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

Spinal cord ischemia may accompany surgical procedures on the aorta or vertebral column. Regional spinal cord blood flow (SCBF) was measured at five vertebral levels in the spinal cords of pentobarbital-anesthetized rats based on the distribution of intravenously injected carbon-14-labeled butanol. In seven normal rats, mean SCBF (+/- standard error of the mean) ranged from 52.7 +/- 5.4 to 68.5 +/- 4.9 ml.min-1.100 gm-1 (depending on the level, being lowest at the thoracic levels) and mean arterial blood pressure (MABP) was 126 mm Hg. Corporal hypothermia (mean rectal temperature 28.1 degrees +/- 0.6 degrees C) was induced by cold exposure in seven other rats, and SCBF, measured immediately thereafter, was significantly elevated at all five levels by 52% to 69% compared to the normal group. However, MABP was elevated in the hypothermic group to 165 +/- 4 mm Hg (p less than 0.0001). Therefore, in seven additional hypothermic rats, MABP was maintained at the control level by withdrawal of arterial blood as necessary. In these animals, SCBF at all levels was still significantly elevated compared with the normal group and the values were nearly identical to those measured in the hypertensive hypothermic rats. It was concluded that hemodynamic autoregulation of SCBF is impaired in the presence of moderate systemic hypothermia in pentobarbital-anesthetized rats.
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PMID:The effect of hypothermia on regional spinal cord blood flow in rats. 270 18

Spinal cord injury occurring as the result of surgical repair of thoracic and thoracoabdominal aortic disease remains a devastating complication. The incidence of postoperative neurologic deficits varies from 4% to 38%. Factors associated with a greater risk for injury include the presence of dissection or extensive thoracoabdominal disease, and a prolonged cross-clamp time. Spinal cord ischemia initiates a deleterious cascade of biochemical events that ultimately result in an increased intracellular calcium concentration. Calcium-activated proteases, lipases, and nucleases mediate the processes that cause cell injury. The accumulation of oxygen-derived free radicals and the occurrence of hyperemia during reperfusion are also contributing causes of spinal cord injury. Increasing the spinal cord blood flow with shunts, oxygenated bypass circuits, cerebrospinal fluid drainage, the intrathecal administration of vasodilators, and the reattachment of intercostal arteries has been tried in an effort to increase spinal cord perfusion. Pharmacologically based measures to prevent spinal cord injury have been pursued, and these have consisted of hypothermia, anesthetic agents, calcium channel blockers, free radical scavengers, and immune system modulation. However, no single technique has proved to be consistently effective in preventing ischemia-induced spinal cord injury.
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PMID:Prevention of spinal cord injury after repair of the thoracic or thoracoabdominal aorta. 781 42

Spinal cord ischemia with resultant paraplegia or paraparesis remains an important clinical problem after operations on the thoracoabdominal aorta. Because hypothermia has a protective effect on ischemic neural tissue, we developed a baboon model of spinal cord ischemia to simulate the situation encountered clinically for resection of aneurysms of the thoracoabdominal aorta and to determine whether profound hypothermia produced by hypothermic cardiopulmonary bypass has a protective effect on spinal cord function. After cardiopulmonary bypass was established, the aorta was clamped distal to the left subclavian artery and proximal to the renal arteries for 60 minutes. Group I animals (n = 9) underwent aortic clamping at normothermia (37 degrees C), and group II animals (n = 9) were cooled to a rectal temperature of 15 degrees C before aortic clamping and underwent cardiopulmonary bypass at this temperature until the aorta was unclamped. Of the eight operative survivors in group I, six animals were paraplegic and two were paraparetic, whereas all six group II animals that survived the procedure were neurologically intact (p = 0.0002). The protective effect of hypothermia was associated with blunting of the hyperemic response of spinal cord blood flow (determined by the radioactive microsphere technique) in the lower thoracic and the lumbar segments of the spinal cord after unclamping of the aorta. Profound hypothermia produced by hypothermic cardiopulmonary bypass may be an effective method of protection of the spinal cord in patients undergoing repair of aneurysms of the thoracoabdominal aorta and may reduce the prevalence of ischemic injury to the spinal cord.
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PMID:Profound systemic hypothermia protects the spinal cord in a primate model of spinal cord ischemia. 824 34

Mild hypothermia to 32 degrees C protected the spinal cords of 5 rabbits subjected to 90 min of surgically created spinal cord ischemia. Spinal cord ischemia was produced in 10 New Zealand White rabbits by transection of four out of the five segmental arteries arising from the abdominal aorta below the renal arteries plus 90-min occlusion of the remaining segmental artery 24 hr later. Of these 10 rabbits, 5 served as controls. Recovery, or failure to recover, as assessed by examining the rabbits for permanent loss of sensory and motor function in the hind limbs, was compared in the two groups. The duration of the ischemia was sufficient to lead to a total or near total loss of sensory and motor function in all control rabbits. These results may have implications for the care of patients subjected to spinal cord ischemia.
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PMID:Mild hypothermia protects against irreversible damage during prolonged spinal cord ischemia. 853 81

Spinal cord ischemia during resection of thoracoabdominal aortic aneurysms (TAA) can result in lower limb neurological deficits. Spinal cord monitoring can only improve outcome if ischemia is detected before irreversible damage has occurred and protective measures are readily available. Monitorin( spinal cord function with motor evoked potentials (MEPs) is a relatively new technique. With MEP. recorded from the muscle (myogenic MEPs), the vulnerable spinal motoneuronal system is exclusively monitored and ischemia is detected within minutes. Using a strategy aimed at maintaining and restoring spinal cord blood supply (distal aortic perfusion, sequential aortic clamping, and selective segmental artery reattachment), early detection of ischemia allows protective measures to be applied and adjusted immediately, ie, reattaching or safely ligating intercostal arteries, increasing proximal o distal aortic pressures as required, or inducing hypothermia. Recent improvements in the technique fo eliciting myogenic MEPs include multi-pulse stimulation paradigms and the use of a circumferentia cathode. This results in robust and reproducible signals, which are less susceptible to anesthetic interference and allow the use of a constant level of neuromuscular blockade. In conclusion, monitoring myogenic MEPs during a TAA repair has become clinically feasible. The fast detection of spinal cord ischemia allows timely guidance of protective measures.
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PMID:Spinal cord monitoring with myogenic motor evoked potentials: early detection of spinal cord ischemia as an integral part of spinal cord protective strategies during thoracoabdominal aneurysm surgery. 946 73

Mild hypothermia and the 21-aminosteroids have both been neuroprotective in several models of cerebral ischemia. In this study we compared the effects of mild hypothermia and the 21-aminosteroid U-74389G, alone and in combination on neurologic and histopathologic outcome after temporary spinal cord ischemia. Forty male anesthetized New Zealand white rabbits were randomized to four groups (n = 10): (a) normothermia (control); (b) U-74389G (3 mg/kg intravenously [i.v.] before aortic occlusion, 1.5 mg/kg i.v. and 10 mg/kg intraperitoneally after occlusion); (c) mild hypothermia (4 degrees C epidural temperature decrease); and (d) mild hypothermia combined with U-74389G. Spinal cord ischemia was produced by 40 min of infrarenal aortic balloon occlusion. Forty-eight hours after the procedure, the neurologic status of the animals was assessed (Tarlov score) and the animals were killed for histologic evaluation. In the normothermic control group, eight of 10 animals became paraplegic. There was a significant reduction of the incidence of paraplegia and overall neurologic deficits and a significant improved Tarlov score in the mild hypothermic group (one animal paraplegic) and in the group with both mild hypothermia and U-74389G (two animals with a mild paraparesis). The histopathologic scores showed significantly less damage in both hypothermic groups. In group 2, U-74389G administration did not improve neurologic or histopathologic outcomes. The results of the current study demonstrate that a slight decrease of intraischemic spinal cord temperature significantly improved neurologic and histopathologic outcomes after experimental spinal cord ischemia. Protection by the 21-aminosteroid at normothermic conditions, or additional protection when U-74389G was added to mild hypothermia, could not be demonstrated.
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PMID:Effect of mild hypothermia and the 21-aminosteroid U-74389G on neurologic and histopathologic outcome after transient spinal cord ischemia in the rabbit. 955 66

1. Spinal cord ischemia evoked a biphasic increase in CSF-Glu during 20 min of ischemia (40%) and at 2 hr after reperfusion (70%) in the nontreated group that was attenuated by all treated groups. But MK-801 (15 micrograms i.t.) did not affect the increased Glu at 2 hr (80%). 2. The argyrophilia observed in laminae II-V at 8 hr after reperfusion was attenuated by hypothermia (33 degrees C) and combination with MK-801, but the attenuation was less with MK-801. 3. Mild hypothermia attenuated the biphasic increase in CSF-Glu and corresponding development of neuronal damage after spinal cord ischemia. 4. Mild hypothermia with NMDA antagonism did not yield any further effects, suggesting that hypothermia itself plays a pivotal role in the protection.
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PMID:Hypothermia prevents biphasic glutamate release and corresponding neuronal degeneration after transient spinal cord ischemia in the rat. 1008 4

Thoracoabdominal aneurysm surgery is associated with a high incidence of morbidity and mortality. Spinal cord ischemia and the risks of paraparesis or paraplegia remain devastating complications. The mechanisms of spinal cord injury involve both acute ischemic injury and delayed reperfusion injury. Blood flow to the spinal cord frequently arises in the segment of the aorta requiring aortic cross clamping. As such, there is an obligate period of blood flow disruption. Multiple strategies have evolved to reduce the ischemic interval and to provide adjunct interventions to reduce the impact of the ischemia. Despite a multidisciplinary approach, a spinal cord ischemia is present in approximately 4 to 16% of patients, depending on the type of aneurysm and other comorbid diseases. Cerebral spinal fluid drainage, distal perfusion techniques, intercostal artery anastomosis, hypothermia techniques, and mechanisms of ischemic preconditioning are interventions employed to reduce the risk of paraplegia after thoracal-abdominal aortic surgery. Surgeons, anesthesiologists, and perfusionist are intimately involved in the decision making as to which interventions will be employed in a given case. Although these adjuncts have been evaluated in multiple animal and human protocols, the efficacy of each intervention when looked at in isolation remains difficult to determine fully. This is attributable, in part, to the complex mechanisms of the patient injury, the inherint risks of the surgical procedure, and the confounding effects of comorbid disease states. Nonetheless, clinicians must have comprehensive understanding of these various interventions and their application. This review serves as an overview of these various interventions with special emphasis on outcome data.
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PMID:Thoracoabdominal aneurysm surgery and the risk of paraplegia: contemporary practice and future directions. 1191 23

The purpose of this study was to investigate the effect of N-acetylcysteine (NAC) on spinal cord ischemia-reperfusion (I-R) in rabbits. Thirty rabbits were divided into five equal groups, group I (sham-operated, no I-R), group II (control, only I-R), group III (I-R+NAC), group IV (I-R+hypothermia), group V (I-R+NAC+hypothermia). Spinal cord ischemia was induced by clamping the aorta both below the left renal artery and above the aortic bifurcation. Forty-eight hours postoperatively, the motor function of the lower limbs was evaluated in each animal according to Tarlov Score. Spinal cord samples were taken to evaluate the histopathological changes. The sham-operated rabbits (group I) showed no neurologic deficit (Score=4). Paraplegia (Score=0) developed in all rabbits in the control group (group II). Administration of 50 mg/kg of NAC (group III) resulted in significant reduction of motor dysfunction (Score=3.1+/-1.3, p=0.002). Application of hypothermia alone (group IV) showed significant recovery of motor functions (Score=3.0+/-1.1, p=0.002), and combination of hypothermia and 50 mg/kg of NAC (group V) showed complete recovery of lower limb motor function (Score=4, p=0.001). Histologic examination of the spinal cord in rabbits with paraplegia revealed several injured neurons. The cords of animals with no motor function deficits showed only minimal cellular infiltrates in the gray matter, and there was good preservation of nerve cells. NAC showed protective effects of the spinal cord. Moderate hypothermia alone also showed protective effects. Combined use of NAC and hypothermia resulted in highly significant recovery of spinal cord function.
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PMID:Neuroprotective effect of N-acetylcysteine and hypothermia on the spinal cord ischemia-reperfusion injury. 1295 48

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


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