Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020672 (hypothermia)
 17,327 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The authors tested the hypothesis that during epidural anesthesia: 1) shivering-like tremor is primarily normal thermoregulatory shivering; 2) hypothermia does not produce a subjective sensation of cold; and 3) injectate temperature does not influence tremor intensity. An epidural catheter was inserted into ten healthy, nonpregnant volunteers randomly assigned to skin-surface warming below the T10 dermatome (warmed group) or no extra warming (unwarmed group). Each volunteer was given two 30-ml epidural injections of 1% lidocaine (16.0 +/- 4.7 degrees C and 40.6 +/- 0.7 degrees C at the catheter tip), in random order separated by at least 3 h. Skin-temperature gradients (forearm-fingertip) and tympanic membrane and average skin temperatures were recorded; significant vasoconstriction was prospectively defined as a gradient greater than or equal to 4 degrees C. Integrated electromyographic (EMG) intensity was recorded from four upper-body muscles. Overall thermal comfort was evaluated using a visual analog scale. Tympanic membrane temperatures decreased significantly in the unwarmed group (n = 6). Tremor occurred following ten of 12 injections in unwarmed volunteers, but only following one of eight injections in the warmed group. Integrated EMG intensity did not differ significantly following epidural injection of warm and cold lidocaine: tremor started when tympanic membrane temperature decreased about 0.5 degrees C and continued until central temperature returned to within 0.5 degrees C of control. Tremor always was preceded by hypothermia and vasoconstriction in the arms. Thermal comfort increased in both groups after epidural injection, with maximal comfort occurring at the lowest tympanic temperatures.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Shivering during epidural anesthesia. 233 97

Systemic hypothermia has neuroprotective effects in experimental models of central nervous system ischemia caused by vascular occlusions. The present study addresses the question as to whether systemic hypothermia can influence the extravasation of plasma proteins following severe spinal cord compression trauma using immunohistochemistry to identify the plasma proteins albumin, fibrinogen and fibronectin. Fifteen rats were assigned to one of three groups and received either thoracic (T) laminectomy or severe spinal cord compression trauma of the T8-9 segment. One group comprised laminectomized animals without compression trauma submitted to a hypothermic procedure in which the core temperature was reduced from 38 degrees to 30 degrees C. The two trauma groups were either submitted to the same hypothermic procedure or kept normothermic during the corresponding time. All animals were killed 24 h following the surgical procedure. The normothermic and hypothermic trauma groups had indications of marked extravasation of albumin, fibrinogen and fibronectin at the site of the injury (T8-9). There was also pronounced extravasation in the cranial and caudal peri-injury zones (T7 and T10) of normothermic injured rats but, with few exceptions, not in the hypothermic ones with the same degree of compression. By measuring the cross-sectional area of the peri-injury zones we found in the hypothermic trauma group a significant reduction of the expansion compared with that present in normothermic injured rats. Our study thus indicates that hypothermia reduces the extravasation of the plasma proteins albumin, fibrinogen and fibronectin following spinal cord compression in the rat. Such a reduction may contribute to neuroprotective effects exerted by hypothermia.
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PMID:Systemic hypothermia following compression injury of rat spinal cord: reduction of plasma protein extravasation demonstrated by immunohistochemistry. 1041 96

The present study addresses the effects of moderate posttraumatic hypothermia (32 degrees C) on the temporal and regional profile of polymorphonuclear leukocyte (PMNL) accumulation after traumatic spinal cord injury (SCI). We hypothesized that posttraumatic hypothermia would reduce the degree of inflammation by reducing PMNL infiltration. Rats underwent moderate spinal cord injury at T10 using the NYU impactor device. In the first study, the temporal profile of myeloperoxidase (MPO) activity (a marker of neutrophil accumulation) under normothermic (37 degrees C) conditions was determined. The animals were allowed to survive for 3 or 24 h, or 3 or 7 days after SCI. Spinal cords were dissected into five segments rostral and caudal to the injury site. Additional animals were studied for the immunocytochemical visualization of MPO. In the second study, rats were sacrificed at 24 h after a monitoring period of normothermia (36.5 degrees C/3 h) or hypothermia (32.4 degrees C/3 h) with their controls. In the time course studies, MPO enzymatic activity was significantly increased at 3 and 24 h within the traumatized T10 segment compared to controls. MPO activity was also increased at 3 h within the rostral T8 and T9 segments and caudal T11 and T12 segments compared to controls. At 24 h after trauma, MPO activity remained elevated within both the rostral and caudal segments compared to control. By 3 days, the levels of MPO activity were reduced compared to the 24-h values but remained significantly different from control. Neutrophils that exhibited MPO immunoreactivity were seen at 6 and 24 h, with a higher number at 3 days. PMNLs were located within the white and gray matter of the lesion and both rostral and caudal to the injury site. Posttraumatic hypothermia reduced MPO activity at 24 h in the injured spinal cord segment, compared to normothermic values. The results of this study indicate that a potential mechanism by which hypothermia improves outcome following SCI is by attenuating posttraumatic inflammation.
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PMID:Posttraumatic hypothermia reduces polymorphonuclear leukocyte accumulation following spinal cord injury in rats. 1077 15

Systemic hypothermia has been shown to exert neuroprotective effects in experimental ischemic CNS models caused by vascular occlusions. The present study addresses the question as to whether systemic hypothermia has similar neuroprotective qualities following severe spinal cord compression trauma using microtubule-associated protein 2 (MAP2) immunohistochemistry combined with the avidin-biotin-peroxidase complex method as marker to identify neuronal and dendritic lesions. Fifteen rats were randomized into three equally sized groups. One group sustained thoracic laminectomy, the others severe spinal cord compression trauma of the T8-9 segment. The control group contained laminectomized animals submitted to a hypothermic procedure in which the esophageal temperature was reduced from 38 degrees C to 30 degrees C. The two trauma groups were either submitted to the same hypothermic procedure or kept normothermic during the corresponding time. All animals were sacrificed 24 h following the surgical procedure. The MAP2 immunostaining in the normothermic trauma group indicated marked reductions in MAP2 antigen in the cranial and caudal peri-injury zones (T7 and T10, respectively). This reduction was much less pronounced in the hypothermic trauma group. In fact, the MAP2 antigen was present in almost equally sized areas in both the hypothermic groups independent of previous laminectomy alone or the addition of trauma. Our study thus indicates that hypothermia has a neuroprotective effect on dendrites of rat spinal cords subjected to compression trauma.
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PMID:Systemic hypothermia following spinal cord compression injury in the rat: an immunohistochemical study on MAP 2 with special reference to dendrite changes. 1104 77

In this work, we are presenting a rat animal model for bladder hyperreflexia after suprasacral spinal cord transection. Our aim was to standardize an animal model that can be useful in studying this condition. After standardizing the animal model in a pilot study, 26 female Sprague-Dawley rats were subjected to spinal cord transection at the level of T10 vertebra. Four animals were subjected to cystometrogram (CMG) 24 hr after spinalization and six rats 3 weeks post-spinalization. These CMGs were compared to that of six normal controls. The detailed description of the model presented in this manuscript, is the final result after several modifications. All the animals consistently developed hyperreflexia after an initial period of spinal shock phase. Expressed volume of urine continued to decrease until it reached a plateau after peaking at 1-week post-spinalization. The attrition rate reached 27.3% after several improvements in the animal model and was mostly from self-inflicted injuries. Post-operative complications included hypothermia, decubitus ulcers, hematuria, urinary tract infection in addition to the unexplained death of two animals. In conclusion, we believe that this animal model closely resembles the clinical condition of hyperreflexia and follows similar course. The relative low cost of this animal model and the easy maintenance makes it a valuable tool to study such a condition.
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PMID:Urinary bladder hyperreflexia: a rat animal model. 1459 17

We developed a simple cooling method for spinal cord protection against ischemic injury during aortic surgery. The neuroprotective effects of our method were investigated using an animal study. Selective spinal hypothermia was produced by means of originally-designed cooling pads placed over the lower thoracic and lumbar vertebral column. Spinal cord ischemia was induced by cross-clamping the thoracic aorta for 60 min in beagle dogs. The neuroprotective effects were evaluated by a multi-modal study. The motor-evoked potentials of the spinal cord resulting from transcranial electric stimulation (MEPs) were recorded during both the ischemic and reperfusion periods. Hindlimb motor function was graded with the Tarlov score, and a histologic examination of the spinal cord injury was performed, at 24 hours after ischemia in animals undergoing hypothermia (hypothermia group: n = 7) or a sham (control group: n = 7). The spinal cord temperatures at the lower thoracic (T10) and lumbar (L3) levels decreased by -9.1 degrees C per hour and -8.1 degrees C per hour, respectively. The amplitude of the MEPs decreased during ischemia in both groups of animals, and significantly recovered during the early phase of aortic reperfusion in the hypothermia group. The Tarlov scores in the hypothermia and control groups were 3.3 +/- 1.0 and 1.1 +/- 1.5 (mean +/- SD, p = 0.015), respectively. Histopathologic study revealed that ischemic injury of the lumbar cord was reduced in the animals undergoing hypothermia. Trans-vertebral regional cooling reduced ischemic spinal cord injury in a canine study. The current method is potentially feasible for clinical use, especially in view of its technical simplicity and few procedure-related complications.
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PMID:Trans-vertebral regional cooling for spinal cord protection during thoracoabdominal aortic surgery: an experimental study. 1462 Oct 27