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F Plum

Publications and source records attributed to F Plum.

At least 19 recordsLinked to original sources
PubMed1979

Selective chromatolysis of neurons in the gerbil brain: a possible consequence of "epileptic" activity produced by common carotid artery occlusion.

Unilateral (50 to 118 minutes) and bilateral (2 to 33 minutes) carotid artery occlusion in gerbils resulted in two distinct types of neuronal alteration: ischemic cell change (ICC) in selectively vulnerable brain regions, and selective chromatolysis (SC) confined to the deeper layers of the cortex, the Sommer sector of zone h-1, and the paramedian region (PM) of the hippocampus. In typical SC the nucleus was eccentric and the Nissl substance was lost in the central eosinophilic cytoplasm. In electron micrographs this area of cytoplasm showed disruption of smooth and rough endoplasmic reticulum with disaggregation of polyribosomes and accumulation of mitochrondria and various dense bodies. SC was identified at 2 to 3 hours and was still recognizable at five days. When bilateral carotid artery occlusion lasted 5 to 6 minutes, SC was seen in the hippocampal Sommer sector and cerebral cortex, while ICC was restricted to the endfolium (h3-5). Unlike ICC, the frequency of SC was not related to the duration of ischemia but probably to the epileptic seizures (overt and subclinical) initiated by ischemia in the gerbil. These changes must be considered when the gerbil is employed as a model of experimental stroke.

Animals↗
PubMed1979

The dynamics of ammonia metabolism in man. Effects of liver disease and hyperammonemia.

The cyclotron-produced radionuclide, 13N, was used to label ammonia and to study its metabolism in a group of 5 normal subjects and 17 patients with liver disease, including 5 with portacaval shunts and 11 with encephalopathy. Arterial ammonia levels were 52-264 micron. The rate of ammonia clearance from the vascular compartment (metabolism) was a linear function of its arterial concentration: mumol/min = 4.71 [NH3]a + 3.76, r = +0.85, P less than 0.005. Quantitative body scans showed that 7.4 +/- 0.3% of the isotope was metabolized by the brain. The brain ammonia utilization rate, calculated from brain and blood activities, was a function of the arterial ammonia concentration: mumol/min per whole brain = 0.375 [NH3]a - 3.6, r = +0.93, P less than 0.005. Assuming that cerebral blood flow and brain weights were normal, 47 +/- 3% of the ammonia was extracted from arterial blood during a single pass through the normal brains. Ammonia uptake was greatest in gray matter. The ammonia utilization reaction(s) appears to take place in a compartment, perhaps in astrocytes, that includes less than 20% of all brain ammonia. In the 11 nonencephalopathic subjects the [NH3]a was 100 +/- 8 micron and the brain ammonia utilization rate was 32 +/- 3 mumol/min per whole brain; in the 11 encephalopathic subjects these were respectively elevated to 149 +/- 18 micron (P less than 0.01), and 53 +/- 7 mumol/min per whole brain (P less than 0.01). In normal subjects, approximately equal to 50% of the arterial ammonia was metabolized by skeletal muscle. In patients with portal-systemic shunting, muscle may become the most important organ for ammonia detoxification. Muscle atrophy may thereby contribute to the development of hyperammonemic encephalopathy with an associated increase in the brain ammonia utilization rate.

Adolescent↗
PubMed1979

Outcome from severe neurological illness; should it influence medical decisions?

Most persons now accept the concept that when brain is dead, self is dead, and are willing to act accordingly. Much more difficult is to decide what to do when illness irreparably deprives the brain of cognitive functions. To facilitate less impassioned discussion of this question, 500 consecutive patients in coma from non-traumatic causes have been studied in the USA and Europe and the outcome has been compared against carefully selected early neurological signs. Medical coma was itself a dangerous sign, with only 15% of patients recovering independence within the first month. Within the first six hours, when most medical decisions are made about applying intensive care, neurological signs predicted with 95% confidence between the extremes of favourable and unfavourable outcomes in as many as a quarter of the patients. Only 5% of patients who failed to regain cognition by the end of one week regained any independence. Other more detailed guidelines were equally informative. If prognostic signs that confidently separate potentially favourable from unfavourable outcomes can be identified in severe neurological illness, perhaps society can more easily help medicine in reaching difficult ethical decisions.

Brain Diseases↗
PubMed1978

Cerebral blood flow and metabolism in chronically hyperammonemic rats: effect of an acute ammonia challenge.

The effects of chronic hyperammonemia on cerebral metabolism were studied in rats four and eight weeks after the construction of a portacaval shunt. Compared to sham-operated controls, shunted animals had increased arterial concentrations of ammonia and glutamine and decreased glutamate. Cerebral blood flow, measured by xenon 133 washout in animals lightly anesthetized with nitrous oxide, increased from a control of 91 +/- 5 (mean +/- SEM) to 139 +/- 20 ml per 100 gm tissue per minute after shunting for eight weeks; however, the cerebral metabolic rate for oxygen was not different from control four or eight weeks after the shunting procedure. Following intraperitoneal administration of a small ammonium acetate load (2.6 mmol/kg), eight-week portacaval animals consistently underwent a fall in cerebral blood flow and cerebral oxygen consumption and developed high-voltage slow waves in the electroencephalogram. Glutamine was produced by the brains of all groups of animals; the cerebral metabolic rate for glutamine was greater than control in eight-week portacaval rats, the only animals to show a net uptake of ammonia into brain. The findings suggest that increased cerebral sensitivity to ammonia, along with nonspecific effects of chronic portal-systemic shunting, may lead to uncoupling of cerebral blood flow and oxidative metabolism.

Ammonia↗
PubMed1977

Ultrastructural characteristics of the brain and blood-brain barrier in experimental seizures.

During experimental seizures, the blood-brain barrier (BBB) is broken; tracer substances such as I131-albumin, Evans blue and horseradish peroxidase (HRP) geographically locate the barrier breakdown primarily in the diencephalon. Using rats, we have induced seizures with electroshocks and demonstrated the breakdown of the BBB with Evans blue and HRP. We have shown that (1) the BBB breakdown is proportional to the number of electroconvulsant shocks (ES) given; (2) the mechanism of increased barrier permeability is primarily by micropinocytosis in the cerebral capillaries, arterioles, and, to a lesser extent, venules; and (3) the stimulus for micropinocytosis and hence BBB breakdown is associated with the abrupt rise in systemic blood pressure and cerebral vasodilatation that accompanies each ES. If the systolic hypertension is abolished via cervical cordotomy, there is little to no breakdown in the BBB.

Animals↗
PubMed1977

A prospective study of nontraumatic coma: methods and results in 310 patients.

Neurological signs and outcome are compared in the first 310 patients from a continuing prospective study of coma not caused by trauma or drugs. Sixteen percent of the patients achieved an independent existence within a month; severe disability or the vegetative state developed in 25% of patients comatose for six hours and in 79% of those still in coma after a week. The chance of regaining an independent existence was greater in patients who, by one day, obeyed commands or moved the limbs appropriately in response to noxious stimuli or who had attained any of the following: orienting eye movements, normal responses to oculocephalic or oculovestibular stimulation, or normal muscle tone. Conversely, the chance of regaining an independent existence fell in patients who, after one day, had either extensor responses of the limbs or failed to move them in response to noxious stimuli or who lacked eye opening, pupillary reactions, corneal responses, or any eye movement in response to oculovestibular or oculocephalic stimulation. Beyond these general guidelines, numbers of patients with particular signs are presently too small for confident prediction of outcome.

Adolescent↗
PubMed1977

George C. Cotzias.

Explore the source record for details and available documents.

History, 20th Century↗
PubMed1977

Effect of acute ammonia intoxication on cerebral metabolism in rats with portacaval shunts.

Rats were made chronically hyperammonemic by portal-systemic shunting and, 8 wk later, were subjected to acute ammonia intoxication by the intraperitoneal injection of 5.2 mmol/kg of ammonium acetate. In free-ranging animals, ammonia treatment induced a brief period of precoma (10-15 min) that progressed into deep, anesthetic coma lasting for several hours and was associated with a high mortality. In paralyzed, artificially ventilated animals that were lightly anesthetized with nitrous oxide, acute ammonia intoxication caused major disturbances of cerebral carbohydrate, amino acid, and energy metabolism that correlated in time with the change in functional state. At 10 min after injection (precoma), the concentrations of most glycolytic intermediates were increased, as was the lactate/pyruvate ratio. Citrate declined, despite a twofold rise in pyruvate, suggesting that the conversion of pyruvate to citrate had been impaired. Concentrations of phosphocreatine, and of the putative neurotransmitters, glutamate and aspartate, declined during precoma, but the concentrations of the adenine nucleotides in the cerebral hemispheres, cerebellum, and brain stem remained within normal limits. At 60 min after injection (coma), ATP declined in all regions of brain; the reduction in total high-energy phosphates was most notable in the brain stem. The findings indicate that cerebral dysfunction in chronic, relapsing ammonia intoxication is not due to primary energy failure. Rather, it is suggested that ammonia-induced depletion of glutamic and aspartic acids, and inhibition of the malate-asparate hydrogen shuttle are the dominant neurochemical lesions.

Adenosine Diphosphate↗