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Biomedical subjects

F Plum

Publications and source records attributed to F Plum.

At least 19 recordsLinked to original sources
PubMed1991

Clinical and pathophysiological effects of piretanide treatment in the nephrotic syndrome.

12 patients with the nephrotic syndrome (N.S.) and normal serum creatinine (less than 1.5 mg/dl) were investigated in a follow-up study over 10 days under diuretic treatment with piretanide (29 +/- 24 pg/ml). Clinical effects, parameters of renal clearance and hemodynamics, metabolic changes and the influence on vasoactive and volume dependent hormonal systems were studied. Piretanide markedly increased urine volume and electrolyte excretion (Vu +53%, UNa +24%, p less than 0.05, after 10 days treatment) but did not significantly alter glomerular filtration rate or renal blood flow. While baseline plasma renin activity was in the normal range and regularly stimulated (2.55 ng/ml x h to 7.7 ng/ml x h) plasma ANP values were elevated (152 +/- 107 pg/ml) at the start of the study and did not significantly change under piretanide treatment. This may be an indicator of sodium retention and a high plasma volume in the primary form of the nephrotic syndrome. Thereby piretanide did not significantly alter the intravascular space.

Adolescent↗
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↗