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Query: UMLS:C0020672 (hypothermia)
 17,327 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The data show that the enucleated eye of the cat can be maintained in apparently physiologically functioning condition by appropriate arterial perfusion. Under appropriate conditions, photically evoked electrical mass responses can be recorded from various parts of the isolated, perfused eye for 8 to 10 hours. ERGs as well as responses from axonal bundles of the optic nerve exhibit shapes, amplitudes and time courses comparable to their counterparts in vivo. Homeostasis of the perfusion ensures the stability of these light-evoked electrical responses. Transient changes in biophysical parameters of the perfusate rapidly induce marked, although reversible, changes in the amplitudes of b-waves of the ERGs. Increases or decreases in the flow rate of the perfusate induce parallel increases or decreases in the amplitudes of the b-waves as well as of the optic nerve responses. Similar alterations in the oxygen concentration of the perfusate induce similar and proportional changes in the amplitudes of the b-waves. It is concluded, that low flow rates of hemoglobin-free perfusate induce hypoxia; consequently, acceleration of the flow can compensate for hypoxia in a certain range. Previous studies on the effects of and recovery after transient hypoxia in mammalian retina are in concordance with the present data. Progressive decrease of temperature induces gradual and reversible reductions in the amplitudes of the b-waves and increases their latencies and peak-times. It is suggested, that initial hypothermia, which occurs during the period of cannulation, reduces the deliterious effects of the coincident unavoidable hypoxia on retinal neuronal elements. Since light-evoked electrical responses can be maintained for many hours in these preparations and since movements of cardiovascular and respiratory origin, invariably present to varying extent in the in vivo experiments, are eliminated, this preparation is suitable for intracellular recordings from neuronal elements of the retina. Potentials were recorded from cells in various layers of the retina of the cat; intracellular recordings from horizontal cells (S-potentials) are described in detail. Spectral analysis of S-potentials allowed to distinguish between three types according to their inputs: a mixed, rod-cone type, which was most frequently encountered, a pure cone- and a pure rod-type. Light- and electronmicroscopic investigation of the retina after perfusion revealed that (1) the extent of cellular damage depends on the flow rate of the perfusate; (2) little cellular damage is observed if medium flow rates, which maintain physiologic responsiveness of the isolated eye to light, were applied for two hours; (3) high flow rates applied for two hours, or medium flow rates applied for 7 hours appear to induce cystic changes in the pigment epithelium, but only minor changes in the cells of the inner nuclear layer.
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PMID:The function of the retina in the perfused eye. 110 95

In a five year period, 39 children (29 boys, 10 girls) aged 2 months to 13 years (mean 7.8 years) were studied who had suffered a major head injury (29 road traffic accidents, six falls, and four non-accidental injury). The injury had been assessed clinically and by cranial computed tomography or cranial ultrasound (in a single baby of 2 months). Initial Glasgow coma scores for all subjects ranged from 3-11 (mean 5.5), intact survivors 5-11 (7.4), minor handicap 4-11 (6.1), major handicap 3-6 (4.3), fatalities 3-6 (4.1). All were treated with sedation, paralysis, hyperventilation (arterial carbon dioxide tension 3.0-3.5 kPa), intracranial pressure monitoring and moderate body surface hypothermia to 32 degrees C. Nine children died and 30 survived (nine intact, 13 minor disability, and eight major disability). The worst cerebral perfusion pressure was over 40 mm Hg in all but one survivor, and less than 40 mm Hg in seven of nine fatalities. Severe hypocapnia both in the first 24 hours and overall was correlated with poor outcomes (dead or major disability), as were bilateral contusions or diffuse axonal injury.
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PMID:Management and outcome of severe head injuries in the Trent region 1985-90. 833 80

Fetal rat neocortex grafted into lesion cavities made in the newborn rat neocortex can exchange multiple axonal connections with the host brain. Most previous studies demonstrating efferent transplant-to-host brain connections have used fluorescent retrograde tracers injected into the host brain (Castro et al. 1985, 1987; Floeter and Jones 1984; O'Leary and Stanfield 1989). Other studies have used anterograde axonal tracing with either tritium-labelled amino acids impregnating the transplant and its efferents (Floeter and Jones 1985) or horseradish peroxidase injected into the transplants (Chang et al. 1984, 1986). In the present study we used the anterograde axonal tracer Phaseolus vulgaris-leucoagglutinin (PHA-L) to examine in detail the course and termination of the efferent neocortical graft fibers. Twenty-six newborn rats had the right frontal cortex forepaw area removed by vacuum aspiration, while anesthetized by hypothermia. A piece of fetal frontal cortex 14-16 embryonic days old (E14-16) was immediately thereafter placed in the lesion, and the recipient rats allowed to survive for 5-7 months. At this time the rats were reoperated under sodium pentobarbital (Nembutal) anesthesia and the transplants iontophoretically injected with PHA-L. Two weeks later the animals were again anesthetized, perfused, and processed for PHA-L immunocytochemistry and routine histology. Analysis of acetylcholinesterase- (AChE) and Nissl-stained sections showed graft survival in 19 of the 26 animals used in this study. When these 19 brains were processed for PHA-L immunocytochemistry, 5 of them were found with certainty to have the PHA-L injection confined to the transplant. Based on these cases PHA-L-reactive fibers arising from labelled transplant neurons were traced into the ipsilateral host neocortex adjacent to the transplant and found to project through the subcortical white matter to the ipsilateral parietal neocortical area 1, and claustrum. Callosal fibers were traced to the contralateral frontal neocortical forelimb and parietal areas. Transplant fibers were also observed to descend through the caudate putamen in the dispersed fiber bundles of the internal capsule to distribute as terminal branches and varicose fibers within the mesencephalic periaqueductal gray, red nucleus, deep mesencephalic nucleus, and intermediate gray of the superior colliculus, as well as in the pontine gray. Similar fibers and terminations were present in the caudate putamen, the reticular, ventrobasal, centrolateral, posterior, and parafascicular thalamic nuclei.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Projections from fetal neocortical transplants placed in the frontal neocortex of newborn rats. A Phaseolus vulgaris-leucoagglutinin tracing study. 149 66

Somatosensory evoked potentials (SEPs) following median nerve stimulation were recorded over Erb's point (N10), neck (N13) and scalp (N20) of 17 neurologically normal patients during hypothermic cardiopulmonary bypass. Anesthesia was induced with fentanyl and 100% oxygen, and supplemented with isoflurane as necessary. All 3 SEPs were recorded at esophageal temperatures (Te) of down to 19.5 degrees C. The central conduction time (CCT, defined as N20-N13 interpeak interval) increased exponentially with decreasing temperature (CCTTe = 1.066(37)-Te X CCT37; r = -0.96). The spinal conduction time (SCT, defined as N13-N10 interpeak interval) also increased exponentially but less steeply than the CCT (SCTTe = 1.047(37)-Te X SCT37; r = -0.89), and the N10 peak latency increased exponentially and least steeply (N10Te = 1.033(37)-Te. N10(37); r = -0.87). Anesthetic doses of fentanyl (75 micrograms/kg) did not affect the SEPs. Isoflurane (inspired concentration, 0.25-2.0%) produced dose-dependent increases in CCT of up to 13% and decreased N20 amplitude. All patients had normal CTs after rewarming and none suffered postoperative neurological deficits. Differences in slopes of the latency-temperature functions indicate that cooling produces more conduction slowing in central than in peripheral segments of the pathway and can be accounted for by estimates of the effects of cooling on synaptic delay and axonal conduction between wrist and cortex. The consistency of SEPs between patients both during stable hypothermia and when temperature was changing suggests their potential as a sensitive monitor of cerebral status during hypothermic cardiopulmonary bypass.
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PMID:Central and spinal somatosensory conduction times during hypothermic cardiopulmonary bypass and some observations on the effects of fentanyl and isoflurane anesthesia. 241 46

This study measured the velocity of fast orthograde axonal transport of incorporated 3H-proline in motoneurones of the sciatic nerve in control rats and in rats with streptozotocin-induced diabetes of 3 weeks duration. Sciatic nerve and abdominal cavity temperatures were monitored throughout the period of measurement of transport velocity, and the rats were warmed to minimise hypothermia at both sites. There was marked abdominal and sciatic nerve hypothermia immediately after operation, and this effect was more intense in diabetic rats than in control rats. In steady state, abdominal cavity temperature (mean +/- SEM) was 38.1 +/- 0.1 degree C in both control and diabetic rats, and the sciatic nerve temperatures were 37.8 +/- 0.1 degree C in controls and 37.1 +/- 0.3 degrees C in diabetic rats. The difference was not statistically significant. The velocities of orthograde axonal transport for the fastest molecules containing 3H-proline were 14.0 +/- 0.9 (SEM)mm/h for controls and 13.9 +/- 1.1 (SEM)mm/h for diabetic rats. Thus, no velocity difference was observed. The findings are discussed in relation to measurements of fast orthograde transport velocity in experimental diabetes in other studies. It is suggested that, where velocity deficits have been seen in diabetic rats, nerve hypothermia should be considered as a contributory factor.
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PMID:Fast orthograde axonal transport in sciatic motoneurones and nerve temperature in streptozotocin-diabetic rats. 241 4

Pattern-reversal-evoked potentials (PREPs), flash-evoked potentials (FEPs), rapid axonal transport in the optic system and body temperature were measured in hooded rats, treated with either saline or the formamidine insecticide/acaricide, chlordimeform (CDM). Rats receiving chlordimeform had low body temperatures when housed at standard laboratory room temperature, 22 degrees C, but not at 30 degrees C. Peak latencies of flash-evoked potentials were prolonged by chlordimeform at 22 degrees C, but not at 30 degrees C. The rate of axonal transport was slowed in chlordimeform-treated hypothermic rats, but not in chlordimeform-treated warmed rats. These findings suggest that the flash-evoked potential and axonal transport changes produced by chlordimeform were an indirect consequence of hypothermia. In contrast, chlordimeform increased pattern-reversal evoked potential peak latencies and peak-to-peak amplitudes independent of body temperature. These findings confirm and extend previous reports of chlordimeform-induced hypothermia, emphasize the importance of changes in body temperature as a possible confounding factor in studies of neuroactive agents and demonstrate that chlordimeform has both body-temperature-dependent and independent actions in the visual system in the rat.
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PMID:Body temperature-dependent and independent actions of chlordimeform on visual evoked potentials and axonal transport in optic system of rat. 242 66

This study measured the velocity of the fast anterograde axonal transport of [3H]-proline-labelled proteins in sciatic motoneurones of rats with streptozotocin diabetes of 12 weeks duration and in age matched controls. Four groups of diabetic animals were studied. One of these groups remained untreated whilst 2 diabetic groups received a long-acting insulin twice weekly to limit body wasting, but to permit regular hyperglycaemia. One insulin-treated group and one other diabetic group received an aldose reductase inhibitor, "Statil" (ICI 128436) by dietary admixture. Neither diabetes alone nor any of the treatment regimes produced any significant alteration of axonal transport velocity. Sciatic nerve temperature was measured concomitantly. A slight nerve hypothermia was seen in the untreated diabetic rats, but not in either insulin-treated group. It is concluded that 2 aspects of diabetes mellitus, namely persistent hyperglycaemia and polyol pathway activity in nervous tissue are without effect on the velocity of fast orthograde axonal transport of proteins.
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PMID:Fast anterograde axonal transport in wasted and non-wasted diabetic rats; effects of aldose reductase inhibition. 243 44

Auditory nerve brain-stem (ABR) and somatosensory evoked responses (SER) were recorded in cats as body temperature was uniformly lowered from 37 to 27 degrees C. Analysis of the results showed that the alterations in the evoked responses were due to disturbances induced both in axonal propagation and synaptic transmission by the hypothermia. By studying the first wave of the SER, which is solely an axonal event, and by assuming reasonable values for the total synaptic delay and axonal propagation times along the ABR pathway, it was concluded that this lesion model induced an effect on synaptic transmission 1.3-1.7 times greater than that on axonal propagation. There was a strong inverse correlation between wave latency and body temperature, with slightly steeper slopes for the longer latency waves. Wave amplitudes were not correlated with temperature. Furthermore, the wave latencies and amplitudes were generally not dependent on stimulus rate.
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PMID:Effects of hypothermia on auditory brain-stem and somatosensory evoked responses. A model of a synaptic and axonal lesion. 246 49

Severe hypothermia and an ascending impairment of shivering are previously undescribed clinical signs in hyperacute experimental allergic encephalomyelitis (EAE) in the Lewis rat. These occurred in hyperacute EAE induced by inoculation with guinea pig spinal cord homogenate and heat-killed Bordetella pertussis. Hypothermia was first detected on day 6-7 post-inoculation, within 12-24 h of the onset of neurological signs, and became more severe as the disease progressed. Rectal temperatures less than or equal to 30 degrees C were common at ambient temperatures of 19-22 degrees C. Shivering was assessed by palpation and by cold tremor electromyography. Shivering was absent in the tail by day 6-7 post-inoculation. The impairment then progressed to affect the hindlimbs, thorax and occasionally the forelimbs. Shivering was absent in hindlimbs with only mild or moderate weakness. Histological studies revealed perivascular inflammation with polymorphonuclear and mononuclear cells, oedema, fibrin deposition, haemorrhage, primary demyelination and axonal degeneration in the spinal cord, dorsal root ganglia and spinal roots. The brainstem was also involved but the cerebral hemispheres, including the hypothalamus, were spared. The close relationship between the severity of hypothermia and the extent of shivering impairment indicates that reduced shivering is an important cause of hypothermia in hyperacute EAE. It is concluded that this impairment of shivering is due not to hypothalamic damage but to lesions elsewhere in the central and peripheral nervous systems.
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PMID:Hypothermia due to an ascending impairment of shivering in hyperacute experimental allergic encephalomyelitis in the Lewis rat. 261 69

The effect of hypoglycaemia (blood glucose 1 mmol/l) on the axonal transport of acetylcholinesterase activity and noradrenaline was examined in non-diabetic rats. Rats were made hypoglycaemic over a 6-h period during which acetylcholinesterase and noradrenaline accumulated proximal to a tight ligature applied to the left sciatic nerve. The hypoglycaemic rats were either kept at room temperature, when they became profoundly hypothermic, or kept in a 31 degrees C incubator to maintain body temperature as close to normal as possible. Hypoglycaemia without temperature control caused marked reductions in the accumulation of acetylcholinesterase activity and of noradrenaline proximal to the ligature. These accumulation deficits were obviated by body heating. The findings indicate that hypoglycaemia impairs fast orthograde axonal transport, but that this effect is a consequence of hypothermia rather than glucopenia.
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PMID:Impaired orthograde axonal transport in acute hypoglycaemia, an effect mediated via hypothermia. 620 28


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