed1988

Dementia due to vascular disease--a multifactorial disorder.

This review was undertaken to evaluate critically the literature pertaining to vascular dementia with the objective of determining a more useful and scientifically supported definition of vascular dementia, its relation to other causes of dementia, and the biologic mechanisms involved in its causation.

Alzheimer Disease↗
PubMed1987

Substantia nigra lesion protects against ischemic damage in the striatum.

The role of striatal dopamine (DA) in mediating ischemic neuronal death was studied in the rat. Two weeks after unilateral substantia nigra lesion, rats were subjected to 20 min of forebrain ischemia by 4-vessel occlusion. Morphological changes and 45Ca uptake were evaluated after 3 days of survival. In the DA-depleted striatum, the degree of ischemic neuronal damage and 45Ca uptake were markedly attenuated compared to the contralateral side. This study is the first to demonstrate that the presence of DA is a prerequisite for the development of ischemic injury in the striatum and that DA depletion protects the striatum from ischemic damage.

Animals↗
PubMed1979

Survival of the ischemic brain: a progress report.

The number of patients with cerebral infarctions increases as the population ages, despite campaigns against hypertension, the greatest risk factor. Cerebral ischemia initiates events that are presumed to defer the stage of irreversible injury. These events cause an increase of perfusion around the central ischemic zone and trigger the Bohr effect, both of which preserve tissue viability. Almost simultaneously, mitochondrial function fails, resulting in insufficient energy for the enzyme systems to control Na and K ion equilibrium. At the same time, protein synthesis slows and cellular respiratory enzymes decrease their activity, initiating an irreversible state of tissue change. Tissue fatty acids increase as a result of dissolution of cell membrane lipoprotein structure. Barbiturates reduce the extent of experimental infarction. Resperine and aminophylline are also effective, but there are no corroborative clinical trials. That ischemic brain damage may be the result of toxic substances in the ischemic tissue represents a new concept.

Adenosine Triphosphate↗
PubMed1977

Effect of insulin hypoglycemia upon cerebral energy metabolism and EEG activity in the rat.

Anesthetized ventilated rats were subjected to insulin-induced hypoglycemia (50 units/kg i.v.) while EEG, ECG, mean arterial pressure, blood gases, arterial pH and rectal temperature were controlled. Animals were sacrificed by rapid transcalvarial freezing of the brain in situ. Glucose, pyruvate and lactate were measured in blood, CSF and cortical tissue, in which additionally glycogen, phosphocreatine, ATP, ADP, AMP, aketoglutarate (aKG), glutamate, oxalacetate, aspartate, ammonia and water content were estimated. ATP/ADP ratio, energy charge (ECh) energy reserve, NADH/NAD+ quotient and intracellular pH were calculated. ECh does not correlate with either dysfunction of carbohydrate depletion, but declines in a threshold fashion when tissue glucose has fallen by over 97% and glycogen by over 60%. The EEG correlates with the degree and duration of carbohydrate depletion in cortical tissue. An isoelectric EEG occurs pari passu with the fall of the ECh. Increase in ammonia and decrease in aKG and Glut are supportive evidence of intrinsic substrate. Lactate decrease during hypoglymecia is not reversed by super-imposed hyqoxia.

Animals↗
PubMed1977

Sequential cerebral biochemical and physiological events in controlled hypoxemia.

Effects of controlled hypoxemia on cerebral functional activity were studied in rats using cyclic adenosine monophosphate (cAMP) and aminergic neurotransmitters in the brain tissue as special references. Evidence is presented that: (1) mild hypoxemic stress (PaO2 60 to 40 torr) may activate cerebral glycolysis with no evidence of anaerobic metabolism but that further reduction of PaO2 impairs cellular respiration, as evidenced by accumulation of glycolytic products; (2) glycogenolysis in the brain tissue, leakage of potassium ions from the brain cell, increase in brain water, and suppression of neural functional activity occur concomitant with accumulation of cAMP and prior to the fall of adenosine triphosphate; (3) the diminution of cerebral high-energy phosphates during hypoxia is associated with and may be caused by hypoxemia-induced neuroglycopenia and occurs at PaO2 15 torr; (4) induced hypoxemia per se does not affect the level or aminergic neurotransmitter substances in brain tissue.

Adenosine Diphosphate↗
PubMed1975

Catecholamines in experimental brain ischemia.

Local cerebral ischemia was produced in rats by internal carotid artery injection of 35 mu carbon microspheres, and brain norepinephrine (NE), dopamine, and cyclic adenosine 3, 5-monophosphate (cAMP) were measured in embolized and intact hemispheres at intervals up to four hours. Sham-operated animals were controls. There was an instantaneous increase of cAMP. Norepinephrine was reduced within two minutes after embolization and remained low for four hours. Dopamine increased by five minutes after embolization and returned to normal after four hours. Results were qualitatively similar, but less, in the nonembolized hemisphere. Accumulation of cAMP is thought to be due to a direct effect of ischemic hypoxia and may be the initiating factor in increased glycolysis that occurs in ischemia. Decrease in NE may be secondary to its generalized release from presynaptic terminals throughout the brain and could be a factor in cortical vasocontriction that follows embolization. Dopamine changes are a reflection of alterations in energy metabolism.

Animals↗
PubMed1975

Effect of hyperventilation on dynamics of cerebral energy metabolism.

Hypocapnia of moderate and extreme degree (Paco2 21.1 and 13.5 torr, respectively)was induced by hyperventilation in rats subjected to the closed system of Lowry inorder to evaluate the effects on utilization rate of cerebral energy metabolites. The tissue levels of high-energy phosphates and calculated intracellular pH did not change, whereas glucose, pyruvate, and lactate increased significantly. The La/Pyratio and NADH/NAD-+ RATIO BOTH INCREASED IN PROPORTION TO THE DEGREE OF HYPOCAPNIA. Utilization rates of glucose, glycogen, and ATP were all significantly reduced by hypocapnia, whereas the utilization rate of phosphocreatine was increased. The rate oftotal high-energy phosphate use was also diminished in proportion to the degree of hypocapnia. The constant value of the energy charge (0.94 plus or minus 0.01) indicates that the energy production rate might also be reduced by hyperventilation; thus the intermediate metabolics and substrates increased. It is concluded that extreme hypocapnia reduces the rate of cerebral energy metabolism significantly.

Adenosine Triphosphate↗