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Biomedical subjects

F Plum

Publications and source records attributed to F Plum.

At least 91 records · Page 5Linked to original sources
PubMed1976

Metabolic anatomy of focal motor seizures.

Contralateral focal seizures occurred in rats following the intracortical injection of penicillin into the anterior motor cortex. The anatomic dimensions of the metabolic response in the focus as well as the spread of increased activity through the brain were studied by autoradiography following intravenous injection of carbon 14-labeled 2-deoxyglucose. Injections of 25 to 200 units of penicillin resulted in mild to severe contralateral motor jerks coincident with repetitive single spike discharges on the electroencephalogram. Concurrent autoradiography revealed a 1.3- to 2.5-fold increase in metabolic activity in discrete areas in ipsilateral cortex, basal ganglia, thalamus, and contralateral cerebellum. Intracortical injections of over 300 units resulted in the development of recurrent contralateral tonic-clonic seizures, with 20% becoming bilateral. In brains of these animals there was activation of bilateral medial frontal cortex, bilateral extrapyramidal system, thalamus, cerebellum, and limbic structures.

Amygdala↗
PubMed1975

Brief hypoxia-ischemia initially damages cerebral neurons.

Rats were studied during cerebral hypoxic ischemia to determine whether neurons or blood vessels suffered the first damage. Ten or more minutes of unilateral carotid artery occlusion combined with systemic hypoxemia (PaO-2, 21 mm Hg) produced neuronal but not vascular damage in the ipsilateral cerebral hemispheres of 18 of 29 rats (62%); two and five minute stresses caused no visible neuronal abnormalities. The longer exposures produced more widespread damage, and neuronal loss and gliomesodermal reaction were evident after prolonged survival. Early neuronal changes correlated with abnormalities of motor behavior (P less than .005). Despite neuronal damage that was sometimes extensive, vascular no-reflow developed in only one of 24 animals after 20 and 30 minutes of hypoxia-ischemia. Production of neuronal and neurological abnormalities in the absence of hypotension or vascular no-reflow indicates that hypoxia-ischemia initially damaged cerebral neurons.

Anesthesia, Inhalation↗
PubMed1975

Can one predict outcome of medical coma?

The combined evaluation of the motor response to stimulation and the oculovestibular (OV) reflex gives useful indicants to the outcome of medical coma. We examined 48 patients during the first 12 h and at 24 h after the onset of medical coma. We excluded patients who had ingested drugs or who had hypothermia. Motor responses to a noxious stimulus were scored on a 6 'best' and 1 'worst' scale, and the presence or absence of oculovestibular responses to icewater irrigations was recorded. Subjects were divided by outcome at three months into three groups: death or persistent vegetative state, severe disability, and moderate disability or good recovery. On the basis of the present series it was often possible to distinguish among the outcomes at or before 24 h. The patient's age and the presence or absence of pupillary responses, spontaneous eye movements and oculocephalic responses were not predictive of outcome, nor were the respiratory pattern, blood gases, blood pressure, heart rate and temperature. A minimal motor score and an absence of oculovestibular responses at 12 h always were assoicated with death. With higher motor scores, the absence of oculovestibular responses at either 12 or 24 h implied an outcome no better than severe disability. The results of the present study imply that early bedside assessments can yield accurate predictive information in medical coma.

Cerebrovascular Disorders↗
PubMed1975

Ischaemic brain damage in the gerbil in the absence of 'no-reflow'.

Approximately 40% of gerbils subjected to one hour of unilateral carotid artery occlusion displayed neurological abnormalities during that time. Most such animals were subsequently found to have ischaemic neuronal alterations within the territory of the ipsilateral middle cerebral artery. In contrast, impaired reperfusion ('no-reflow') rarely occurred and cannot therefore be implicated in the pathogenesis of ischaemic brain damage.

Animals↗
PubMed1975

Whole-brain blood flow and oxygen metabolism in the rat during nitrous oxide anesthesia.

The Kety-Schmidt washout technique has been modified to measure whole-brain blood flow and metabolism in the rat. During nitrous oxide anesthesia, 14 rats exhaled (133)Xe, and continuous and simultaneous arterial and cerebral venous samples were drawn from a femoral artery and the transverse sinus of the brain. Extracerebral contamination of the venous sample was minimal, and equilibration of (133)Xe in brain tissue and blood was obtained after 10-24 min of inhalation. Cerebral blood flow was calculated from the total activity of the mechanically integrated arterial and venous samples according to the principle of Scheinberg and Stead. At a mean Paco2 of 40 mmHg, CBF averaged 98 +/- 6 (SEM) ml/100 g-min and CMRO2 averaged 5.4 +/- 0.7 (SEM) ml/100 g-min. CBF changed 2.4% with each millimeter Hg change of Paco2 while CMRO2 changed only insignificantly. The values obtained for CBF are higher than reported for man and large laboratory animals bur reflect the proportionately greater amount of gray matter in the rat brain.

Anesthesia, Inhalation↗
PubMed1974

Alpha-ketoglutaramate: increased concentrations in the cerebrospinal fluid of patients in hepatic coma.

alpha-Ketoglutaramate, a deaminated metabolite of glutamine not previously identified in biological tissues, was measured in the cerebrospinal fluid of human subjects and found to be increased three- to tenfold in patients with hepatic coma. When perfused into the cerebral lateral ventricles of rats, alpha-ketoglutaramate (10 mM) depressed the animals' nocturnal locomotor activity, and at higher doses induced circling behavior and myoclonus. The concentration of alpha-ketoglutaramate in cerebrospinal fluid appears to be a reliable diagnostic indicator of hepatic coma, and its accumulation may contribute to the pathogenesis of this disease.

Amides↗