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)

The effects of calmodulin antagonists trifluoperazine (TFP) and calmidazolium (CMZ) and of ethmozine (a phenothiazine without anticalmodulin activity) on the postischemic recovery in the perfused working rat hearts were studied. In the hearts subjected to 25 min zero-flow ischemia coronary flow, cardiac output, MVO2 and external work recovered to about 50% of the preischemic values during 40 min of reperfusion. TFP (5 x 10(-7) M and 10(-6) M) or CMZ (10(-7) M) improved the functional recovery to 75-94% whereas 5 x 10(-7) M ethmozine was not effective. In all experimental groups a prolongation of the ischemic period caused a progressive deterioration of the functional recovery while the total postischemic LDH release showed an initial gradual rise followed by a later decay. TFP and CMZ prolonged the time-to-half decay of the hemodynamic functions (tHF50) by 4-7 min and the time-to-peak of total LDH release (tLDHmax) by 5-10 min. In the hearts subjected to 0.2 ml/min low-flow ischemia tHF50 and tLDHmax were increased to 40 min, CMZ prolonged these times by further 5-10 min. Thus, TFP and CMZ delayed the development of the myocardial ischemic injury. Although other interpretations are possible, our data are consistent with the hypothesis that calmodulin-sensitive process is involved in the ischemic damage of the myocardium.
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PMID:Antagonists of calmodulin delay injury development in the severely ischemic perfused working rat heart. 307 8

The effect of ATP-MgCl2 treatment was investigated on the biochemical changes of preserved kidneys and on the functional recovery of hypoxically damaged and autotransplanted canine kidneys. We observed that ATP-MgCl2 administered before or during simple hypothermic storage did not protect the integrity of preserved kidney cells, as measured by enzyme wash-out (LDH and NAG) or by lactate release. If the compound was administered after 120 min or 180 min clamping of the renal artery, the solitary kidney showed a faster regeneration as measured by changes in serum creatinine level. The survival rates were significantly higher in the treated groups. Without warm ischemia of the kidney all of the autotransplanted dogs survived after surgery. After 60 min of warm ischemia the mortality rate was 100%, and the mean survival time in average 5 days. If ATP-MgCl2 was administered after the 60 min of warm ischemia, an improved recovery of the graft function was observed
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PMID:Effect of ATP-MgCl2 treatment on kidney preservation and on recovery of graft function. 701 Apr 79

The use of salicylate as a chemical trap for .OH represents a simple and convenient alternative to the use of spin trapping techniques to study oxidative injury in isolated perfused organs. In these systems, salicylate is included in the perfusion buffer at concentrations ranging from 0.1 to 2 mM depending on the detection apparatus employed. In our studies, we have used a coulometric detector, which has a theoretical efficiency of 100% as compared to 1-5% for the standard glassy carbon electrode. We have been able to generate reproducible results by inclusion of only 100 microM salicylate, a concentration demonstrated not to affect pre- or post-ischemic cardiac function. In initial studies, we observed an increase in perfusate 2,5-dihydroxybenzoic acid consistent with an early post-ischemic burst of .OH, not unlike that reported using spin trapping techniques. Since then we and others have used this technique to examine possible relationships between .OH formation and treatments that alter post-ischemic cardiac functional recovery. For example, preischemic loading of hearts with copper results in increases in post-ischemic dysfunction and LDH release that were associated with an increase in 2,5-dihydroxybenzoate and by inference, .OH formation. Alternatively, we have reported that the nitroxide spin label, TEMPO, reputed to be a superoxide dismutase mimetic, decreased post-ischemic arrhythmias and 2,5-dihydroxybenzoate formation. Most recently, we have observed that preischemic loading of hearts with zinc-bis-histidinate results in improved post-ischemic cardiac function and decreased LDH release; changes that were associated with decreased 2,5-dihydroxybenzoate formation. These studies indicate that under certain conditions, salicylate is a valuable alternative to spin trapping techniques to probe the role of .OH in cardiac oxidative injury, particularly when applied to the isolated perfused heart preparation.
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PMID:Salicylate trapping of .OH as a tool for studying post-ischemic oxidative injury in the isolated rat heart. 783 50

Preexisting magnesium deficiency may alter the susceptibility of rat hearts to postischemic oxidative injury (free radicals). This was examined in rats maintained for 3 weeks on a magnesium-deficient (Mg-D) diet with or without concurrent vitamin E treatment (1.2 mg/day, SC). Magnesium-sufficient (Mg-S) rats received the same diet supplemented with 100 mmol Mg/kg feed. Following sacrifice, isolated working hearts were subjected to 30-, 40-, or 60-min global ischemia and 30-min reperfusion. Postischemic production of free radicals was monitored using electron spin resonance (ESR) spectroscopy and spin trapping with alpha-phenyl-N-tert butylnitrone (PBN, 3 mM final); preischemic and postischemic effluent samples were collected and then extracted with toluene. PBN/alkoxyl adduct(s) (PBN/RO.; alpha H = 1.93 G, alpha N = 13.63 G) were the dominant signals detected in untreated Mg-S and Mg-D postischemic hearts, with comparably higher signal intensities observed for the Mg-D group following any ischemic duration. Time courses of postischemic PBN/RO. detection were biphasic for both groups (maxima: 2-4 and 8.5-12.5 min), and linear relationships between the extent of PBN/RO. production and the severity of both mechanical dysfunction and tissue injury were determined. Following each duration of ischemia, Mg-D hearts displayed greater levels of total PBN adduct production (1.7-2.0 times higher) and lower recovery of cardiac function (42-48% less) than Mg-S hearts. Pretreating Mg-D rats with vitamin E prior to imposing 40-min ischemia/reperfusion, led to a 49% reduction in total PBN/RO. production, a 55% lower LDH release and a 2.2-fold improvement in functional recovery, compared to untreated Mg-D hearts. These data suggest that magnesium deficiency predisposes postischemic hearts to enhanced oxidative injury and functional loss, and that antioxidants may offer significant protection against the pro-oxidant influence(s) of magnesium deficiency.
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PMID:Magnesium-deficiency potentiates free radical production associated with postischemic injury to rat hearts: vitamin E affords protection. 807 Jun 74

This study was designed to assess whether the protective effect of ischemic preconditioning can be adapted for myocardium undergoing 6 h of no-flow ischemia. Twelve isolated rat hearts were either perfused with oxygen-bicarbonated Krebs-Henseleit buffer in the Langendorff mode for 35 min (n=6), or perfused in the same way for 20 min, following 5 min of global normothermic ischemia and 100 min of buffer-perfusion (n=6). The 12 hearts were then preserved for 6 h in HTK solution at 4 degrees C, followed by 30 min of reperfusion. Recovery of cardiac function, metabolic activity and intracellular free calcium concentration were compared between the two groups. After 6 h ischemia, the hearts that underwent preconditioning showed better recovery of left ventricular developed pressure (P<0.01), a lower end-diastolic pressure level (P<0.05), less creatine kinase leakage and a lower calcium concentration. There was no statistical difference in the recovery rate of coronary flow and leakage rate of LDH between the two groups. In conclusion, this experiment demonstrates that ischemic preconditioning improved myocardial functional recovery after 6 h of hypothermic ischemic preservation in the isolated rat heart. Preconditioning might be a potential mechanism for preserving the heart against long-term ischemia/reperfusion injury.
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PMID:Cardioprotective efficacy of ischemic preconditioning on long-term myocardial ischemia. 946 84

A 63-year-old man, whose father died of malignant lymphoma, developed subacutely cauda equina/conus medullaris syndrome progressed over 3 months. Initial radicular pain, ascending motor and sensory paralysis without sacral sparing, vesicorectal dysfunction were similar with signs of spinal dural arteriovenous fistula. However, mild inflammatory signs, raised serum LDH, predominantly of LDH 3, lymphocytic pleocytosis and elevated beta 2 microglobulin in CSF suggested neurolymphomatosis. It was not supported, however, after CSF immunocytochemistry, myelogram, CT, Gd-MRI and Ga scan. Spinal cord/nerve root vascular syndromes of intravascular lymphomatosis (IVL) according to Glass J et al. was suspected because of the unique neurological progression similar to Foix-Alajouanine syndrome, hypoxia without abnormalities in chest X-ray film, response to steroids and raised serum soluble IL-2 receptor. Multiple biopsies were performed with negative results. However, after all muscle biopsy confirmed IVL. The lower spinal irradiation was not effective. But CHOP regimen supplemented by granulocyte colony-stimulating factor (G-CSF) brought about swift neurological improvement and protection from late complications. Self-limiting polyneuropathy emerged during the biweekly CHOP therapy, 6 courses for 12 weeks. Eventually he was neurologically improving 10 months after the chemotherapy and adrenal enlargement, which was possibly of metastasis, was only against complete remission. This case was good outcome by biweekly CHOP using G-CSF when compared with very high mortality in reported IVL cases besides vincristine neurotoxicity under compromised blood-brain/nerve barrier due to IVL might affect the functional recovery. This case with IVL implied raised soluble IL-2 receptor and progressive cauda equina syndrome/ascending myelopathy as diagnostic clues, and efficiency of muscle biopsy to confirm IVL.
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PMID:[A 63-year-old man with progressive cauda equina/conus medullaris syndrome]. 998 61

The effects of low-intensity, prolonged swimming on functional recovery of the rat heart (Langendorff preparations) from ischaemia-reperfusion (I/R) were investigated. Three groups of rats (120 days old) were used: sedentary rats (S) and rats exercised by a single bout of swimming lasting 5 (E5) or 8 h (E8), respectively. The effect of exercise on the response to I/R was related to an index of oxidative damage such as lipid peroxidation, as well as to the tissue antioxidant capacity and the response of heart tissue to in vitro oxidative stress. The intrinsic performance of E5 Langendorff preparations paced at 220 beats x min(-1) was also determined. A group of sedentary animals was used for H2O2-treated preparations. The effect of antioxidant treatment on inotropic recovery during reperfusion was studied on preparations from 5 or 8 h swimming vitamin E-treated (EVT5 and EVT8 and 5 or 8 h swimming untreated (EVU5 and EVU8) rats. Hearts from exercised animals displayed a reduced preischaemic inotropism, which in E5 rats was accompanied by an increase in the intrinsic heart rate. The lower intrinsic cardiac inotropism of E5 animals was confirmed in the paced preparations. The reduced contractility found in control hearts after addition of H2O2 to perfusion medium suggested that the low inotropism of E5 and E8 hearts was due to an exercise-induced increase in reactive oxygen species. Inotropic recovery during reperfusion was low in the S hearts, was significantly increased in the E5 hearts, and was again reduced to the S level in the E8 hearts. In the E8 hearts the indexes of cellular damage (LDH release) and oxidative stress increased, and antioxidant capacity decreased, while in E5 hearts there was no evidence of significant changes in such parameters. Performance and reperfusion recovery of hearts from 5 h swimming rats was not affected by vitamin E treatment, while those of hearts from 8 h swimming rats was the highest observed. We suggest that the higher inotropic recovery during reperfusion in the hearts from the E5 rats is related to the negative inotropic effect of exercise. The fall in recovery following the 8 h exercise was instead related to the increased oxidative stress.
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PMID:Effects of prolonged aerobic exercise on myocardial responses to ischaemia-reperfusion in the rat. 1142 51

To study the effects of different pH HEPES-KH reperfusate solution on immature myocardial protection, isolated perfused Langendorff model from immature rabbit hearts were developed formed. Control group (C) was perfused only with pH 7.4 HEPES-KH solution for 90 min. Ischemia/reperfusion group (group I/R) was perfused with pH 7.4 HEPES-KH solution before ischemia or after ischemia. Experimental group (group E), after ischemia, was perfused with pH 6.8, pH 7.1 and pH 7.4 HEPES-KH solutions for 5 min, 5 min, and 20 min, respectively. The left ventricular function recovery, MWC, LDH and CK leakage, MDA, ATP content, and SOD activity were determined. Our results showed that the left ventricular function recovery, ATP content and SOD activity in group E were higher than those of group I/R (P < 0.05). MWC, MDA content, LDH and CK leakage in group E were lower than those of group I/R (P < 0.05). These findings suggested that pH paradox might be one of important mechanisms for immature myocardial ischemia-reperfusion injury, and acidic perfusate, at the beginning of reperfusion, might attenuate pH paradox and ameliorate functional recovery in isolated perfused immature rabbit hearts.
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PMID:Acidic HEPES-KH reperfusion enhances myocardial protection in immature rabbits. 1265 46

Severe dietary Mg restriction (Mg(9), 9% of recommended daily allowance [RDA], plasma Mg = 0.25 mM) induces a pro-inflammatory neurogenic response in rats (substance P [SP]), and the associated increases in oxidative stress in vivo and cardiac susceptibility to ischemia/reperfusion (I/R) injury were previously shown to be attenuated by SP receptor blockade and antioxidant treatment. The present study assessed if less severe dietary Mg restriction modulates the extent of both the neurogenic/oxidative responses in vivo and I/R injury in vitro. Male Sprague-Dawley rats maintained on Mg(40) (40% RDA, plasma Mg = 0.6 mM) or Mg(100) (100% RDA, plasma Mg = 0.8 mM) diets were assessed for plasma SP levels (CHEM-ELISA) during the first 3 weeks and were compared with the Mg(9) group; red blood cell (RBC) glutathione and plasma malondialdehyde levels were compared at 3 weeks in Mg(9), Mg(20) (plasma Mg = 0.4 mM), Mg(40), and Mg(100) rats; and 40-min global ischemia/30-min reperfusion hearts from 7-week-old Mg(20), Mg(40), and Mg(100) rats were compared with respect to functional recovery (cardiac work, and diastolic, systolic, and developed pressures), tissue LDH release, and free radical production (ESR spectroscopy and alpha-phenyl-N-tert butylnitrone [PBN; 3 mM] spin trapping). The Mg(40) diet induced smaller elevations in plasma SP (50% lower) compared with Mg(9), but with a nearly identical time course. RBC glutathione and plasma malondialdehyde levels revealed a direct relationship between the severity of oxidative stress and hypomagnesemia. The dominant lipid free radical species detected in all I/R groups was the alkoxyl radical (PBN/alkoxyl: alpha(H) = 1.93 G, alpha(N) = 13.63 G); however, Mg(40) and Mg(20) hearts exhibited 2.7- and 3.9-fold higher alkoxyl levels, 40% and 65% greater LDH release, and lower functional recovery (Mg(20) < Mg(40)) compared with Mg(100). Our data suggest that varying dietary Mg intake directly influences the magnitude of the neurogenic/oxidative responses in vivo and the resultant myocardial tolerance to I/R stress.
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PMID:Dietary magnesium intake influences circulating pro-inflammatory neuropeptide levels and loss of myocardial tolerance to postischemic stress. 1277 97

This study investigated the effects of Ginkgo biloba (EGb 761) extract on seeded Schwann cells within poly(DL-lactic acid-co-glycolic acid) (PLGA) conduits by in vitro and in vivo trials for peripheral nerve regeneration. The seeding efficiency of Schwann cells in serum-deprived culture medium, which simulated the environment of mechanical trauma on an injured nerve site, was improved by adding different dosages of EGb 761 (0, 1, 10, 20, 50, 100, 200 microg/mL). The analytical results showed enhanced cell attachment and survival, reduced LDH release and increased MTT values, particularly in the range 10-100 microg/mL. The PLGA nerve conduits seeded with Schwann cells (6 x 10(3) cells) and filled with gelatin containing EGb 761 (0, 10, 50, 100 microg/mL) were implanted to 10-mm right sciatic nerve defects in rats. Autograft was performed as another control. Electromyography was assessed based on the motor unit action potential (MUAP) and fibrillation potential (Fib) at 2, 4, and 6 weeks during all periods. The specimens of the experimental and control groups were harvested for histological analysis at 6 weeks after surgery. The Fib was found to gradually decay, and the MUAP was found not to be present until 4 weeks after surgery. Meanwhile, the experimental groups were all statically better than the control group (without EGb 761) and autografts were observed at 6 weeks, especially at the concentration of 10 microg/mL, where there was higher amplitude of MUAP and a significantly larger number of myelinated axons. This study concluded that a proper concentration of EGb 761 (10-50 microg/mL) promoted seeding efficiency of Schwann cells in a tissue-engineered PLGA conduit. Addition of EGb 761 in Schwann cells-seeded conduit could increase the total number of myelinated axons in nerve regeneration and improve peripheral nerve functional recovery.
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PMID:In vitro and in vivo effects of Ginkgo biloba extract EGb 761 on seeded Schwann cells within poly(DL-lactic acid-co-glycolic acid) conduits for peripheral nerve regeneration. 1538 88


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