Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Pyruvate dehydrogenase complex (PDHC) is a major enzyme of glucose metabolism. Dichloroacetate (DCA) is a noncompetitive inhibitor of PDHC kinase, an enzyme that inactivates PDHC. We examined the effects of DCA on extracellular lactate and pyruvate concentration changes and spinal somatosensory evoked potentials (SSEP) in ischemic rabbit spinal cords. In the first group of 26 animals, the aorta was occluded until postsynaptic SSEP waves were completely suppressed for 10 min, a period of ischemia that causes neurologic deficits in 50% of untreated animals. DCA (25 mg/kg) was given to 13 of these animals before ischemia. In the second group of 24 animals, the aorta was occluded until the postsynaptic SSEP waves were absent for 20 min, a period of ischemia that produces paraplegia in 100% of untreated animals. DCA (25 mg/kg) was given to 16 of these animals just before the aortic occlusion was released. After occlusion, extracellular spinal lactate concentrations increased abruptly while pyruvate concentrations fell. Both lactate and pyruvate concentrations reached a plateau during the ischemic period but increased when the aortic balloon was deflated. DCA-treated animals had lower lactate and pyruvate peak concentrations during reperfusion, as well as more rapid and greater recovery of SSEP at 2 h after reperfusion. DCA did not alter spinal metabolism during the ischemia but appeared to produce a more rapid shift to glucose metabolism on reperfusion. Thus, DCA treatment resulted in better electrophysiological recovery after both moderate and severe ischemia, either by reducing lactic acidosis or by increasing the recovery rate of aerobic energy production.
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PMID:Reduction in spinal cord postischemic lactic acidosis and functional improvement with dichloroacetate. 234 14

Although it was initially performed in 1935, aortic fenestration has been infrequently employed and reported in recent years. We have continued to use fenestration for descending aortic dissection with complicating organ ischemia (lower-extremity ischemia, renal ischemia, and paraplegia). Our technique involves complete transection of the infrarenal abdominal aorta, removal of a generous intimal flap proximally, and reconstitution of layers distally. We report our experience with 12 patients, all of whom survived the operative procedure. Nine patients were discharged from the hospital, and with a mean follow-up of 6.8 years, 7 are still alive. Fenestration immediately restored organ perfusion in all but 1 of the patients, and no patient died of late rupture. We recommend fenestration for descending aortic dissection in patients presenting with organ ischemia. Fenestration is not recommended for acute dissection with rupture or for chronic enlarging dissection.
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PMID:Fenestration revisited. A safe and effective procedure for descending aortic dissection. 234 78

A 60-year-old man suffered from paraplegia after the operation for thoracic aortic aneurysm and died 10 months after the operation. Detailed examination on the distribution of spinal cord lesions and of the locations of anterior radicular arteries revealed that the spinal cord ischemia occurred at the mid-thoracic segments between T-6 and T-10; the artery of Adamkiewicz entered at T-12; another radicular artery entered at T-4. We concluded that the spinal cord ischemia was caused by the interruption of the radicular artery at T-4 and that the segments nourished by the blood flow of the artery of Adamkiewicz were intact. We suggest that in some patients important radicular arteries other than the artery of Adamkiewicz are essential to preserve blood flow to the upper or middle thoracic spinal segments.
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PMID:[A case report of paraplegia following an operation for thoracic aortic aneurysm--with special reference to pathological findings of the spinal cord]. 234 13

Hyperglycemia has been shown to exacerbate neurological deficit associated with central nervous system ischemia. Iodoacetate or dichloroacetate was administered intraperitoneally to rats in a study to examine the role of glycolysis in hyperglycemic exacerbation of neurological deficit. Sprague-Dawley rats were injected with saline, iodoacetate, or dichloroacetate and then made paraplegic by temporary occlusion for 10, 12, 13, or 15 minutes of the right and left subclavian arteries and the aorta distal to the left subclavian artery. Glycolytic blockage by iodoacetate was lethal in doses of 15 mg/kg or more, whereas rats receiving 10 mg/kg survived but showed no significant neurological improvement compared to the saline-treated control group. Dichloroacetate, 500 mg/kg, protected neurological function, which suggests a possible detrimental role for lactate accumulation and the benefit of maintaining tricarboxylic acid cycle activity by stimulating pyruvate dehydrogenase. The protection seen with dichloroacetate depended on the severity of ischemic injury. Dichloroacetate administration had a minimal effect on neurological outcome with occlusion periods of 13 and 15 minutes, mild improvement with 12 minutes of occlusion, and a significant protective effect with a 10-minute occlusion period. The dose-response nature of ischemic injury and neurological outcome in this rat model of paraplegia therefore appears to play an important role in determining the effect observed with a specific intervention.
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PMID:Neurological protection by dichloroacetate depending on the severity of injury in the paraplegic rat. 235 11

From 1970 to 1985, 49 patients were operated for traumatic aortic rupture (TAR) in 2 university hospitals. Protection of distal ischemia was performed 31 times with a left heart bypass (LHB), 5 times with a heparin coated shunt and, 13 times using simple aortic cross-clamping combined with pharmacological vasodilatation. Total mortality was 17 out of 49, 5 during and 12 after the operation, 2 of them being directly related to systemic heparinization during LHB. In the LHB and shunt groups there was one postoperative paraplegia out of 35 patients, while 4 from the 13 patients operated without a shunt developed paraplegia. If risk factors such as long cross-clamping time, hypotension, extensive laceration of the inner curvature of the aorta, or cross-clamping of the aortic arch at a high level are anticipated, LHB or the shunt technique must be considered to avoid paraplegia. A repair without a shunting procedure should be limited to those cases in which the individual surgeon believes that he can do the operation within 30 minutes aortic cross-clamping time.
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PMID:Spinal cord injury following surgery for acute traumatic rupture of the thoracic aorta. 242 44

This animal experiment was in succession to the research on paraplegia caused by spinal cord local ischemia in an animal model. Immediately after the operative production of local spinal cord ischemia, pedicled omentum spinal transposition onto the ischemic segments of spinal cord was performed. The animals recovered from paraplegia around two months afterwards. Spinal cord specimens showed adhesion of omentum to the spinal cord without compression. Omental vessels grew into the cord. Gross sections of specimen stained with Nissl method revealed that normal structure of nerve cells were preserved but number of nerve cell decreased.
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PMID:The effect of transposition of pedicled omentum to spinal cord ischemia segments. An animal experiment. 250 9

Local spinal cord ischemia model was established in 11 adult dogs. The anterior spinal artery, posterior spinal artery and radicular artery were cauterized with bipolar cautery. Ischemia of this segment of spinal cord was thus produced followed by paraplegia. The pathological findings of this spinal cord segment were softening and necrosis. The establishment of this animal model of segmental spinal cord ischemia is beneficial to scientific research in basic medicine and clinical practice.
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PMID:Paraplegia caused by local spinal cord ischemia. An animal spinal cord ischemia model. 250 49

The pressure difference between the mean distal aortic pressure (MDAP) and the cerebrospinal fluid pressure (CSFP), defined as the spinal cord perfusion pressure (SCPP), as well as somatosensory evoked potentials (SEP) were monitored intraoperatively to detect and prevent intraoperative spinal cord ischemia in 24 patients who required cross-clamping of the descending thoracic aorta. A temporary axillo-femoral shunt, utilizing a 10 mm woven Dacron tube graft, was employed in 10 patients and partial cardiopulmonary bypass was employed in fourteen. Ischemic SEP changes were seen in six patients. Two patients, whose SCPPs were 32 and 35 mmHg, showed a complete loss of SEP and subsequently developed paraplegia. In the other four cases, increase of the MDAP and/or withdrawal of cerebrospinal fluid were performed to increase the SCPP to more than 60 mmHg when ischemic SEP changes occurred. The SEP gradually recovered in two of these cases. The ischemic SEP changes seen in one patient, who had the longest aortic cross-clamping time, (175 minutes) returned to normal immediately after unclamping. In another case, who had a thoracoabdominal aortic aneurysm, the intercostal arteries were reimplanted since the ischemic SEP changes did not revert. These four patients recovered without any neurological deficit. In the other 18 cases without ischemic SEP change, SCPP was kept at more than 40 mmHg during aortic cross-clamping. We conclude that the SCPP should be maintained at more than 40 mmHg during aortic occlusion, and increased to more than 60 mmHg when ischemic SEP changes occur, by increasing MDAP and/or withdrawing cerebrospinal fluid in order to prevent postoperative paraplegia.
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PMID:[Prevention of spinal cord ischemia after cross-clamping of the thoracic aorta--monitoring of spinal cord perfusion pressure and somatosensory evoked potentials]. 260 Apr 66

A previous article (Part I) described the patient population and operative management of 666 patients who had surgery for nonruptured abdominal aortic aneurysms. This article details the perioperative complications and, by chi-square and logistic regression analysis, identifies the variables that are associated with each complication. In summarizing the results (below) the incidence of each complication is listed, along with the predictive risk factors in parentheses that have significance levels less than 0.05. Vascular morbidity data are as follows: intraoperative bleeding, 4.8%; postoperative bleeding requiring transfusion, 2.3% or repeat operation, 1.4% (large volume of blood transfusion and/or use of an autotransfusion device); intraoperative limb ischemia, 3.5%; graft thrombosis, 0.9% (femoropopliteal disease and/or distal anastomosis at the femoral level); distal thromboembolism, 3.3% (male sex, femoral popliteal disease, and/or intraoperative graft thrombosis); amputation, 1.2%; graft infection, 1 case. General morbidity data are as follows: cerebrovascular event, 0.6%; paraplegia, 1 case; cardiac event, 15.1% (age, previous episode of congestive heart failure, and/or electrocardiogram [ECG] evidence of a previous myocardial infarction); myocardial infarction, 5.2% (advancing age, angina, and/or prolonged aortic cross-clamp time); congestive heart failure, 8.9% (previous history of congestive heart failure, ECG evidence of ischemia, and/or chronic obstructive lung disease); arrhythmia requiring treatment, 10.5% (preoperative ventricular premature beats and/or respiratory failure requiring ventilation for more than 48 hours); new arrhythmia, 8.4% (angina and/or chronic obstructive lung disease); respiratory failure, 8.4% (chronic obstructive lung disease, large volume of blood transfused, and/or occurrence of postoperative bleeding, cerebrovascular accident, congestive heart failure, or myocardial infarction); renal damage with rise in creatinine or blood urea nitrogen, 5.4% and/or renal failure requiring dialysis, 0.6% (elevated preoperative creatinine, suprarenal aortic cross-clamping, and/or renal vein ligation); diarrhea without evidence of ischemia colitis, 7.1% and ischemic colitis, 0.6% (pelvic flow interrupted); prolonged ileus, 11.0% (aortoiliac occlusive disease, deterioration of renal function, prolonged ventilation, and/or preoperative history of angina); superficial wound infection, 1.5% and deep infection, 0.5% (femoral anastomosis and/or female sex); coagulopathy, 1.1% (large volume of blood transfused).(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Multicenter prospective study of nonruptured abdominal aortic aneurysm. Part II. Variables predicting morbidity and mortality. 264 60

A simple yet reliable model of spinal cord ischemia has been previously developed by inserting a Swan-Ganz catheter into the abdominal aorta of rabbits and inflating the balloon just inferior to the renal arteries. Recent investigations have shown that paraplegia is consistently reproduced if the balloon remains inflated for 20 min after loss of the N3 component of the somatosensory evoked potential. Because of its high reliability, this model has been frequently and successfully used to determine the efficacy of pharmacological agents thought to provide protection against spinal cord ischemia. Results from the present report demonstrate that a similar degree of reliability can be achieved in this model for testing motor activity. A simple method of evoking highly reproducible motor potentials, that can be percutaneously recorded from the spinal cord in response to cortical stimulation, was developed. Predictable and repeatable changes in the configuration of the corticomotor evoked potential were found during spinal cord ischemia and reperfusion. With this added dimension of functional assessment, future application of the current spinal cord ischemia model have been greatly expanded.
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PMID:Alterations in the corticomotor evoked potential following spinal cord ischemia. 275 75


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