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Metabolic Recovery (metabolic + recovery)

Distribution by Scientific Domains
Medical Sciences75%

Selected Abstracts

Nitric oxide bioavailability modulates the dynamics of microvascular oxygen exchange during recovery from contractions

ACTA PHYSIOLOGICA, Issue 2 2010
D. M. Hirai
Abstract Aim:, Lowered microvascular PO2 (PO2mv) during the exercise off-transient likely impairs muscle metabolic recovery and limits the capacity to perform repetitive tasks. The current investigation explored the impact of altered nitric oxide (NO) bioavailability on PO2mv during recovery from contractions in healthy skeletal muscle. We hypothesized that increased NO bioavailability (sodium nitroprusside: SNP) would enhance PO2mv and speed its recovery kinetics while decreased NO bioavailability (l -nitro arginine methyl ester: l -NAME) would reduce PO2mv and slow its recovery kinetics. Methods:,PO2mv was measured by phosphorescence quenching during transitions (rest,1 Hz twitch-contractions for 3 min,recovery) in the spinotrapezius muscle of Sprague,Dawley rats under SNP (300 ,m), Krebs-Henseleit (Control) and l -NAME (1.5 mm) superfusion conditions. Results:, Relative to recovery in Control, SNP resulted in greater overall microvascular oxygenation as assessed by the area under the PO2mv curve (PO2 AREA; Control: 3471 ± 292 mmHg s; SNP: 4307 ± 282 mmHg s; P < 0.05) and faster off-kinetics as evidenced by the mean response time (MRToff; Control: 60.2 ± 6.9 s; SNP: 34.8 ± 5.7 s; P < 0.05), whereas l -NAME produced lower PO2 AREA (2339 ± 444 mmHg s; P < 0.05) and slower MRToff (86.6 ± 14.5 s; P < 0.05). Conclusion:, NO bioavailability plays a key role in determining the matching of O2 delivery-to-O2 uptake and thus the upstream O2 pressure driving capillary-myocyte O2 flux (i.e. PO2mv) following cessation of contractions in healthy skeletal muscle. Additionally, these data support a mechanistic link between reduced NO bioavailability and prolonged muscle metabolic recovery commonly observed in ageing and diseased populations. [source]

Influence of lipophilicity and stereochemistry at the C7 position on the cardioprotective and antioxidant effect of ginkgolides during rat heart ischemia and reperfusion,

DRUG DEVELOPMENT RESEARCH, Issue 3 2005
Ludovic Billottet
Abstract The extent to which the cardioprotective effect of ginkgolides is related to their lipophilicity rather than to their anti-platelet activating factor (PAF) effect was addressed in isolated rat hearts submitted to ischemia and reperfusion. A new derivative of ginkgolide C (1), the 7-,- O -(4-methylphenyl) ginkgolide C (4) was synthesized and compared to 7- O -(4-methylphenyl) ginkgolide C (2) that had the same absolute configuration at C7 as 1 for its lipophilicity, anti-PAF activity, and cardioprotective and antioxidant effects. Using reversed-phase high-performance liquid chromatography HPLC, 4 and 2 were found to be significantly more lipophilic (i.e., log kw of 3.42±0.05 and 3.64±0.07, respectively) than 1 (1.15±0.03) and the strong PAF inhibitor ginkgolide B (GkB; 1.65±0.03). The anti-PAF activities (IC50 values in ,M) were 8.2, 17.1, and 2.2 for 4, 1, and GkB, respectively, while 2 was inactive. In preischemic and/or reperfused hearts perfused with ginkgolides at 0.7 ,M: (i) 2 and 4 were more efficient in improving postischemic hemodynamic and metabolic recovery than 1, (ii) a key-step in cardioprotection occurred during ischemia where 2 and 4 limited myocardial ATP depletion and contracture development, (iii) a strong anti-lipoperoxidant effect was observed with 2 and 4, but not 1. In vivo administration of 2 to rats (4 mg/kg/day for 20 days) was more effective than that of 1 regarding ischemic heart protection, suggesting a positive role for lipophilicity. It was concluded that a high lipophilicity is not an absolute prerequisite for a strong anti-PAF effect for ginkgolides, whereas it appears essential for cardioprotection. Drug Dev. Res. 64:157,171, 2005. © 2005 Wiley-Liss, Inc. [source]

Hepatic Volume Measurements in Dogs with Extrahepatic Congenital Portosystemic Shunts before and after Surgical Attenuation

JOURNAL OF VETERINARY INTERNAL MEDICINE, Issue 1 2010
A. Kummeling
Background: In dogs with congenital portosystemic shunts (CPSS), the ability of the hypoplastic liver to grow is considered important for recovery after surgical shunt attenuation. Objectives: This study investigated hepatic growth after extrahepatic shunt attenuation in dogs using magnetic resonance imaging (MRI) and computed tomography (CT). Animals: Ten client-owned dogs with single extrahepatic CPSS. Methods: Abdominal MRI, CT, or both were performed before and 8 days, 1, and 2 months after shunt attenuation. Liver volumes were calculated from the areas of the MRI or CT images. Results: Before surgery, median liver volume was 18.2 cm3/kg body weight. Liver volume increased significantly after surgery. Growth was highest between days 0 and 8 and decreased afterward. Median liver volume was 28.8 cm3/kg at 2 months after attenuation. No significant differences in growth were found between dogs with complete or partial shunt closure or between dogs with complete or incomplete metabolic recovery. Volumes measured from consecutively performed MRI and CT images correlated well (r= 0.980), but volumes from MRI images were significantly larger than volumes from CT images (6.8%; P= .008). Conclusion and Clinical Importance: After shunt attenuation, rapid normalization of liver size was observed. Hepatic growth was not decreased in dogs after partial closure of CPSS or in dogs with subclinical, persistent shunting 2 months after surgery. CT is the preferred imaging method for volumetric estimation because of speed. [source]

Cystic fibrosis transmembrane conductance regulator in human muscle: Dysfunction causes abnormal metabolic recovery in exercise

ANNALS OF NEUROLOGY, Issue 6 2010
Anne-Marie Lamhonwah PhD
Objective Individuals with cystic fibrosis (CF) have exercise intolerance and skeletal muscle weakness not solely attributable to physical inactivity or pulmonary function abnormalities. CF transmembrane conductance regulator (CFTR) has been demonstrated in human bronchial smooth and cardiac muscle. Using 31P-magnetic resonance spectroscopy of skeletal muscle, we showed CF patients to have lower resting muscle adenosine triphosphate and delayed phosphocreatine recovery times after high-intensity exercise, suggesting abnormal muscle aerobic metabolism; and higher end-exercise pH values, suggesting altered bicarbonate transport. Our objective was to study CFTR expression in human skeletal muscle. Methods and Results We studied CFTR expression in human skeletal muscle by Western blot with anti-CFTR antibody (Ab) L12B4 and demonstrated a single band with expected molecular weight of 168kDa. We isolated the cDNA by reverse transcription polymerase chain reaction and directly sequenced a 975bp segment (c. 3,600,4,575) that was identical to the human CFTR sequence. We showed punctate staining of CFTR in sarcoplasm and sarcolemma by immunofluorescence microscopy with L12B4 Ab and secondary Alexa 488-labeled Ab. We confirmed CFTR expression in the sarcotubular network and sarcolemma by electron microscopy, using immunogold-labeled anti-CFTR Ab. We observed activation of CFTR Cl, channels with iodide efflux, on addition of forskolin, 3-isobutyl-1-methyl-xanthine, and 8-chlorphenylthio,cyclic adenosine monophosphate, in wild-type C57BL/6J isolated muscle fibers in contrast to no efflux from mutant F508del-CFTR muscle. Interpretation We speculate that a defect in sarcoplasmic reticulum CFTR Cl, channels could alter the electrochemical gradient, causing dysregulation of Ca2+ homeostasis, for example, ryanodine receptor or sarco(endo)plasmic reticulum Ca2+ adenosine triphosphatases essential to excitation-contraction coupling leading to exercise intolerance and muscle weakness in CF. ANN NEUROL 2010 [source]