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)

EEG and somatosensory evoked potentials were recorded in anesthetized rats before and up to 24 h after 30 min of global forebrain ischemia. Before ischemia, SEP (sweep time 1000 ms) included primary (N25P50) components and late potentials of low amplitude. During ischemia, SEP and EEG were isoelectric. During postischemic recirculation SEP evoked by stimulation at 1.0 Hz remained severely suppressed for 24 h, although long-latency potentials (> 100 ms) recovered. Using a very low stimulation frequency of 0.1 Hz, late components strongly increased in amplitude and the overall evoked activity in the averaged post-stimulus-EEG reached 90% of control. These results demonstrate that the SEP evoked at very low stimulation frequency may serve as an early indicator of functional brain recovery after prolonged cerebro-circulatory arrest.
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PMID:[Evoked potentials following cerebral ischemia in the rat: the effect of the stimulus frequency]. 142 91

The effects of endothelin 1 (ET-1; 300 pmol/rat intracarotid) on somatosensory evoked potential were investigated in rats. ET-1 led to an amplitude reduction, peak latency prolongations and waveform disturbances. There was a large interindividual variability. The late cortical components were more affected than the earlier potentials at a thalamic or cortical level. ET-1-induced SEP changes developed quickly after the drug injection and persisted for at least 30 min. It is assumed that the observed effects probably reflect the occurrence of a progressively developing ischemia subsequent to ET-1 administration. Moreover, the pattern of ET-1-induced changes suggests a greater sensitivity of the synaptic transmission to the ischemic influence than the axonal conduction.
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PMID:Effect of endothelin on somatosensory evoked potentials in rats. 147 35

Postoperative paraplegia is a relatively rare complication in reconstructive surgery for coarctation of the aorta and the operative treatment is usually performed without any adjuncts. A 59-year-old male patient underwent replacement of descending thoracic aorta with vascular prosthesis under the monitoring of SEP and spinal cord perfusion pressure (SCPP) [pressure difference between mean distal aortic pressure (MDAP) and the cerebrospinal fluid pressure (CSFP)]. During cross-clamping of the aorta, MDAP decreased from 61 to 40 mmHg and CSFP increased from 6 to 15 mmHg, SCPP was 25 mmHg, and the amplitude of the SEP waves rapidly decreased. As the ischemic changes of spinal cord were suspected, the aortic cross-clamping was released. The amplitude of SEP recovered to the preoperative level immediately after de-clamping. In order to prevent spinal cord ischemia, the partial cardio-pulmonary bypass was employed, and SCPP was maintained above 60 mmHg, so that SEP did not show any ischemic changes during cross-clamping of the aorta. The patient did not develop any neurological deficit postoperatively. The monitoring of SEP and SCPP appears to be useful for prevention of postoperative paraplegia in the surgical treatment for coarctation of the aorta.
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PMID:[Reconstructive surgery in 59-year-old patient with coarctation of aorta under the monitoring of somatosensory evoked potential and spinal cord perfusion pressure]. 156 47

The feline infusion model of brain edema was used to evaluate the role of bradykinin in the etiology and pathophysiology of vasogenic brain edema. Bradykinin (3 or 90 ug in 600 microL saline) did not alter normocapnic regional cerebral blood flow (rCBF) nor induce specific changes in either the somatosensory (SEP) or motor (MEP) evoked potentials. The mean increases in ICP (from 4.5 to 16.1 mmHg) and peri-infusion white matter water content (from 69.4 to 79.8 ml/100 g tissue), mean decrease in lumped craniospinal compliance (from 0.040 to 0.014 ml/mmHg) and local histological changes were all similar to those after 600 microL saline infusion. The interstitial bradykinin infusion caused focal blood-brain-barrier (BBB) opening to Evans Blue dye and was chemotaxic for granulocytes. After the infusion there was a global loss of rCBF CO2 reactivity but there was no ischemia at normocapnia. These results show that bradykinin in brain edema fluid, at concentrations greater than those found in neuropathological conditions, can open the BBB of normal cerebral parenchymal capillaries and cause vascular dysregulation. In neuropathological conditions bradykinin may therefore potentiate formation of vasogenic brain edema but does not contribute to perilesional brain dysfunction.
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PMID:The role of bradykinin in the etiology of vasogenic brain edema and perilesional brain dysfunction. 159 96

A model of cerebral ischemia by microsphere embolization in the rabbit was monitored with somatosensory evoked potentials by median nerve stimulation (SEPs) and by flash visual evoked potential (VEPs). The degree of SEP alterations paralleled the type of lesions (focal or multifocal ischemia or diffuse oedema). Alterations present at the first hour after ischemia were generally unchanged during the follow-up, which ended at the 24th hour. The prevalence of VEP alterations was low (only 16% in focal ischemia). These results are compared to EEG modifications performed in the same animals.
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PMID:Evoked potentials monitoring of a cerebral focal ischemia model. 175 17

Several authors have demonstrated a correlation between short latency somatosensory evoked potentials (short latency SEPs) and cerebral blood flow (CBF). It is also known that ischemia may modify the amplitude of the cortical SEP while its latency is less sensitive to CBF fluctuations. Phychotropic drugs--Oxiracetam, SAMe, Naloxone, L-acetylcarnitine and GM1--affect some parameters of the early components of cortical SEPs, chiefly the amplitude, which makes SEP recording a useful method for monitoring pharmacological activity in acute stroke.
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PMID:Effects of psychotropic drugs on somatosensory evoked potentials in cerebral ischemia. 187 7

SEP (somatosensory evoked potential) monitoring was carried out on seven patients with vertebro-basilar aneurysms during balloon occlusion test, during operation, or after operation. In the patient (case 5) with basilar tip aneurysm, the amplitude of N20 remarkably decreased and this finding closely correlated with disturbed consciousness during transient balloon occlusion of the basilar artery. In another patient (case 6) with vertebral dissecting aneurysm, cerebellar retraction caused transient prolongation of N20 latency during operation. In another case, postoperative SEP monitoring revealed marked reduction of N20 amplitude in the patient (case 7) who showed disturbed consciousness and bilateral oculomotor palsy after operation for basilar aneurysms, but who showed no abnormality in postoperative ABR (auditory evoked brainstem response). The other four patients showed no neurological deterioration and no SEP change during transient balloon occlusion of the parent arteries. Because of the high rate of "false-negative" findings, it remains unclear whether SEP monitoring during surgery for vertebrobasilar aneurysms is of value to predict postoperative deficit due to brainstem ischemia. In our study, however, the changes of SEP were well correlated with neurological deterioration and/or the location of postoperative infarction. In conclusion, SEP monitoring during balloon occlusion tests or operations for vertebro-basilar aneurysms is considered to be useful in predicting ischemic complication of the brainstem caused by the occlusion of the parent artery. However other methodologies have to be developed in order to monitor the pyramidal tract and reticular activating system of the brainstem more accurately.
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PMID:[SEP monitoring during balloon occlusion test or operation for vertebro-basilar aneurysms]. 204 48

Dazoxiben, a selective TXA2 synthetase inhibitor, was studied in the incubating sections of porcine basilar arteries with arachidonic acid (AA) 50 mumols/L and calcimycin (calcium inophore A-23187) 50 mumol/L. TXB2 and 6-keto-PGF1 alpha were determined by radioimmunoassay. Leukotrienes (LT) were extracted and purified with SEP-PAK column, identified by HPLC and determined by bioassay with ileum of guinea pig. The results showed that the production of TXB2 was unaltered whether or not the incubation of arteries were induced by AA or calcimycin. Dazoxiben and indomethacin 0.05-50 mumols/L had no effects on the production of TXB2. However, dazoxiben 0.5, 5 and 50 mumols/L increased the production of 6-keto-PGF1 alpha by 16.3%, 19.0% and 30.7%, respectively. Indomethacin 0.5, 5 and 50 mumols/L decreased the production of 6-keto-PGF1 alpha by 22.3%, 24.9% and 24.0%, respectively. Meanwhile dazoxiben 1, 10 and 100 mumols/L decreased the production of LT by 33.4%, 45.6% and 66.4%, respectively. These results suggest that the protective effect of dazoxiben on the damages which resulted from brain ischemia may be related to the change of TAX2/PGI2 balance in the brain tissue as well as the inhibition of production of LT.
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PMID:[Effect of dazoxiben on the metabolism of arachidonic acid in isolated porcine basilar arteries]. 212 32

Twenty hogs were administered the following procedures before, during, and after overdistraction of the spinal column at T5-T6: somatosensory (SEP) and neurogenic-motor evoked potentials (NMEPs), hydrogen clearance procedures, Stagnara wake-up tests, and aortic-injection of silastic plastic. To ensure that overdistraction was possible, a nonosseous, circumferential osteotomy was made at T5-T6 and distraction applied in one-ratchet increments using Harrington instrumentation. Overdistraction was maintained for 3, 5, 6, 10, 15, 20, 25, or 30 minutes. Results indicated that the duration of overdistraction, as represented by lost NMEPs, was always correlated with the animal's clinical status on wake-up test. If overdistraction was maintained more than 6 minutes, 100% of the animals demonstrated positive wake-up results; if maintained between 5 and 6 minutes, 75% demonstrated positive wake-up results; and if maintained less than 5 minutes, only 25% demonstrated positive wake-up results. Time-to-loss of the NMEPs and SEPs, after onset of overdistraction, fell within two groups: slow and fast. In the slow group, it required slightly more than 20 minutes (mean = 20.6) for the potentials to be lost, while in the fast-loss group data were lost in slightly less than 4 minutes (mean = 3.6). Blood flow studies and inspection of the spinal cord revealed that the mechanism of action for the slow group appeared to be ischemia of the spinal cord that extended several centimeters above and below the site of maximum distraction. In the fast-loss group, it appeared that gross structural damage, with some very localized ischemia, were the mechanisms of actions influencing the integrity of the spinal cord.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Relationship between duration of spinal cord ischemia and postoperative neurologic deficits in animals. 221 5

Paraplegia secondary to spinal cord ischemia is a too frequent devastating complication of thoracic aneurysm surgery. We examined the ability of veno-arterial bypass (VAB) to ensure adequate spinal cord blood flow during aortic cross-clamping by monitoring spinal cord function via somatosensory evoked potentials (SEP's) and postoperative motor function. Dogs were placed on VAB using a heparin-bonded roller pump circuit without systemic heparinization. SEP latency and amplitude were monitored continuously. The respirator FIO2 was set at 100% while the aorta was cross-clamped for one hour with the bypass adjusted to keep distal arterial pressure at greater than 60 mmHg. After one hour the aorta was unclamped, bypass discontinued, and the animals recovered. SEP's were always present during VAB as long as the distal pressure was kept at greater than 60 mmHg. There were several transient hypotensive episodes (less than 5 min) which were accompanied by reversible loss of SEP's. None of the animals displayed any gait abnormalities post-op. These findings using this simple bypass technique suggest the following conclusions: (1) SEP's degenerate (increased latency and decreased amplitude) in response to hypoxia; (2) spinal cord function can be maintained for up to one hour during hypoxic conditions; (3) SEP's can be used to monitor sensory spinal cord function under these conditions; and (4) heparinless VAB can provide spinal cord protection while also allowing monitoring of SEP's to ensure adequate spinal cord perfusion.
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PMID:Preservation of spinal cord function and prevention of paralysis during aortic occlusion via veno-arterial bypass. 292 82


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