UMLS:C0599766 - FACTA Search

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Query: UMLS:C0599766 (functional recovery)
13,441 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Activation of areas of the health hemisphere seems to play a role in functional recovery from stroke. We studied cerebral blood flow changes during motor and mental activity in patients with cortical ischemic lesions. We simultaneously measured blood flow velocity in the two middle cerebral arteries of 45 patients with single cortical ischemic lesions and good functional recovery and of 16 healthy controls by means of bilateral transcranial Doppler ultrasonography during a 2-minute sequential thumb-to-finger opposition task, alternately performed with the right and left hands, and during a 1-minute word-fluency task. Twenty-five patients had left cortical lesions, 12 with previous motor deficit alone and 13 with associated motor deficit and Broca's aphasia. Twenty patients had right cortical lesions with previous motor deficit. With respect to baseline values, the increase of flow velocity in the middle cerebral artery contralateral to the hand performing the motor task was comparable in controls and patients, regardless of the side of the lesion and the hand (normal or recovered) involved in the task. During movement of the recovered hand, the increase of flow velocity in the ipsilateral middle cerebral artery was significantly greater (p < 0.001, two-way ANOVA) than the increase during movement of the normal hand in both controls and patients. During performance of the word-fluency task, the increase of flow velocity in the left middle cerebral artery was comparable in controls and patients.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Involvement of the healthy hemisphere in recovery from aphasia and motor deficit in patients with cortical ischemic infarction: a transcranial Doppler study. 747 74

This study was undertaken to determine the effect of dichloroacetate (DCA) on myocardial functional and metabolic recovery following global ischemia. Sixteen isolated rabbit hearts were subjected to 120 minutes of mildly hypothermic (34 degrees C) cardioplegic arrest with multi-dose, modified St. Thomas' cardioplegia. Following ischemia, hearts were reperfused with either a physiologic salt solution (PSS) as controls, (CON, N = 10), or PSS containing DCA (DCA, N = 6) at a concentration of 1 mmol/L. Functional and metabolic indices were determined at baseline and at 15, 30, and 45 minutes of reperfusion. Results were analyzed using analysis of variance (ANOVA, Sheffe F test) and significance was defined as P < 0.05. Functional recovery was significantly better in hearts reperfused with DCA. Developed pressure (DP) recovered to 62 +/- 4% of baseline in DCA hearts, compared to 37 +/- 8% in CON hearts. Recovery of dP/dt was also improved in DCA versus CON hearts (67 +/- 5 v 43 +/- 10%). Coronary blood flow was not different between groups either at baseline or during reperfusion, but myocardial oxygen consumption (MVO2) was increased in the DCA versus CON hearts (71 +/- 10% of baseline, v 51 +/- 19%). Diastolic compliance during reperfusion was improved in those hearts receiving DCA, as was myocardial mechanical use efficiency (DP/MVO2). Correction of myocardial tissue pH to baseline values was similar in both groups, indicating that the beneficial effect on functional recovery seen with DCA was not solely related to amelioration of acidosis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Dichloroacetate enhances myocardial functional and metabolic recovery following global ischemia. 820 12

Recent findings indicate that ischemia/reperfusion (IR) is associated with phospholipase C (PLC)-induced inositol 1,4,5-triphosphate production, as well as abnormal sarcoplasmic reticulum (SR) Ca2+ release. Therefore, we hypothesized that increased SR Ca2+ release may contribute to Ca2+ overload and myocardial stunning. Neomycin (NEO) was used to inhibit PLC, and sodium dantrolene (DAN) was used to inhibit myocardial SR Ca2+ release. The purposes of this study were (1) to determine if PLC inhibition would reduce IR-induced ventricular dysfunction, (2) to examine ventricular function during inhibition of SR Ca2+ release prior to ischemia, and (3) to examine the influence of SR Ca2+ release inhibition on post-IR ventricular function. Left ventricular developed pressure (DP) and +/- dP/dt of isolated crystalloid perfused rat heart (Langendorff apparatus) paced at 350 bpm were compared before and after global IR (38 degrees C, 20 min I, 40 min R) to assess functional recovery. PLC was inhibited with NEO (10 microM x 5 min prior to ischemia), and SR Ca2+ release was retarded with DAN (12.5 microM) in 0.05% DMSO (vehicle) infused for 3 min via the aortic cannula 13 min prior to ischemia. No effect on DP was observed during NEO or DAN infusion. NEO and DAN pretreatment each improved recovery of DP (% recovery +/- SEM) following IR: control, 46.5 +/- 5.1%; NEO + IR, 71.0 +/- 6.3%,* vehicle + IR, 44.4 +/- 2.9%; DAN + IR, 71.0 +/- 4.7%, *, # (*P < 0.05 vs control IR, #P < 0.05 vs vehicle + IR, ANOVA, Scheffe F test, n = 5 all groups). We conclude that SR Ca2+ release during IR contributes to myocardial stunning.
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PMID:Inhibition of sarcoplasmic reticulum calcium release reduces myocardial stunning. 836 Nov 66

The ATP-sensitive K+ channel (K[ATP] channel) has been implicated in the mechanism of ischemic preconditioning. We compared the protective effects of ischemic preconditioning and a highly selective K(ATP) channel opener, BMS 180448, in human myocardium. BMS 180448 was either used alone or in combination with the K(ATP) channel blocker glibenclamide. Human atrial trabeculae derived from the right atrial appendage were suspended in an organ bath, superfused with oxygenated Tyrode's solution at 37degrees C, and paced at 1 Hz. Experimental groups (n = 6 in each) were as follows: (1) control (C)--90 minutes hypoxic substrate-free perfusion at 3 Hz (simulated ischemia), followed by 120 minutes of reoxygenation with substrate at 1 Hz (reperfusion); (2) preconditioning (PC)--3 minutes simulated ischemia, 7 minutes reperfusion, followed by 90 minutes simulated ischemia and 120 minutes reperfusion; (3) BMS 180448 (BMS)--exposure to the drug for 5 minutes prior to 90 minutes simulated ischemia and 120 minutes reperfusion; (4) BMS 180448 + glibenclamide (BMS + G)--glibenclamide exposure for 10 minutes, and BMS for 5 minutes prior to 90 minutes simulated ischemia and 120 minutes reperfusion. Force of contraction prior to the commencement of the protocol was assigned the arbitrary value of 100%. Percentage recovery of contractile function at 120 minutes reperfusion was used as the endpoint. BMS (59.2 +/- 8.6%) and preconditioning (50.5 +/- 3.6% ) produced a similar degree of recovery of function at the end of 120 minutes of reperfusion; this was significantly different from the untreated control group (20.8 +/- 3.5%, p < 0.05, ANOVA). When glibenclamide was added prior to BMS, protection was lost (20.5 +/- 2.7%). In this human atrial preparation, a highly selective K(ATP) channel opener mimicked the protective effect of ischemic preconditioning. This protective effect of BMS was abolished by glibenclamide. These findings confirm that the mechanism of ischemic preconditioning in human muscle may be mediated via opening of the K(ATP) channel.
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PMID:Comparison of the protective effects of a highly selective ATP-sensitive potassium channel opener and ischemic preconditioning in isolated human atrial muscle. 931 Feb 76

The ATP-sensitive potassium channel (KATP channel) has been implicated in the mechanism underlying ischaemic preconditioning protection. This study based on human atrium compared the protective effects of ischaemic preconditioning with pre-operative nicorandil (a KATP channel opener with nitrate actions). We also examined the added effect of ischaemic preconditioning to that of nicorandil on ischaemic protection. The protective effects of other KATP channel openers devoid of nitrate actions were also examined. Atrial trabeculae harvested from patients undergoing routine myocardial revascularisation were divided on the basis of whether patients had been ingesting nicorandil orally preoperatively. Trabeculae were superfused with oxygenated Tyrode's solution and following stabilisation underwent 90 minutes simulated ischaemia followed by 120 minutes reoxygenation (n = 6 per group). Atrial trabeculae exposed to nicorandil underwent either no treatment (N), or ischaemic preconditioning (N + PC) using 3 minutes simulated ischaemia and 7 minutes reoxygenation prior to the 90 minutes simulated ischaemia. Similarly trabeculae not exposed to nicorandil underwent either no treatment, controls (C), or ischaemic preconditioning (PC). The experimental endpoint was recovery of contractile function presented as percentage baseline function. Further groups were examined using other KATP channels openers with and without ischaemic preconditioning. In the control group, following 120 minutes reoxygentation the recovery of function reached 28.8 +/- 3.5%. In contrast, exposure to nicorandil alone improved recovery of function (55.5% +/- 5.3) to a similar extent as PC (55.3% +/- 2.5) when compared to controls (p < 0.05, ANOVA). The addition of ischaemic preconditioning to nicorandil exposure abolished protection (29.7% +/- 3.1 ). Findings were confirmed using the other KATP channels openers. Clinically available nicorandil appears to afford ischaemic protection to isolated human atrial muscle. The addition of a short ischaemic episode to nicorandil exposure seems to completely abolish this protection. Although the mechanism underlying this effect remains unknown, we believe that this observation may have clinical implications.
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PMID:Ischaemic preconditioning may abolish the protection afforded by ATP-sensitive potassium channel openers in isolated human atrial muscle. 934 32

A detailed examination of the histopathological features of the clip compression injury in mice was performed to understand the relationships between neurological function and existing pathology of the spinal cord. Adult, female CD1 mice underwent three grades of extradural clip compression injury (3-g, 8-g, and 24-g FEJOTA mouse clips), transection, and sham injury at T3-4. Quantitative behavioural assessments were performed for 4 weeks following SCI. After 4 weeks, Fluoro-Gold was introduced caudal to the SCI site, at T9, and was retrogradely transported for 5 days to the origin of spared axons through the injury site. Counts of retrogradely labeled neurons in the brain-stem, midbrain, and sensory-motor cortex indicated that the number of intact descending axons that traversed the lesion decreased with increasing injury severity (F > 28; df = 4; p < 0.0001; one-way ANOVA). Independent linear correlation analyses were performed between indices of neurological recovery (BBB and IP test), counts of retrogradely labeled neurons and morphometric assessments of normal residual tissue at the injury epicenter. The BBB test correlated strongly with the amount of residual tissue at the injury epicenter (R = 0.945, df = 28, p < 0.0001). Counts of neurons retrogradely labeled with Fluoro-Gold were also strongly correlated with the BBB scores. The extrapyramidal (raphespinal, reticulospinal, vestibulospinal, and rubrospinal) tracts had Pearson correlation coefficients (R) of 0.814, 0.812, 0.813, and 0.747, respectively (df = 28, p < 0.0001). The pyramidal (corticospinal) tract had a correlation of R = 0.747, df = 28, p < 0.0001 with the BBB scores. The IP scores also correlated strongly with the persistence of extrapyramidal (raphespinal, reticulospinal, vestibulospinal and rubrospinal) tracts with correlation coefficients of 0.801, 0.782, 0.790, and 0.836, respectively (df = 28, p < 0.0001). These data indicate that the counts of retrogradely labeled neurons at the origin of distinct descending motor pathways are predictors of the variance of the functional recovery measured by the BBB and IP tests following spinal cord injury. In addition, we provide a detailed neuroanatomical study of clip compression injury in mice that can be used to study the molecular mechanisms of SCI in knockout and transgenic mice.
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PMID:Development and characterization of a novel, graded model of clip compressive spinal cord injury in the mouse: Part 2. Quantitative neuroanatomical assessment and analysis of the relationships between axonal tracts, residual tissue, and locomotor recovery. 1189 22

Secondary injury following traumatic spinal cord injury is induced by the activation of a number of cellular and molecular changes. RhoA, a small GTPase, regulates the organization of the actin cytoskeleton, gene expression, cell proliferation, and has been implicated in the regenerative process. This study was undertaken to investigate the involvement of the RhoA signaling pathway in the secondary injury that follows traumatic spinal cord injury in rats. RhoA mRNA and protein expressions were enhanced significantly in the injured spinal cord 1 week after surgery (P<0.05, ANOVA). C3 exozyme (RhoA inhibitor), Y-27632 (selective Rho kinase inhibitor), and Fasudil (non-selective protein kinase inhibitor) were administered after spinal cord injury, and the subjects were evaluated for 5 weeks as per BBB locomotor score. Poor rat response interrupted the C3 experiment. Y-27632 slightly, but significantly (P<0.05, ANOVA), delayed the recovery. Fasudil significantly improved the BBB score (P<0.05, ANOVA). In conclusion, spinal cord injury activates the RhoA/Rho-kinase alpha, beta associated pathway. However, their role in secondary injury or in the improvement of functional recovery remains unclear. Fasudil might exert a cytoprotective effect by mechanisms other than inhibiting Rho-kinase alpha, beta.
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PMID:A possible role of RhoA/Rho-kinase in experimental spinal cord injury in rat. 1248 Jan 55

Recently, locomotor training has been shown to improve overground locomotion in patients with spinal cord injury (SCI). This has triggered renewed interest in the role of exercise in rehabilitation after SCI. However, there are no mouse models for voluntary exercise and recovery of function following SCI. Here, we report voluntary wheel running improves recovery from a SCI in mice. C57Bl/10 female mice received a 60-kdyne T9 contusion injury with an IH impactor after 3 weeks of voluntary wheel running or 3 weeks of standard single housing conditions. Following a 7-day recovery period, running mice were returned to their running wheels. Weekly open-field behavior measured locomotor recovery using the Basso, Beattie and Bresnahan (BBB) locomotor rating scale and the Basso Mouse Scale (BMS) locomotor rating scale, a scale recently developed specifically for mice. Initial experiments using standard rung wheels show that wheel running impaired recovery, but subsequent experiments using a modified flat-surface wheel show improved recovery with exercise. By 14 days post SCI, the modified flat-surface running group had significantly higher BBB and BMS scores than the sedentary group. A repeated measures ANOVA shows locomotor recovery of modified flat-surface running mice was significantly improved compared to sedentary animals (p < 0.05). Locomotor assessment using a ladder beam task also shows a significant improvement in the modified flat-surface runners (p < 0.05). Finally, fibronectin staining shows no significant difference in lesion size between the two groups. These data represent the first mouse model showing voluntary exercise improves recovery after SCI.
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PMID:Voluntary wheel running improves recovery from a moderate spinal cord injury. 1566 10

A study of the effect of weak, interrupted sinusoidal low frequency magnetic field (ISMF) stimulation on regeneration of the rat sciatic nerve was carried out. In the experiment, 60 Wistar rats were used: 24 rats underwent unilateral sciatic nerve transection injury and immediate surgical nerve repair, 24 rats underwent unilateral sciatic nerve crush injury, and the remaining 12 rats underwent a sham surgery. Half of the animals (n = 12) with either sciatic nerve lesion were randomly chosen and exposed between a pair of Helmholtz coils for 3 weeks post-injury, 4 h/day, to an interrupted (active period to pause ratio = 1.4 s/0.8 s) sinusoidal 50 Hz magnetic field of 0.5 mT. The other half of the animals (n = 12) and six rats with sham surgery were used for two separate controls. Functional recovery was followed for 6 weeks for the crush injuries and 7(1/2) months for the transection injuries by video assisted footprint analysis in static conditions and quantified using a recently revised static sciatic index (SSI) formula. We ascertained that the magnetic field influence was weak, but certainly detectable in both injury models. The accuracy of ISMF influence detection, determined by the one-way repeated measures ANOVA test, was better for the crush injury model: F(1, 198) = 9.0144, P = .003, than for the transection injury model: F(1, 198) = 6.4826, P = .012. The Student-Newman-Keuls range test for each response day yielded significant differences (P < .05) between the exposed and control groups early in the beginning of functional recovery and later on from the points adjacent to the beginning of the plateau, or 95% of functional recovery, and the end of observation. These differences probably reflect the ISMF systemic effect on the neuron cell bodies and increased and more efficient reinnervation of the periphery.
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PMID:Effect of weak, interrupted sinusoidal low frequency magnetic field on neural regeneration in rats: functional evaluation. 1588 58

Statins exert beneficial effects in brain diseases including stroke. Here, we investigated whether oral prophylactic atorvastatin provides long-term neuroprotection and functional recovery in permanent middle cerebral artery occlusion (pMCAO), and whether cerebral hemodynamics are affected. Male Long-Evans rats were treated with 10 mg/kg oral atorvastatin for 14 days and subjected to pMCAO. Cerebral hemodynamics were measured by bolus tracking MRI and laser Doppler flowmetry (LDF). Infarct volume was quantified at 1 week by T2-MRI and at 3 weeks by histology. Rats were also subjected to neuroscoring and cylinder test. The number of animals per group was 10. The infarct volumes were 100.8 +/- 8.2 and 47.3 +/- 5.5 mm(3) in vehicle, and 68.7 +/- 11.0 and 28.6 +/- 3.82 mm(3) in atorvastatin group at 7 and 21 days post-ischemia, respectively (mean +/- SEM). Atorvastatin significantly reduced infarct volume both at 7 and 21 days (P = 0.04 and 0.03, respectively, 1-way ANOVA). Interestingly, no improvement in cerebral hemodynamic parameters was observed in atorvastatin treated animals. The vehicle group recovered normal neuroscore at day 13, whereas atorvastatin group recovered already at day 10 after pMCAO. All treatment groups preferred to use the unaffected forelimb for rearing in Cylinder test, whereas the defected forelimb use was minimal in all groups. These results suggest that oral atorvastatin protects cerebral tissue against the subsequent pMCAO without influencing cerebral hemodynamic parameters, and it may well be that persons with ongoing atorvastatin treatment benefit in the incidence of stroke.
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PMID:Long-term protective effect of atorvastatin in permanent focal cerebral ischemia. 1602 89

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