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Biomedical subjects

F Plum

Publications and source records attributed to F Plum.

At least 37 records · Page 2Linked 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↗
PubMed1989

The effects of extracellular acidosis on neurons and glia in vitro.

Cerebral lactic acid, a product of ischemic anaerobic glycolysis, may directly contribute to ischemic brain damage in vivo. In this study we evaluated the effects of extracellular acid exposure on 7-day-old cultures of embryonic rat forebrain. Mixed neuronal and glial cultures were exposed to either lactic or hydrochloric acid to compare the toxicities of relatively permeable and impermeable acids. Neurons were relatively resistant to extra-cellular HCl acidosis, often surviving 10-min exposures to pH 3.8. In the same cultures, immunochemically defined astrocytes survived 10-min HCl exposures to a maximum acidity of pH 4.2. Similarly, axonal bundles defasciculated in HCl-titrated media below pH 4.4, although their constituent fibers often survived pH 3.8. Cell death occurred at higher pH in cultures subjected to lactic acidosis than in those exposed to HCl. Over half of forebrain neurons and glia subjected for 10 min to lactic acidification failed to survive exposure to pH 4.9. Longer 1-h lactic acid incubations resulted in cell death below pH 5.2. The potent cytotoxicity of lactic acid may be a direct result of the relatively rapid transfer of its neutral protonated form across cell membranes. This process would rapidly deplete intracellular buffer stores, resulting in unchecked cytosolic acidification. Neuronal and glial death from extracellular acidosis may therefore be a function of both the degree and the rapidity of intracellular acidification.

Acidosis↗
PubMed1988

MRI demonstrates descending transtentorial herniation.

Descending cerebral transtentorial herniation (DTH) is a serious and often fatal complication of intracranial mass lesions. The condition can be inferred from clinical neurologic signs, but has not been visualized during life. Using midsagittal magnetic resonance images (MRIs), we compared vertical brainstem position on 50 images from normals and 21 images from 15 clinically stable patients with large supratentorial tumors. The length of Twining's line (T), the perpendicular distance from T to the pontomesencephalic junction (T-PMJ), and from T to the apex of the midbrain aqueduct (T-A) were measured. We also measured lateral shifts of the diencephalon and midbrain on axial images. T-PMJ decreased from 2.04 +/- 0.06 mm in normals to 0.94 +/- 0.2 mm in patients with large cerebral tumors (p less than 0.0001). Similarly, T-A decreased from 6.35 +/- 0.13 mm in normals to 4.83 +/- 0.35 mm in patients (p = 0.001). Lateral diencephalic-midbrain shifts often accompanied DTH but to an unpredictable degree. Either lateral or downward brainstem shift could occur alone and did not necessarily produce specific neurologic signs or an altered state of consciousness. Anatomic DTH occurs in life, it can be quantified with MRI, and in slowly developing cerebral mass lesions the process can precede the appearance of neurologic signs and symptoms that indicate lower-diencephalic or midbrain dysfunction.

Brain Diseases↗
PubMed1987

Differences in cerebral blood flow and glucose utilization in vegetative versus locked-in patients.

Positron emission tomographic studies of regional cerebral metabolic rate for glucose (rCMRGlc) and cerebral blood flow were performed in 7 vegetative and 3 locked-in patients to determine objectively the level of brain function underlying these clinical states. Cortical gray rCMRGlc in the vegetative patients was 2.73 +/- 0.13 (mean +/- SEM) mg/100 gm/min, less than half the normal value of 6.82 +/- 0.23 (p less than 0.001). Cerebral blood flow exhibited similar but more variable reductions. By contrast, cortical rCMRGlc in the locked-in patients was 5.08 +/- 0.69, a 25% reduction (p less than 0.02) from normal. The massive reduction in vegetative rCMRGlc involved not only the cerebral cortex but also the basal nuclei and cerebellum. Such metabolic hypoactivity has precedent only in deep anesthesia and supports clinical evidence that cerebral cognitive function is lost in the vegetative state, leaving a body that can no longer think or experience pain.

Adolescent↗
PubMed1987

Hydrogen ions kill brain at concentrations reached in ischemia.

Elevation of brain glucose before the onset of nearly complete ischemia leads to increased lactic acid within brain. When excessive, such acidosis may be a necessary factor for converting selective neuronal loss to brain infarction from nearly complete ischemia. To examine the potential neurotoxicity of excessive lactic acid concentrations, we microinjected (0.5 microliter/min) 150 mM sodium lactate solutions (adjusted to 6.50-4.00 pH) for 20 min into parietal cortex of anesthetized rats. Interstitial pH (pH0) was monitored with hydrogen ion-selective microelectrodes. Animals were allowed to recover for 24 h before injection zones were examined with the light microscope. Injectants produced brain necrosis in a histological pattern resembling ischemic infarction only when pH0 was less than or equal to 5.30. Nonlethal injections showed only needle tract injuries. Abrupt deterioration of brain acid-base homeostatic mechanisms correlated with necrosis since pH0 returned to baseline more slowly after lethal tissue injections than after nonlethal ones. The slowed return of pH0 to baseline after the severely acidic injections may reflect altered function of plasma membrane antiport systems for pH regulation and loss of brain hydrogen ion buffers.

Acidosis↗
PubMed1987

Delayed hippocampal damage in humans following cardiorespiratory arrest.

Transient ischemia in animals produces delayed cell death in vulnerable hippocampal neurons. To see if this occurs in humans, we reexamined brain slides from all patients with anoxic-ischemic encephalopathy and a well-documented cardiorespiratory arrest. Eight patients dying 18 hours or less after cardiac arrest had minimal damage in hippocampus and moderate damage in cerebral cortex and putamen. Six patients living 24 hours or more had severe damage in all four regions. The increase in damage with time postarrest was significant only in the hippocampus. Delayed hippocampal injury now documented in humans provides a target for possible therapy that can be initiated after cardiopulmonary resuscitation.

Adult↗
PubMed1986

Carbonic acid buffer changes during complete brain ischemia.

Simultaneous measurements of tissue PCO2 (PtCO2), interstitial H+ concentration ([H+]o), and tissue lactate content were used to examine changes in interstitial HCO3- concentration ([HCO3-]o) during complete ischemia. In normoglycemic rats (blood glucose of 6-8 mM; neocortical ischemic-induced lactate content 8-12 mmol/kg) [H+]o increased from 7.22 +/- 0.02 to 6.79 +/- 0.02 pH (n = 3). By contrast, in hyperglycemic rats (blood glucose 18-75 mM; ischemic-induced lactate content 19-31 mmol/kg) [H+]o rose by a significantly larger amount to 6.19 +/- 0.02 pH (n = 7). Given that HCO3- is the predominant interstitial H+ buffer, changes in peak PtCO2 show why peak [H+]o were bimodally distributed compared with lactate content. Between 8 and 12 mmol/kg lactate, when peak PtCO2 rose from 99 to 186 Torr but [H+]o was constant at 6.79 pH, calculated [HCO3-]o increased from 11.9 to 21.9 mM. Then after transitional changes, peak PtCO2 and [H+]o remained constant at 389 +/- 9 Torr (n = 7) and 6.19 pH despite the fact that tissue lactate ranged from 19 to 31 mmol/kg lactate, respectively; [HCO3-]o must have remained constant at 12.3 +/- 0.7 mM (n = 7). Since ischemic brain continued to produce another 12 more mmol/kg of lactic acid above 19 mmol/kg lactate without further changes in PtCO2 or [H+]o, H+ and HCO3- must have been heterogeneously compartmented. The continued lactic acid production occurred in a compartment that occupied 36% of neocortical space. This compartment is likely to represent glial cells.

Animals↗
PubMed1986

Epidemiology of aging and its effects on the nervous system.

Aging emerges as a condition of major concern in relation to humane and economic aspects of health care for the balance of this century and future times to come. Persons in the United States older than age 65 years are expected to more than double in number between now and the year 2020. Already, one out of every five people 85 years and older in the United States is a patient in a nursing home, with neurologic diseases being responsible for the infirmity for well over half. Inherited and degenerative diseases of the nervous system are overwhelmingly a problem of aging. To solve the problem will demand the most vigorous effort and cooperation on the part of both public and private health resources.

Aging↗
PubMed1986

The pathophysiology of dementia.

Dementia is a symptom of a variety of specific structural brain diseases as well as several system degenerations. Alzheimer's disease presently is the commonest cause in the developed world, causing a cortical-subcortical degeneration of ascending cholinergic neurons and large pyramidal cells in the cerebral cortex. Clinically, the disease reflects predominantly deterioration of function in the association cortex. Pharmacologically and pathologically, abnormalities are more diffuse and extend into sensorimotor cortical areas as well.

Aged↗