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)

To characterize the changes in axonal function in the motor and somatosensory tracts of the cord after spinal cord injury (SCI) and to correlate these changes with spinal cord blood flow (SCBF), the relationships among the severity of SCI, motor and somatosensory evoked potentials (MEPs and SSEPs) and SCBF were examined. Fifteen rats received a 1.5 g (n = 5), 20 g (n = 5) or 56 g (n = 5) clip compression injury of the cord at C8. SCBF at the injury site was measured by the hydrogen clearance technique 35 min before and 30 min after SCI. Concomitantly MEPs from the cord at T10 (MEP-C) and from the sciatic nerve (MEP-N) and SSEPs were recorded. A linear relationship (r = -0.89, P less than 0.002) was found between the severity of SCI and the reduction in SCBF at the injury site. Linear discriminant analysis revealed that both the MEP (P less than 0.0001) and SSEP (P less than 0.003) were significantly related to the severity of SCI. Furthermore, the amplitude of the MEP (r = 0.65, P less than 0.0001) and SSEP (r = 0.58, P less than 0.001) was significantly correlated with the posttraumatic SCBF. Multiple regression revealed that both the severity of cord injury and the degree of posttraumatic ischemia were significantly related to axonal dysfunction after SCI. While the MEP was more sensitive to injury than the SSEP, the SSEP more accurately distinguished between mild and moderate severities of cord injury. Axonal conduction in the motor and somatosensory tracts of the cord was significantly correlated with the reduction in posttraumatic SCBF and, therefore, these data provide quantitative evidence linking posttraumatic ischemia to axonal dysfunction following acute cord injury. Furthermore, this study validates the hypothesis that the combined recording of MEPs and SSEPs is an accurate technique to assess the physiological integrity of the cord after injury.
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PMID:The relationships among the severity of spinal cord injury, motor and somatosensory evoked potentials and spinal cord blood flow. 247 26

Hemodynamic responses (blood pressure, as well as cardiac output (CO), peripheral and CNS blood flow changes measured via radioactive microspheres) were analyzed in anesthetized rats 2 min following intrathecal (IT) administration (10 microliters) of either 5-ion control solution or 20 nmol of dynorphin A(1-13) into the lower thoracic space (T10-T12). Mean arterial pressure (MAP) significantly increased within 2 min following IT dynorphin A(1-13) due to rise in total peripheral resistance, whereas CO significantly declined. Two minutes post-IT-dynorphin A(1-13) administration spinal cord blood flow also significantly decreased for 2 cm anterior and 1 cm posterior from the tip of the spinal catheter, which reflected a significant elevation in tissue flow resistance of spinal cord vessels in spite of the reduction of CO. As well, tissue blood flow resistance was also increased at this time in the kidneys and adrenal glands. The results indicate that within 2 min after intrathecal dynorphin A(1-13) administration an acute increase in blood flow resistance of spinal cord vessels around the tip of the spinal catheter occurs, at a time when the animal is also hypertensive. It is suggested that the associated pressor response may, in part, be caused by dynorphin A evoking localized ischemia.
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PMID:Intrathecal dynorphin A administration causes pressor responses in rats associated with an increased resistance to spinal cord blood flow. 256 52

The effect of lumbar epidural anesthesia on myocardial wall motion was compared in two groups of patients using precordial two-dimensional echocardiography (2DE). All patients were scheduled to undergo lower abdominal or peripheral surgery. Group 1 included five healthy ASA PS 1 subjects and group 2 included 10 patients with coronary artery disease (CAD). In all patients 12.5 ml of 2% lidocaine HCl was injected into the lumbar epidural space, and systolic and diastolic blood pressures, and heart rate were continuously monitored. 2DE evaluation was performed before and at 10, 20, 30, and 60 min (T10-T60) after epidural lidocaine injection. The left ventricular wall was divided into 16 segments for parasternal long-axis, short-axis and apical four-chamber views. The wall motion of each segment was graded on a scale from 1 (dyskinesia) to 6 (hyperkinesia), with 5 representing normal motion. A decrease in segmental wall motion greater than or equal to 2 grades was considered indicative of ischemia. Plasma lidocaine and catecholamine levels were measured before and 10, 20, and 60 min after epidural lidocaine injection. Peak plasma lidocaine levels in groups 1 and 2 were 2.79 +/- 1.06 micrograms/ml (mean +/- SD) and 2.58 +/- 1.48 micrograms/ml at 10 min, respectively (NS). Plasma epinephrine and norepinephrine levels were unchanged from baseline. Systolic pressures decreased significantly in group 2 from T10 to T60. Diastolic pressure decreased significantly in the same group from T20 to T60, and in group 1 only at T10. Mean arterial pressure decreased significantly in both groups at T30, without change in heart rate.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Abnormalities in myocardial segmental wall motion during lumbar epidural anesthesia. 229 27

Somatosensory evoked potentials were used to locate intercostal arteries critical to spinal cord blood flow in nine dogs. To mimic a clinical situation, the proximal descending thoracic aorta (left subclavian artery to T7) was excluded with cross-clamps, and partial pulsatile left atrial-femoral artery bypass was instituted to maintain distal aortic pressure at 100 mm Hg. Progressively lower aortic segments were excluded (T7-10, T10-L1, L1-3, L3-6, L6-7) until loss of somatosensory evolved potentials occurred. Spinal cord blood flow measurements at the time of evoked potential loss revealed significant ischemia (p less than 0.02 versus baseline) in the excluded segment in seven animals but normal spinal cord blood flow in the remainder of the cord. Upon reperfusion, significant reactive hyperemia (p less than 0.02) was noted only in previously ischemic cord segments. Two animals exhibited no change in somatosensory evoked potentials or spinal cord blood flow despite exclusion of the entire thoracoabdominal aorta, presumably as a result of spinal collaterals. Loss of somatosensory evoked potentials despite adequate distal perfusion indicates that critical intercostal vessels have been excluded from systemic and bypass circulations. Use of evoked potential measurements in both experimental and clinical situations provides a means for assessing adequacy of spinal cord blood flow during cross-clamping and can alert the surgeon to the need for reimplantation of critical intercostal arteries during surgical resection of the thoracoabdominal aorta.
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PMID:Monitoring of somatosensory evoked potentials during surgical procedures on the thoracoabdominal aorta. III. Intraoperative identification of vessels critical to spinal cord blood supply. 361 27

The neuroprotective potential of halothane anesthesia was explored in a weight-drop model of spinal trauma in the rat (N = 252). In initial experiments, animals were subjected to 25, 50 or 100 g cm impact injuries at T10 during pentobarbital or halothane anesthesia and their outcomes determined using somatosensory-evoked potentials, blinded neurologic evaluations for two weeks, and post-mortem analysis of spinal serotonin levels. Subsequently, halothane anesthesia was combined with either pentobarbital or nitrous oxide or given as a late treatment to pentobarbital anesthetized rats subjected to 50 g cm injuries. A series of acute studies were then performed in order to assess the hemodynamic and respiratory concomitants of halothane vs. pentobarbital, as well as the effect of mechanical ventilation and bicarbonate treatment upon halothane neuroprotection. Finally, the effect of a 50 g cm impact upon local white matter spinal cord blood flow was measured during halothane or pentobarbital anesthesia using laser-Doppler flowmetry. Results demonstrate an active neuroprotective action for halothane anesthesia that is not altered by the presence of other anesthetics and is most prominent at severe injury levels. The data suggest the importance of immediate injury responses in this action. Late halothane treatment was ineffective when given as early as 10 minutes postinjury while both the electrophysiological and hemodynamic effects of halothane vs. pentobarbital were apparent during this 10 minute period. Thus, halothane was associated with the prevention of spinal ischemia during the first 10 minutes after trauma in comparison to pentobarbital.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Halothane anesthesia is neuroprotective in experimental spinal cord injury: early hemodynamic mechanisms of action. 848 42

Numerous factors are involved in the spread of secondary damage in spinal cord after traumatic injury, including ischemia, edema, increased excitatory amino acids, and oxidative damage to the tissue from reactive oxygen species. Neutrophils and macrophages can produce reactive oxygen species when activated and thus may contribute to the lipid peroxidation that is known to occur after spinal cord injury. This study examined the rostral-caudal distribution of neutrophils and macrophages/microglia at 4, 6, 24, and 48 h after contusion injury to the T10 spinal cord of rat (10 g weight, 50 mm drop). Neutrophils were located predominantly in necrotic regions, with a time course that peaked at 24 h as measured with assays of myeloperoxidase activity (MPO). The sharpest peak of MPO activity was localized between 4 mm rostral and caudal to the injury. Macrophages/microglia were visualized with antibodies against ED1 and OX-42. Numerous cells with a phagocytic morphology were present by 24 h, with a higher number by 48 h. These cells were predominantly located within the gray matter and dorsal funiculus white matter. The number of cells gradually declined through 6 mm rostral and caudal to the lesion. OX-42 staining also revealed reactive microglia with blunt processes, particularly at levels distant to the lesion. The number of macrophages/microglia was significantly correlated with the amount of tissue damage at each level. Treatments to decrease the inflammatory response are likely to be beneficial to recovery of function after traumatic spinal cord injury.
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PMID:Acute inflammatory response in spinal cord following impact injury. 958 56

We report the case of a 66-year-old man who had a descending thoracic aneurysm, diagnosed as aortitis syndrome. He subsequently underwent an aneurysmectomy under simultaneous sensory and motor spinal cord monitoring. Spinal cord ischemia was diagnosed during prosthetic replacement of the aneurysm by changes in evoked spinal cord potentials and motor evoked potentials from the lumbar spinal cord enlargement and 2 pairs of intercostal arteries were reconstructed at the level of T9 and 10. After surgery, the patient developed paraparesis below T10, but the resulting neurological deficits were overcome with postoperative rehabilitation. Simultaneous monitoring of evoked spinal cord potentials and motor evoked potentials were useful in evaluating spinal cord ischemia during aortic aneurysm surgery and in determing whether intercostal arteries should be reconstructed.
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PMID:Three different approaches to spinal cord monitoring for the prediction of spinal cord ischemia during thoracic aortic aneurysm surgery. 982 91

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

Spinal cord infarctions are rare and due to heterogeneous etiologies. The aim of the study was to analyze the MR imaging findings and evaluate their correlations with clinical symptoms in ischemic spinal cord lesions. MR images and clinical features of 16 patients (11 male, 5 female) with typical sudden onset of neurological deficits caused by spinal cord ischemia were evaluated. MR imaging was performed within 2 h to 14 days after the initial neurological symptoms. Eight patients had follow-up examinations including contrast-enhanced MR imaging. MR abnormalities were best demonstrated on sagittal T2-weighted images, with "pencil-like" hyperintensities (16/16) and cord enlargement (9/16). Axial T2-weighted images showed bilateral (13/16) and unilateral (3/16) hyperintensities according, in 15 patients, to anterior spinal artery (ASA) territory, with three of them located particularly in the spinal sulcal artery territory. In one patient only the posterior spinal artery (PSA) territory was involved. Spinal cord was affected at the cervical level (especially C2-C3) in seven patients, at the upper thoracic level (T3-T5) in two patients and at the thoracolumbar region including the conus medullaris (T10-L1) in seven patients. Presumed etiologies were vascular surgery (3 patients), infrarenal aortic aneurysm (1 patient), bilateral vertebral artery dissection (1 patient), hypotension (1 patient), spine operation (1 patient), excessive cocaine misuse (1 patient) and cardioembolic vertebral artery occlusion (1 patient); six of seven patients with unclear etiologies had vascular risk factors such as hypertension, diabetes and cigarette smoking. MR imaging is therefore useful in detecting spinal cord infarction, with axial T2-weighted images showing hyperintensities in the ASA territory in 15 of 16 patients. Contrary to the presumed spinal cord watershed at the lower cervical and upper thoracic level, and despite numerous central arteries in the cervical cord, our data suggest a high ischemic vulnerability of the cervical spinal cord at level C2-C3.
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PMID:Spinal cord infarction: MR imaging and clinical features in 16 cases. 1238 37

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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