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Biomedical subjects

R C Wiggins

Publications and source records attributed to R C Wiggins.

At least 127 records · Page 7Linked to original sources
PubMed1981

The diagnosis of primary hyperaldosteronism.

An aldosterone-suppression test based on a simple method of extracellular-fluid volume expansion over three days reliably discriminated between patients with aldosterone-producing adenomas, idiopathic adrenal hyperplasia, and essential benign hypertension. In patients with primary hyperaldosteronism adrenal-vein plasma aldosterone/cortisol concentration ratios successfully lateralised all 21 adenomas. In patients with an adenoma the contralateral adrenal gland was always suppressed, as indicated by a ratio which was less than that seen in the lower inferior vena cava, whereas in patients with hyperplasia the adrenal-vein aldosterone/cortisol concentration ratio from each adrenal was always greater than that seen in the lower inferior vena cava. Thus adrenal-vein sampling not only lateralises solitary adenomas but also discriminates between patients with an adenoma or hyperplasia. However, in view of the diagnostic reliability of the suppression test, it is suggested that adrenal-vein sampling is unnecessary in hyperaldosteronism due to adrenal hyperplasia.

Adenoma↗
PubMed1981

Halothane accumulation in rat brain and liver.

Halothane concentrations (microgram/g wet weight) was measured in rat brain and liver following exposure to various concentrations of halothane in air. Because of the difficulty of determining the amount of a volatile compound in brain, we analyzed tissue fixed by two different methods. The apparent concentration of halothane in brain was higher following direct decapitation into liquid nitrogen, than after decapitation, removal of fresh tissue, and then freezing. However, the relative effects of altering the inspired concentration were essentially the same in each case. Thus, absolute quantitative accuracy remains a point for discussion; however, we can reach several conclusions regarding the relative accumulation of halothane in brain tissue following various conditions of exposure. Resultant tissue concentrations of halothane were not linearly related to ambient concentrations. Above an inspired concentrations of 1.0%, an increase to 1.5% inspired concentration caused little further increase in the halothane concentration in brain, although the liver concentration increased in proportion to the dose increase. Below an inspired concentration of 0.5%, tissue concentrations were less expected, probably as a result of metabolic degradation occurring at a rate that becomes more noticeable at lower inspired concentrations. Body size was shown to be an important variable affecting the time required for each tissue to reach equilibrium at a given inspired concentration. These data indicate that tissue concentrations at low exposure levels may be less than proportional at dose and that concentrations in small laboratory animals may be expected to exceed values in humans under equivalent conditions of exposure.

Animals↗
PubMed1981

Cerebral energy metabolism during the onset and recovery from halothane anesthesia.

Halothane (1%) was administered to twenty-two gram female Swiss-Albino mice which were sacrificed at times of 15 seconds, 45 seconds, 79 seconds and 5 minutes. Additional animals were exposed for 5 minutes and sacrificed 10 minutes after removal from halothane (recovery). Selected energy metabolites were measured in 100-500 nanogram samples from the inferior colliculus and the ascending reticular activating system. Results from this study showed an increase in glucose levels at 79 seconds, when the animals first lost their righting response. The glucose increase was similar in the inferior colliculus and reticular formation. ATP and phosphocreatine were increased at 45 seconds, and during the sleep period in the ascending reticular activating system, and returned to normal during the recovery period. In the inferior colliculus. ATP was similarly increased from 45 seconds throughout the time course, whereas phosphocreatine was elevated at 79 seconds, and during recovery only. These data suggest a decrease in utilization of energy metabolites during halothane anesthesia, both in cells of the inferior colliculus and ascending reticular activating system.

Adenosine Triphosphate↗
PubMed1981

The relative numbers of oligodendroglia in different brain regions of normal and postnatally undernourished rats.

The relative numbers of oligodendroglia were compared in representative brain regions of 21 day old undernourished and control rats. As a result of postnatal undernutrition which produced half normal body weights and a 10-15 percent reduction in brain weight, the relative numbers of oligodendroglia were slightly increased in photomicrographs of corticospinal tract (a motor tract), medial lemniscus (a sensory tract), red nucleus (a motor nucleus) and somatosensory cortex. Relative numbers were reduced in the corpus callosum, and the thickness of the corpus callosum was significantly reduced. Cell sizes of oligodendroglia were essentially normal throughout the brain, although some reductions of 5 to 6 percent were observed. Areas of brain structures in cross section were essentially unchanged. We have previously hypothesized that nutritionally induced brain hypomyelination results from a reduction in the specific numbers of oligodendroglia and consequently a lasting reduction in the brain myelin concentration. The present results are inconsistent with this hypothesis, as both the density of oligodendroglia and sizes of brain regions are essentially normal. We know from prior work using the same model of nutritional deprivation that myelin synthesis is greatly reduced. Consequently an important depressant effect of undernourishment on oligodendroglia in the developing brain involves either the communication between axons and oligodendroglia leading to myelin induction or the synthetic capacity to make myelin.

Animals↗
PubMed1981

A morphometric comparison of central and peripheral hypomyelination induced by postnatal undernourishment of rats.

Developing Long-Evans rats were undernourished to produce a body-weight deficit of 39% at the age of weaning. Well-nourished litter mates were used as controls. Morphometric analyses were made of pyramidal tracts and posterior tibial nerves of each animal. In measuring pyramidal tract, we observed that axonal circumferences of myelinated fibers were smaller in the undernourished rats and that the number of myelin lamellae per axon appeared reduced by a small amount. The most striking observation in the undernourished rats compared to the controls was that the proportion of myelinated fibers was decreased by 40% at 20 days of age. Axon circumferences of nonmyelinated axons were not measured. Similar decreases were observed in myelinated axon circumference and myelin lamellae of posterior tibial nerves of undernourished rats. Because of sampling problems, we did not attempt to compare the proportion of myelinated and nonmyelinated fibers in posterior tibial nerves of undernourished and well-nourished rats. These morphometric data, particularly the reduction of myelinated fibers, are consistent with biochemical studies of brain hypomyelination in undernourished rats. The data indicate that the mechanism of hypomyelination in nutritionally deprived rats involves a failure of the "trigger" by which myelin-forming cells begin to sheath axons in myelin.

Animals↗
PubMed1981

Chronic halothane modification of eeg-like activity recorded from somatosensory cortex and deep nuclei in freely behaving rats.

Chronic exposure to the anesthetic agent halothane has been implicated in morphological and biochemical alterations of central nervous system tissue. In the present experiments, analysis of electroencephalographic (EEG) recordings has been used to examine effects on brain electrical activity. EEGs were recorded from freely behaving rats with stereotaxically implanted permanent semimicroelectrodes. Recordings were taken from the somatosensory cortex (SC), nucleus parafasciculus thalami (PF), mesencephalic central gray (CG), and the ventromedial hypothalamus (VMH) before (control) and after 28 and 56 days of chronic intermittent halothane administration (0.5%, 3 hr/day, 5 days/week). On each recording day (0, 28 and 56), EEGs were obtained prior to halothane exposure and following exposure to 0.25%, 0.5% and 1.5% halothane. In halothane-naive rats (day 0), the EEG dominant frequency (DF) showed a dose-response pattern consisting of an initial increase with 0.25% (significant only for the PF) followed by suppression at 0.5% and a marked significant decrease in all regions at 1.5%. On day 28, the pre-drug DF recorded from three of four regions showed a slowing trend. Additionally, with 1.5% halothane, only the SC DF was significantly decreased. Following 56 days of intermittent exposure, the pre-drug EEG frequencies were significantly decreased in all regions as compared to naive values. Subsequent administration of 0.25% halothane produced a significant increase in all regional DFs which was also obtained with 0.5% and with 1.5% for the CG and VMH. The high DF values from the PF, CG and VMH at 0.5% and from the CG and VMH at 1.5% represent statistically significant increases over naive 1.5% values. Chronic halothane exposure is thus shown to progressively alter EEG activity and the EEG pattern of dose-responsiveness in four brain regions.

Anesthetics, Inhalation↗
PubMed1980

Brain cyclic nucleotide and energy metabolite responses to subanesthetic and anesthetic concentrations of halothane.

Adult rats were exposed to 0.5, 1.0 and 1.5% halothane, delivered in air, for 1 h. Whole brain 3',5'-cyclic adenosine monophosphate (cAMP) of halothane-exposed rats showed only a slight increase relative to control values. 3',5'-Cyclic guanosine monophosphate (cGMP) was increased significantly in halothane-exposed rats, and the response was directly related to the halothane concentrations. Adenosine triphosphate (ATP) and phosphocreatine (PC) remained unchanged relative to control values. Correspondence of these values to apparent discrepancies in the literature is discussed.

Adenosine Triphosphate↗
PubMed1980

The effect of postnatal undernourishment on epileptiform kindling of dorsal hippocampus.

Rats were undernourished postnatally from birth through 20 days of age. They were subsequently tested for susceptibility to motor seizures kindled in hippocampus in adulthood. Compared to littermate control animals the postnatally undernourished rats were more susceptible to the kindling treatment. We conclude that early postnatal undernourishment has a permanent effect on susceptibility of the hippocampus to electrically-induced seizures.

Animals↗
PubMed1980

Pattern of myelin breakdown during sciatic nerve Wallerian degeneration: reversal of the order of assembly.

Myelin sheaths of rapidly growing rats were sequentially labeled with the 3H and 14C isotopes of leucine as precursors of protein synthesis. The two injections were separated by time intervals ranging from 2 to 12 d. Wallerian degeneration was initiated by sciatic nerve neurotomy at 2 or 10 d after the second injection of radioactivity. After 5 d of degeneration, myelin was purified and the ratio of isotopes was determined in the delipidated protein. Regardless of the order in which the two isotopes were administered, the relative recovery of radioactivity resultant from the second injection was greatly reduced in degenerating nerves compared with sham-operated controls. Radioactivity incorporated from the first injection was also reduced, but to a lesser extent. Consequently, the isotope ratio corresponding to the first/second injection was greater in degenerating nerves than in controls, and the ratio increased in proportion to the time interval separating the two injections. The magnitude of the effect of degeneration was only slightly greater when degeneration was initiated 2 d after the second injection than when initiated 10 d after the last injection. Consequently, myelin disintegration rather than diminished incorporation of radioactivity accounts for the losses of radioactivity. Furthermore, the pattern of myelin degeneration preferentially involves the last myelin to be formed.

Animals↗
PubMed1980

A halothane-related effect on rat brain myelination: a comparison of chronic prenatal or postnatal exposure.

Rats were exposed to 0.5% halothane in air for 8 h per day during the intervals (1) 5 days postconception to birth, (2) birth to 5 days postnatal age, or (3) birth to 10 days postnatal age. Controls were exposed to an equivalent flow of air. Prenatal exposure had no significant effect on body or brain weight and no subsequent effect on the relative synthesis of brain subcellular membranes. Five days of postnatal exposure caused a 10% reduction in body and brain weight and a 10% relative reduction in the synthesis of brain myelin. The effect persisted throughout the period rapid postnatal brain myelination. Ten days of postnatal exposure produced equivalent, more severe effects on body and brain weights and a more severe effect on myelin synthesis. Postnatal exposure had no apparent effect on the relative synthesis of non-myelin particulate proteins.

Animals↗
PubMed1980

Brain cyclic nucleotide responses to anesthesia with halothane delivered in air or purified oxygen.

Inhalation of either 0.5% or 1.0% halothane in air caused a slight decrease in the cAMP concentration in rat cerebral cortex and cerebellum. During recovery, concentrations returned to normal in 3 h, or less. In contrast, cGMP decreased sixfold in cerebellum, but increased twofold in cortex. Recovery time for cerebellum was several hours. When oxygen was used as the carrier gas for halothane delivery, cAMP in the cortex doubled, in striking contrast to the case with halothane in air. Oxygen alone had no apparent effect. The cGMP effect of halothane delivered in oxygen appeared the same as for halothane in air. Thus, the cAMP effects of brain halothane are related to the enrichment of oxygen.

Anesthesia, Inhalation↗