Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0599766 (functional recovery)
 13,441 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Temperature is known to influence the extent of anoxic/ischemic injury in gray matter of the brain. We tested the hypothesis that small changes in temperature during anoxic exposure could affect the degree of functional injury seen in white matter, using the isolated rat optic nerve, a typical CNS white matter tract (Foster et al., 1982). Functional recovery after anoxia was monitored by quantitative assessment of the compound action potential (CAP) area. Small changes in ambient temperature, within a range of 32 to 42 degrees C, mildly affected the CAP of the optic nerve under normoxic conditions. Reducing the temperature to < 37 degrees C caused a reversible increase in the CAP area and in the latencies of all three CAP peaks; increasing the temperature to > 37 degrees C had opposite effects. Functional recovery of white matter following 60 min of anoxia was strongly influenced by temperature during the period of anoxia. The average recovery of the CAP, relative to control, after 60 min of anoxia administered at 37 degrees C was 35.4 +/- 7%; when the temperature was lowered by 2.5 degrees C (i.e., to 34.5 degrees C) for the period of anoxic exposure, the extent of functional recovery improved to 64.6 +/- 15% (p < 0.00001). Lowering the temperature to 32 degrees C during anoxic exposure for 60 min resulted in even greater functional recovery (100.5 +/- 14% of the control CAP area). Conversely, if temperature was increased to > 37 degrees C during anoxia, the functional outcome worsened, e.g., CAP recovery at 42 degrees C was 8.5 +/- 7% (p < 0.00001). Hypothermia (i.e., 32 degrees C) for 30 min immediately following anoxia at 37 degrees C did not improve the functional outcome. Many processes within the brain are temperature sensitive, including O2 consumption, and it is not clear which of these is most relevant to the observed effects of temperature on recovery of white matter from anoxic injury. Unlike the situation in gray matter, the temperature dependency of anoxic injury cannot be related to reduced release of excitotoxins like glutamate, because neurotransmitters play no role in the pathophysiology of anoxic damage in white matter (Ransom et al., 1990a). It is more likely that temperature affects the rate of ion transport by the Na(+)-Ca2+ exchanger, the transporter responsible for intracellular Ca2+ loading during anoxia in white matter, and/or the rate of some destructive intracellular enzymatic mechanism(s) activated by pathological increases in intracellular Ca2+.
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PMID:Effects of temperature on evoked electrical activity and anoxic injury in CNS white matter. 140 Jun 52

The effect of the xanthine derivative propentofylline (HWA 285) on metabolic and functional recovery in rabbit spinal cord after 20 and 30 min ischemia and 4 days of reperfusion was investigated. Pre-treatment with 20 mg/kg significantly improved recovery of the energy state in the spinal cord, however, without significant functional recovery of hindlimbs. In contrary, post-treatment with HWA 285 recovered the energy state to pre-ischemic value and also significantly improved functional recovery. These findings suggest that the neuroprotective mechanism of HWA 285 in the spinal cord is not associated with inhibition of glutamate release as supposed to operate in the gerbil brain.
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PMID:Amelioration of ischemic spinal cord damage by postischemic treatment with propentofylline (HWA 285). 142 40

Glutamate, aspartate, GABA, glycine and taurine levels have been measured in rat thalamus and in cerebral cortex at different time intervals (3rd, 7th, 15th, 30th day) after cerebellectomy. A decrease in glutamate, aspartate and GABA was detected at the 7th day after cerebellectomy in the thalamus and at the 15th day in the cerebral cortex; at the 30th day after cerebellectomy the levels of these amino acids in the thalamus and in the cerebral cortex were observed to have recovered to control values. No statistically significant difference in glycine and taurine levels in the thalamus and in the cerebral cortex after cerebellectomy could be seen. These results show that the functional recovery process after cerebellar injury is associated with a complex modification of amino acid levels in thalamus and in cerebral cortex.
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PMID:Neurotransmitter amino acid levels in rat thalamus and cerebral cortex after cerebellectomy. 168 98

Explanted rat hearts were subjected to cardioplegic arrest by 3 minutes' perfusion with oxygenated St. Thomas' Hospital solution no. 2 and then were stored by immersion in the same solution at 4 degrees C. Prearrest and postischemic left ventricular functions were compared by means of an isolated working heart apparatus. Hearts (n = 8 per group) arrested and stored for up to 8 hours all resumed the spontaneous rhythm of contraction during reperfusion for 30 minutes at 37 degrees C. There was good recovery of aortic flow rate (105% +/- 3%) against a pressure of 100 cm H2O, of heart rate (102% +/- 2%), and of aortic pressure (86% +/- 5% of prearrest values). Hearts stored for 10 and 20 hours showed poor or no postischemic recovery of cardiac pump function (aortic flow, 16% +/- 11% and 0%, respectively). Enrichment of St. Thomas' Hospital solution with L-glutamate (20 mmol/L) also failed to improve functional recovery of hearts subjected to 10 hours of storage, but hearts treated with St. Thomas' Hospital solution containing L-aspartate (20 mmol/L) or L-aspartate plus L-glutamate (20 mmol/L each) reestablished aortic flow rates of 99% +/- 5% and 93% +/- 4%, respectively. These results indicate that the addition of L-aspartate to St. Thomas' Hospital solution improves the functional recovery and extends the safe preservation of explanted hearts stored at 4 degrees C.
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PMID:L-aspartate improves the functional recovery of explanted hearts stored in St. Thomas' Hospital cardioplegic solution at 4 degrees C. 230 69

The common practice of using alkalotic cardioplegic solutions is not supported by experimental evidence. The present study was conducted to assess the effects of varying the pH (7.00, 7.40, and 7.70 at 20 degrees C) of a glutamate-containing cardioplegic solution on intracellular pH, high-energy phosphate content, and postarrest functional recovery and to compare the effects of various buffers (glutamate, bicarbonate, TRIS, and histidine) at a given pH (7.00 and 7.40). Isolated perfused rat hearts were subjected to 2 hours of cardioplegic arrest at 15 degrees C followed by 30 minutes of reperfusion. Intracellular pH and high-energy phosphate content were measured at 4 minute intervals by phosphorus 31 nuclear magnetic resonance spectroscopy. These data were correlated with postischemic recovery of function. There was no significant difference between the intracellular pH values recorded at the end of arrest in the three glutamate-containing groups. However, the acidotic solution (pH 7.00) resulted in better preservation than the alkalotic solution (pH 7.70), as evidenced by a higher creatine phosphate content at the end of arrest (61% +/- 9% of control values versus 30% +/- 9% [mean +/- standard error of the mean], p less than 0.05), a higher adenosine triphosphate content at the end of reperfusion (102% +/- 5% versus 82% +/- 6%, p less than 0.05), and a faster recovery of aortic flow (at 3 minutes of reperfusion, 91% +/- 11% versus 51% +/- 11%, p less than 0.05). Subsequent comparison of buffers showed that bicarbonate, TRIS, and histidine were equally effective in maintaining intracellular pH close to control values during arrest. Conversely, the use of glutamate resulted in a more pronounced fall in intracellular pH, which correlated with a better preservation of adenosine triphosphate and a better functional recovery than in the other groups. Overall, the greatest extent of preservation was provided by the pH 7.00 glutamate-containing cardioplegic solution. We conclude that additional protection can be conferred to the cold, chemically arrested heart by combining mild intracellular acidosis, which lowers metabolic needs during arrest, most likely through a limitation of calcium overload, and provision of glutamate, which may act as a substrate for anaerobic energy production while allowing intracellular pH to be kept within the appropriate range.
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PMID:Influence of the pH of cardioplegic solutions on intracellular pH, high-energy phosphates, and postarrest performance. Protective effects of acidotic, glutamate-containing cardioplegic perfusates. 241 Jul 46

Using 31P-NMR and haemodynamical measurements, this work assesses different aspects of myocardial preservation improvement during a global ischaemia, based on a simultaneous and correlated study of high-energy phosphorylated compounds, intracellular pH and left ventricular function. Isolated perfused working rat hearts were subjected to 2 or 3 h of hypothermic ischaemia followed by 30 or 45 min of reperfusion. A study of the influence of pH and buffer used in cardioplegic solutions has demonstrated a better preservation of high-energy phosphates and an improved functional recovery when using a pH 7.0, glutamate - containing solution. Protection provided by cardioplegia can be enhanced by the appropriate use of a fluorocarbon-oxygenated cardioplegic reperfusate. The use of nifedipine, a calcium antagonist, in the cardioplegic solutions, does not provide any additional protection under hypothermic conditions.
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PMID:31P-NMR study of high-energy phosphorylated compounds metabolism and intracellular pH in the perfused rat heart. 242 95

This study tests the hypothesis that failure to minimize left ventricular oxygen demands by venting during reperfusion diminishes recovery after controlled blood cardioplegic reperfusion. Of 25 dogs undergoing 2 hours of left anterior descending coronary occlusion, nine were reperfused with normal blood without bypass and five were reperfused with normal blood during total vented bypass. Eleven other dogs were reperfused with aspartate-glutamate-enriched, diltiazem-supplemented blood cardioplegic solution for 20 minutes during cardiopulmonary bypass; the left ventricle was decompressed by venting in only five of them. Regional systolic shortening was measured by ultrasonic crystals and myocardial damage estimated from triphenyltetrazolium chloride staining. All segments developed systolic bulging during ischemia (-23% systolic shortening, p less than 0.05), with no segmental recovery after reperfusion with normal blood without bypass (-27% systolic shortening, p less than 0.05) and negligible recovery following reperfusion with normal blood during total vented bypass (6 +/- 2%, p less than 0.05). In contrast, there was immediate recovery of regional contractility (+ 53% systolic shortening, p less than 0.05) in bypassed hearts reperfused with aspartate-glutamate-enriched, diltiazem-supplemented blood cardioplegic solution when venting was used and triphenyltetrazolium chloride nonstaining fell from 43% to 12% (p less than 0.05). Conversely, there was no postischemic recovery (-8% systolic shortening, p less than 0.05) when the same blood cardioplegic reperfusate was given over a comparable time without venting; triphenyltetrazolium chloride damage increased to 25% (p less than 0.05). Minimizing O2 demands by left ventricular decompression with venting during blood cardioplegic reperfusion is essential to ensure immediate functional recovery and limit histochemical damage.
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PMID:Reperfusion conditions: critical importance of total ventricular decompression during regional reperfusion. 287 23

A variety of putative neurotransmitters has been described in the red nucleus (RN). Measurement of neurotransmitter biochemical markers and study of their specific localizations using morphological techniques in lesion and deafferentation of the RN indicate the participation of glutamate (Glu) in corticorubral transmission and the presence of GABA in RN intrinsic neurones. The cerebellorubral projection may contain at least two populations of fibres, the one using acetylcholine and the other Glu as neurotransmitter. The presence of a serotoninergic input was also demonstrated. Selective deafferentations of the RN, particularly from its cerebellar input, result in biochemical and immunohistochemical responses indicative of increased corticorubral glutamatergic and local GABAergic transmission. These adaptive changes of neuronal transmission as well as the previously described sprouting of corticorubral nerve terminals may contribute to functional recovery after cerebellectomy in adult animals.
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PMID:Putative neurotransmitters in the red nucleus and their involvement in postlesion adaptive mechanisms. 289 48

The objective of the present study was to analyze the anatomical basis of the A5 depressor response and to test if the putative neurotransmitter noradrenaline is involved in the response. Two approaches were used; one was neuroanatomical and the other was pharmacological. First, the retrograde transport method in which two fluorescent markers (Fast blue and rhodamine microspheres) was used in combination with the indirect immunofluorescence technique to establish that A5 catecholamine neurons project to both the spinal cord and the region of the nucleus tractus solitarii (NTS). Second, we analyzed the effects of 6-hydroxydopamine (6-OHDA) lesions of the spinal cord and/or NTS area on the A5 depressor response. This response was elicited by a 80-nl microinjection of L-glutamate (500 mM) into the A5 region in pentobarbital anesthetized rats; it was characterized by a decrease in blood pressure and heart rate. After destruction of various noradrenergic terminal fields we have found that intraspinal injections of 6-OHDA caused a 30% reduction in the blood pressure component of the A5 depressor response and a transient depression of the bradycardic response. This result suggests that only a small portion of the A5 depressor response depends on the descending A5 spinal pathway. Injections of 6-OHDA into the NTS region caused a transient depression of the A5 depressor response, and by 7-14 days postinjection, the response returned to normal. After combined 6-OHDA injections into the spinal cord and NTS area, the blood pressure and heart rate components of the A5 depressor response were reduced to 80% of the control level at 3 days postinjection. By 14 days, even with severe depletion of noradrenaline in the spinal cord (96%) and a moderate depletion of noradrenaline in the NTS (50%), the A5 response was restored to about 80% of its original magnitude, suggesting some type of functional recovery occurs in this system. Third, the blood pressure decrease elicited by L-glutamate stimulation of the A5 cell group was unaffected by pharmacological blockade of the heart. In addition, this response appeared to be normal in rats that had both their autonomic supply to the heart blocked pharmacologically and their spinal cord noradrenaline levels depleted (14 days after intraspinal 6-OHDA injections). These data suggest that the major A5 depressor response operates mainly by inhibition of the sympathetic outflow involved in control of total peripheral resistance and that this system is controlled by a descending spinal pathway which probably does not use noradrenaline as a neurotransmitter.
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PMID:Descending noradrenergic pathways involved in the A5 depressor response. 309 95

Transient global amnesia has been explained by epileptic mechanisms or transient ischemic attacks affecting the hippocampus. None of these two mechanisms appear likely. The animal experimental phenomenon entitled spreading depression of cortical electrical activity (SD) or spreading depression of Leao has been implicated in migraine pathogenesis and may be relevant to transient global amnesia. In experimental animals, SD in the hippocampus causes a temporary functional ablation lasting minutes to hours with full functional recovery. Glutamate, which is present in large amounts in the hippocampus, may experimentally elicit spreading depression, and strong emotional events may possibly liberate glutamate and bring about this reaction in human patients.
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PMID:Leao's spreading depression in the hippocampus explains transient global amnesia. A hypothesis. 370 31


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