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Query: UMLS:C0022116 (ischemia)
91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Paraplegia or paraparesis caused by temporary cross-clamping of the aorta is a devastating sequela in patients after surgery of the thoracoabdominal aorta. No effective clinical method is available to protect the spinal cord from ischemic reperfusion injury. A small animal (rat) model of spinal cord ischemia is established to better understand the pathophysiological events and to evaluate potential treatments. Eighty-one male Sprague-Dawley rats weighing 300 g to 350 g were used for model development (45) and treatment evaluation (36). The heparinized and anesthetized rat was supported by a respirator following tracheostomy. The thoracic aorta was cannulated via the left carotid artery for post-clamping intra-aortic treatment solution administration. After thoracotomy, the aorta was freed and temporarily clamped just distal to the left subclavian artery and just proximal to the diaphragm for different time intervals: 0, 5, 10, 15, 20, 25, 30, 35, and 40 minutes (five animals per group). The motor function of the lower extremities postoperatively showed consistent impairment after 30 minutes clamping (5/5 rats were paralyzed), and this time interval was used for treatment evaluation. For each treatment, six animals per group were used, and direct local intra-aortic infusion of physiologic solution (2 mL) at different temperatures with or without buffer substances was given immediately after double cross-clamp to protect the ischemic spinal cord. Arterial blood (2 mL) was infused in the control group. The data indicate that the addition of HCO3-(20 mM) to the hypothermic (15 degrees C) solution offered complete protection of the spinal cord from ischemic injury.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Third place winner of the Conrad Jobst Award in the gold medal paper competition. Prevention of spinal cord dysfunction in a new model of spinal cord ischemia. 783 75

Forty-three patients undergoing repair of a thoracoabdominal aortic aneurysm were monitored to evaluate spinal cord ischemia, as evidenced by somatosensory evoked potentials (SEPs). All patients were operated on using left heart bypass. In 34 patients (80%), staged clamping was used. Except for cerebrospinal fluid (CSF) drainage in 15 patients (35%), no other protective measures to preserve spinal cord function were used. The overall incidence of immediate onset paraplegia was 7%, and of immediate onset paraparesis was 5%; neither was limited only to those patients in whom potentials were lost. In 18 patients (42%), no change in the evoked potentials occurred; one of these patients (5%) awoke paraplegic after operation, and two others had a delayed onset paraplegia. In 13 patients (30%), evoked potentials were lost despite adequate perfusion; in 12 of them, potentials returned gradually, with one immediate paraplegia (8%), and in one potentials did not return at all, with subsequent immediate paraplegia (100%). In 12 patients (28%), evoked potentials decreased without being lost completely, and then recovered; in this group there were no immediate paraplegias. No relationship could be demonstrated between the extinction time, the recovery time, or the duration of loss of evoked potentials with postoperative neurological outcome. Intraoperative monitoring of SEPs is a good indicator of spinal cord ischemia, although we found a 5% incidence of false negatives. SEP monitoring offers an improvement in surgical strategy, and allows safer operations for thoracoabdominal aneurysms.
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PMID:Somatosensory evoked potentials during exclusion and reperfusion of critical aortic segments in thoracoabdominal aortic aneurysm surgery. 784 50

Between 1978 and 1992, 70 patients were operated for type B aortic dissection (tear in the descending aorta without involvement of the ascending aorta). 15/70 (21%) patients had an acute dissection (onset of symptoms < 24 h), 19/70 (27%) a subacute dissection (onset of symptoms < 14 days), and 36/70 (51) a chronic dissection (onset of symptoms > 14 days). The indications for surgery in cases of acute dissection were: hematothorax, oliguria, leg ischemia and persistent pain. Persistent hypertension was an additional indication in cases of subacute dissection. In large majority (93%) of chronic dissections the indication for surgery was enlarged aortic diameter. In 86% (60/70) graft replacement of the aorta was performed, in 6% (4/70) extra-anatomic bypass, in 3% (2/70) fenestration, in 3% (2/70) thrombendarterectomy, in 3% (2/70). The overall mortality was 17% (12/70); 27% of acute dissection, 26% for subacute dissection, and 8% for chronic dissection. The morbidity for acute dissection was 73%, of subacute dissection 43%, and of chronic dissection 12%. The most frequent complications were: leg ischemia (8 patients), renal failure (4 patients), paraparesis (4 patients) and sepsis (2 patients). No paraparesis was encountered in surgery of the chronic dissection. Conservative treatment was tried in all acute B-dissections, with surgical therapy being reserved for complications of the dissection, such as rupture, such as rupture, risk of rupture (hematothorax, large aortic diameter resp. expansion, persistent hypertension, persistent pain) or ischemia of distal vascular beds. Long-term survival for chronic type B dissections is good. Strong control of risk factors (hypertension) is essential.
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PMID:[Type B aortic dissections: surgical technique and results]. 787 97

Paraplegia may occur after transient aortic occlusion as a consequence of primary ischemia to the spinal cord or injury during the reperfusion period. In animal models of ischemia/reperfusion there is evidence that reperfusion injury may be modulated partially by neutrophils. The efficacy of the neutrophil adherence blocking murine monoclonal antibody (MAb 60.3) was assessed in spinal cord ischemia/reperfusion in rabbits. Spinal cord ischemia was accomplished by balloon catheter occlusion of the infrarenal aorta. Neurologic assessment was graded as normal, partial neurologic deficit, or complete paralysis. Electrophysiologic monitoring with somatosensory evoked potentials was used to determine the optimal length of time of occlusion. Animals were treated randomly with 2 mg/kg of intravenous Mab 60.3 (n = 8) or saline solution (n = 9) with the investigator unaware of treatment. Mean occlusion times were no different between groups (control, 32.7 +/- 3.6 minutes versus MAb, 32.4 +/- 6.0 minutes). Five (55%) saline-treated and four (50%) MAb 60.3-treated animals became paraplegic. Animals with initial paraparesis all progressed to flaccid paraplegia within 24 hours. We conclude that spinal cord injury after transient aortic occlusion is independent of the CD11/CD18 glycoprotein complex of the neutrophil. Injury in this setting may occur during ischemia and thus may not be dependent on neutrophils or reperfusion.
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PMID:Inhibition of neutrophil adhesion does not prevent ischemic spinal cord injury. 794 51

The usefulness of spinal motor evoked potential by transcranial stimulation of the motor cortex (MEPT) in detecting spinal ischemia and predicting postoperative neurological dysfunction was evaluated using a model of spinal ischemia. Group 1 was comprised of 11 dogs used for measuring the basic wave form of spinal MEPT. The normal spinal MEPT response curve consists of two major peaks: peak I and peak II. The latency of peak I and peak II at T13-L1 was 6.0 +/- 0.6 and 7.1 +/- 0.6 msec, and the amplitude, 3.3 +/- 1.6 and 6.1 +/- 2.6 microV, respectively. Group 2 was comprised of six animals subjected to spinal ischemia, in which a time-related deterioration of the MEPT as well as evoked spinal cord potential (ESP) was demonstrated. The time taken until the loss of peak I and peak II was 19.2 +/- 5.3 and 21.7 +/- 6.2 min, respectively, while the time taken until the loss of ESP was 36.7 +/- 14.0 min. In group 3, comprised of seven animals, the aorta was unclamped and the animals were allowed to recover when the spinal MEPT had disappeared. Four had paraparesis immediately after the operation, two had a normal gait, one died, and one developed spastic paraplegia after 24 h. We concluded that the change in spinal MEPT during spinal ischemia occurred earlier than the change in ESP, and that the loss of MEPT suggested irreversible spinal cord damage.
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PMID:An experimental study on spinal cord ischemia during cross-clamping of the thoracic aorta: the monitoring of spinal cord ischemia with motor evoked potential by transcranial stimulation of the cerebral cortex in dogs. 811 20

Evoked spinal cord potentials elicited by direct stimulation of the cord were used to monitor spinal cord ischemia in 68 patients undergoing temporary occlusion of the thoracic aorta (29 thoracic nondissecting aortic aneurysms, 9 nondissecting thoracoabdominal aneurysms, and 30 dissecting aneurysms). "Immediate" postoperative paraplegia developed in three patients and "immediate" paraparesis developed in one, whereas "delayed" paraplegia developed in two others. During aortic crossclamping, four response patterns of the spinal cord potentials were obtained: (1) no change (n = 53), (2) change with return (n = 10), (3) change with inconsistent return (n = 2), and (4) change without return (n = 3). Neurologic complications occurred in 2%, 0%, 100% of these groups, respectively. Delayed paraplegia developed on the second postoperative day in only one patient with a false-negative result, and the potentials correlated well with this patient's clinical neurologic recovery. The aortic crossclamp time was significantly longer in the patients with "change with inconsistent return" and "change without return" than in the other two groups (p < 0.01). Femoral artery pressure and the cardiopulmonary bypass flow rate were also significantly lower in these groups than in the other two groups (p < 0.02 and p < 0.01, respectively). We conclude that intraoperative monitoring of direct spinal cord responses is useful for the early detection of spinal cord ischemia for assessing the efficacy of surgical countermeasures.
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PMID:Clinical application of evoked spinal cord potentials elicited by direct stimulation of the cord during temporary occlusion of the thoracic aorta. 819 98

Revascularization of the spinal arteries with thoracic aortic aneurysm were performed on nineteen patients using partial extracorporeal bypass. They were 16 men and 3 women. Age range were from 33 to 70 years (mean 49.9 +/- 10.3 years). There were eleven patients of dissecting aneurysm (DeBakey type IIIb in eight patients, type I in two patients and type IIIa in one patient), and eight patients of non-dissecting thoracoabdominal aneurysm (including two patients with ruptured aneurysm). The number of revascularized spinal arteries were 60 pairs (average 3.2 pairs per each patient). The revascularized spinal arteries were localized between levels T4 and L5.36 pairs of the 60 existed between levels T8 and L2 from where the artery of Adamkiewicz arises. Seven patients (eleven spinal arteries) underwent selective angiography of the revascularized spinal arteries postoperatively, and the anterior spinal artery and the artery of Adamkiewicz was identified in three patients. Two patients died within one month, one from MOF and the another from intestinal perforation respectively (operative mortality 11.1%). One patient, with ruptured thoracoabdominal aortic aneurysm showed paraparesis postoperatively, but no paraplegia was found in any patients. We recommend that not only the artery of Adamkiewicz but also the spinal arteries at the midthoracic area from T4 to T8 should be revascularized, to prevent postoperative paraplegia. Replacing of extended thoracic aneurysm, our method (using partial extracorporeal circulation and segmental aortic clamping) was thought to prevent spinal cord ischemia.
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PMID:[Angiographic evaluation of reconstructed spinal arteries in thoracic aortic aneurysm surgery]. 822 9

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

The potential usefulness of somatosensory evoked potential monitoring during aortic cross-clamping is slowly being realized. In addition, the protection of endangered spinal nervous tissue during aortic cross-clamping has not been sufficiently evaluated. To test the pharmacologic protective efficacy of various agents, we recorded spinal evoked somatosensory potentials (bipolar epidural catheter) in dogs under controlled conditions (N2O/O2-enflurane anesthesia) following clamping of the aorta for 1 hour. There were 5 groups of animals: those treated with different medications, such as prostaglandin E1 (PGE1), prostacyclin (PGI2), superoxide dismutase (SOD), and PGE1 plus SOD for pharmacologic protection during ischemia, and the controls. The time to recovery of evoked potentials during the reperfusion period was 36 minutes in the controls, 15.9 minutes in the SOD group (p < 0.01), 12.5 minutes in the PGE1 group (p < 0.001), 10.8 minutes in the PGI2 group (p < 0.001), and 3.8 minutes in the combination group (p < 0.001). In addition, treatment resulted in a better neurologic outcome on the seventh postoperative day when compared with the control group. While in the control group only 1 animal could walk (9%), 7 of 12 in the PGE1 group (58%), 4 of 12 in the SOD group (33.8%), 8 of 12 in the PGI2 group (66.7%), and all animals in the combination group (100%) could walk. We computed an exponential correlation that related the mean time of potential recovery during reperfusion with Tarlov scoring (grade 0 = paraplegia; grade 1 = paraplegia with little movements; grade 2 = paraparesis; grade 3 = paraparesis with some problems; grade 4 = normal motor function) in the various groups.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Somatosensory evoked potential, a prognostic tool for the recovery of motor function following malperfusion of the spinal cord: studies in dogs. 834 72

A case of watershed infarction in the spinal cord is reported. The patient underwent bronchial artery embolization for control of massive hemoptysis. The bronchial arteriogram was carefully examined and focused on blood supply to the spinal cord prior to embolization. Acute paraparesis followed the embolization procedure even though there was no visible spinal supply on the arteriogram. Magnetic resonance imaging showed a hyperintensity lesion over the watershed region which is located at the central portion of the upper thoracic cord. This case is reported to emphasize the significant role which angiographically invisible small vessels can play in the blood supply to the spinal cord. The vascular system of the spinal cord and the prevention of spinal cord ischemia secondary to embolization are further discussed here.
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PMID:Watershed infarction of spinal cord after the embolization of bronchial artery: a case report. 870 83


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