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)

The aim of this study was to investigate the effects of L-arginine (L-Arg) on neurological function, histopathology, and expression of hypoxia-inducible factor-1 alpha (HIF-1alpha) following spinal cord ischemia in rats, and the interaction between therapy with the nitric oxide donor L-Arg and up-regulation of the expression of HIF-1alpha. Thirty Wistar rats weighing between 200 and 250 g were divided into three groups, each containing 10 rats: group 1, sham operation; group 2, untreated ischemia-reperfusion (I-R); group 3, I-R plus L-Arg treatment. Spinal cord ischemia was applied for 20 min. There were no significant differences in mean arterial pressures, temperatures, and blood gas levels among the groups. In group 2, malondialdehyde values were significantly increased compared with groups 1 and 3. The rats with aortic occlusion in group 2 had paraplegia or paraparesis. In group 3, all animals were neurologically intact. In group 3, spinal motor neurons did not decrease significantly, and little proliferation of microglia was observed compared with those in group 2. In group 2, spinal motor neurons in ventral gray matter decreased significantly compared with those in groups 1 and 3. HIF-1alpha-positive immunostaining was mildly detected in group 2 animals. The expression of immunoreactive cells was intensely increased in spinal cord tissue from I-R/L-Arg rats. In conclusion, our findings suggest that HIF-1alpha-positive immunostaining may be critical factors in the pathophysiology of inflammatory spinal cord injury induced by I-R. Nitric oxide may play an important role in the immunohistochemical expression of these molecules, and the neuroprotective benefit of L-Arg may be attributed to preventing neural cell necrosis.
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PMID:The effects of L-arginine on neurological function, histopathology, and expression of hypoxia-inducible factor-1 alpha following spinal cord ischemia in rats. 1646 55

We investigated the interaction between nicorandil, a K(+)ATP channel opener, and morphine on motor function after a noninjurious interval of spinal cord ischemia in the rat. Spinal ischemia was induced by aortic occlusion for 6 min with a balloon catheter in Sprague-Dawley rats. All animals received intrathecal (IT) injection of morphine (1-60 microg) 1 h after ischemia. In addition to IT injection of morphine, group M (control), group MN (combination of morphine and nicorandil), and group MNG (combination of morphine, nicorandil, and glibenclamide) received IT saline, nicorandil (10 microg), and both glibenclamide (10 microg) and nicorandil (10 microg) after 150 min of reperfusion, respectively. A quantal bioassay for the effect of IT morphine on neurological function after ischemia was performed to calculate 50% effective dose values (ED50) for inducing paraparesis at 3 h of reperfusion. The ED50 in group M and group MN was 15.1 +/- 4.9 microg and 2.9 +/- 1.0 microg of IT morphine, respectively (P < 0.05). In Group MNG, the dose-response curve shifted back to the right and the ED50 for inducing paraparesis was 11.6 +/- 4.7 microg of IT morphine. The present study demonstrates that IT small-dose morphine combined with nicorandil induces spastic paraparesis after noninjurious interval of spinal cord ischemia in the rat.
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PMID:Intrathecal nicorandil and small-dose morphine can induce spastic paraparesis after a noninjurious interval of spinal cord ischemia in the rat. 1655 26

Acute distal aortic dissection rarely causes spinal cord ischemia presenting with paraplegia or paraparesis. Spinal cord involvement has poor outcomes, and there is no established effective treatment for this disorder. In this report we describe the acute conservative treatment of two cases of paraplegia/paraparesis due to acute type B aortic dissection. Early reversal of lower-limb dysmobility was achieved.
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PMID:Treatment methods for spinal cord injury caused by acute type B aortic dissection. 1713 Mar 11

A patient developed spastic paraparesis after surgery with ultrasound lithothripsy and litholapaxy of fragments of a renal calyceal calculus in middle-upper diverticulum. It was first assumed that the event could be due to transient spinal ischemia, caused by vasospasm of Adamkiewicz artery, secondary to blood engorgement of the area around the vessel. In order to clarify possible implications of medical liability, the Authors took into account the etio-pathogenetic mechanisms of the complication and analyzed the medico-legal aspects, with particular reference to the indication for surgery, which was not absolute in the case under scrutiny. In connection with the latter aspect, the Authors considered the conclusions of a recent sentence of the Court of Milan, whereby, despite the negative opinion of the experts specifically appointed, a case of medical liability was identified as a consequence of algodystrophy resulting from a cardiosurgical intervention. According to the Court, it is for the medical staff to demonstrate that they did all they could to prevent the complication and that such complication did not arise from a mistake on their part.
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PMID:Spastic paraparesis as a complication of percutaneous nephrolithothripsy (PNL) on a calyceal calculus of the left kidney. 1830 29

Spinal cord hematomas are remarkably uncommon. Even more rare are spontaneous spinal subdural hematomas without underlying pathological changes. In some patients, compression of the spinal cord by spinal subdural hematoma has led to acute paraplegia. Spontaneous spinal subdural hematomas occur most often in the thoracic spine and are manifested by sudden back pain that radiates to the upper or lower extremities or to the trunk and variable degrees of motor, sensory, and autonomic disturbances. Clinicians should consider spontaneous spinal subdural hematoma when patients who are taking anticoagulants report back or radicular pain and the development of paraparesis, because early diagnosis is essential for preventing irreversible paralysis. Diagnosis of spontaneous spinal subdural hematoma requires prompt radiological assessment; magnetic resonance imaging is the preferred method. Treatment includes emergent decompressive laminectomy and evacuation of the hematoma to prevent or minimize permanent neurological damage caused by spinal cord compression, ischemia, and spinal cord injury.
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PMID:Spontaneous spinal subdural hematoma: Case study. 1977 Apr 15

Thoracoabdominal aortic aneurysms (TAAAs) have a dismal natural history that frequently necessitates surgical repair, but such repairs sometimes result in paraplegia and paraparesis. To reduce the risk of these complications, intraoperative monitoring of spinal cord motor evoked potentials (MEPs) can be used to guide TAAA repair procedures and may potentially minimize spinal cord ischemia. However, the use of MEP monitoring techniques requires important changes to anesthetic management, entails certain risks, and has important contraindications.
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PMID:Motor evoked potentials in thoracoabdominal aortic surgery: CON. 2045 55

Paralysis and paraparesis are dreaded complications of thoracic endovascular aortic repair (TEVAR) that occur with an incidence of 2%-6%. Risks factors include the type of thoracic aortic pathology treated, coverage of the left subclavian artery origin without revascularization, concomitant infrarenal abdominal aortic aneurysm repair, extent of stent graft coverage of the thoracic aorta, and renal failure. Cerebral spinal fluid (CSF) drains have been advocated as one of several protective strategies to prevent spinal cord ischemia. This case discussion briefly addresses the evidence supporting the use of CSF drains in patients undergoing TEVAR and offers an algorithm for managing CSF drains.
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PMID:Spinal cord protection with a cerebrospinal fluid drain in a patient undergoing thoracic endovascular aortic repair. 2068 36

Paraplegia or paraparesis after otherwise successful thoracic or thoracoabdominal aortic reconstruction is a devastating complication for both patient and physician. Various strategies have been developed to minimize the incidence of neurological complications after aortic surgery. The incidence of spinal cord ischemia and subsequent neurological complications has been correlated with (1) the duration and severity of ischemia, (2) failure to establish a spinal cord blood supply, and (3) reperfusion injury. Preoperative identification of the arteria radicularis magna, the artery of Adamkiewicz, facilitates identification of critical intercostal vessels for reimplantation, resulting in reestablishing spinal cord blood flow. Techniques for monitoring spinal cord function using evoked potentials have been developed, and surgical techniques have evolved to reduce the duration of ischemia. Furthermore, sequentially sacrificing all the intercostal arteries while maintaining collateral circulation to the cord has produced good outcomes. The severity of ischemia can be minimized by using cerebrospinal fluid drainage, hypothermia, distal bypass, managing the blood pressure, and adjunctive pharmacological therapy. Reperfusion injury can be reduced with the use of antioxidant therapy. Recent advances in endovascular stentgrafting have reduced the incidence of postoperative spinal complications, especially among high-risk patients.
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PMID:Fighting spinal cord complication during surgery for thoracoabdominal aortic disease. 2130 33

Postoperative paraplegia is a serious complication of reconstructive surgery on the thoracoabdominal or descending thoracic aorta, and the major cause is thought to be spinal cord ischemia during and after the procedure. Due to advances in anesthetic and surgical techniques, the incidence of intractable neurological complications has declined, but the rate of paraplegia or paraparesis is still within the range of 5-16%. Many methods have been devised to prevent this complication, such as 1) distal perfusion, 2) reimplantation of segmental arteries, 3) detection of the Adamkiewicz artery, 4) hypothermia, 5) cerebrospinal fluid drainage, 6) multisegmental aortic clamping, 7) motor-evoked potential monitoring, 8) epidural perfusion cooling, and 9) selective perfusion of the intercostal arteries and they can be utilized in combination.
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PMID:[Open surgery of thoracoabdominal aortic aneurysm]. 2138 94

In recent decades great advances have been made in surgical procedures for treating thoracic and thoracoabdominal aorta defects. Associated mortality and morbidity rates have dropped considerably, mainly in major reference centers, but nonetheless continue to be significant. The need for new strategies to reduce mortality and morbidity has made endovascular approaches an attractive alternative for high-risk surgical patients. The most feared complications of these procedures include paraparesis and paraplegia, which have devastating consequences on patients' quality of life. We provide an updated review of the pathophysiology of spinal cord ischemia in open and endovascular surgery, as well as perioperative measures designed to protect the spinal cord in both types of procedure.
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PMID:[Spinal cord protection during open and endovascular surgery in thoracic and thoracoabdominal aorta diseases]. 2142 27


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