Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:2.3.1.21 (CPT)
4,580 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Type II carnitine palmitoyltransferase deficiency is the most common cause of exercise-induced rhabdomyolysis, myoglobinuria, and proximal muscle weakness and pain in young adults. A lack of this enzyme impairs mitochondrial oxidation of long-chain fatty acids and can lead to rhabdomyolysis, myoglobinuria, and renal failure. Carnitine palmitoyltransferase deficiency, unusual but not rare, is often detected by finding elevated creatine phosphokinase level in a routine blood chemistry panel. A case of carnitine palmitoyltransferase deficiency in a college athlete is presented, and the disorder is compared with defective myophosphorylation in McArdle's disease, the next most frequent cause of similar symptoms.
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PMID:Carnitine palmitoyltransferase deficiency in a college athlete: a case report and literature review. 759 92

The cold pressor test is used in the clinical testing of the autonomic nervous system. However, little is known about changes in the autonomic control of the cardiovascular system during repeated challenge with cold. Heart rate (HR), respiratory sinus arrhythmia (RSA), T-wave amplitude of ECG (TWA), blood pressure, body temperature and perceived pain were recorded in 18 male subjects during three CPTs which consisted of four minutes immersion of the left hand into cold water at 1 degree C. Breathing during CPT was either spontaneous or paced at 0.23 Hz or 0.1 Hz. Pain intensity and HR decreased and TWA increased during the cold immersion and in the resting period preceding cold in the second and third trials. Systolic and pulse blood pressure increased in resting periods in the third trial. RSA increased in the second and third cold challenge during paced breathing at 0.1 Hz only. A decrease in body temperature (0.48 degree C) at the end of the experiment correlated marginally with HR changes. Our study shows that sustained cardiovascular changes are induced by the first challenge with cold, and persist or increase with repeated cold pressor tests.
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PMID:Cardiovascular adjustments and pain during repeated cold pressor test. 872 92

The present study examined the spinal antinociceptive effects of adenosine analogs and inhibitors of adenosine kinase and adenosine deaminase in the carrageenan-induced thermal hyperalgesia model in the rat. The possible enhancement of the antinociceptive effects of adenosine kinase inhibitors by an adenosine deaminase inhibitor also was investigated. Unilateral hindpaw inflammation was induced by an intraplantar injection of lambda carrageenan (2 mg/100 microl), which consistently produced significant paw swelling and thermal hyperalgesia. Drugs were administered intrathecally, either by acute percutaneous lumbar puncture (individual agents and combinations) or via an intrathecal catheter surgically implanted 7-10 days prior to drug testing (antagonist experiments). N6-cyclohexyladenosine (CHA; adenosine A1 receptor agonist; 0.01-1 nmol), 2-[p-(2-carboxyethyl)phenylethylamino]-5'-N-ethylcarboxamidoadenos ine (CGS21680; adenosine A2A receptor agonist; 0.1-10 nmol), 5'-amino-5'-deoxyadenosine (NH2dAdo; adenosine kinase inhibitor: 10-300 nmol), and 5-iodotubercidin (ITU; adenosine kinase inhibitor; 0.1-100 nmol) produced, to varying extents, dose-dependent antinociception. No analgesia was seen following injection of 2'-deoxycoformycin (dCF; an adenosine deaminase inhibitor; 100-300 nmol). Reversal of drug effects by caffeine (non-selective adenosine A1/A2 receptor antagonist; 515 nmol) confirmed the involvement of the adenosine receptor, while antagonism by 8-cyclopentyl-1,3-dimethylxanthine (CPT; adenosine A1 receptor antagonist; 242 nmol), but not 3,7-dimethyl-1-propargylxanthine (DMPX; adenosine A2A receptor antagonist; 242 nmol), evidenced an adenosine A1 receptor mediated spinal antinociception by NH2dAdo. dCF (100 nmol), which was inactive by itself, enhanced the effects of 10 nmol and 30 nmol NH2dAdo. Enhancement of the antinociceptive effect of ITU by dCF was less pronounced. None of the antinociceptive drug regimens had any effect on paw swelling. These results demonstrate that both directly and indirectly acting adenosine agents, when administered spinally, produce antinociception through activation of spinal adenosine A1 receptors in an inflammatory model of thermal hyperalgesia. The spinal antinociceptive effects of selected adenosine kinase inhibitors can be significantly augmented when administered simultaneously with an adenosine deaminase inhibitor.
Pain 1998 Feb
PMID:Antinociception by adenosine analogs and inhibitors of adenosine metabolism in an inflammatory thermal hyperalgesia model in the rat. 952 Feb 38

An 18-year-old female athlete presented with severe, incapacitating pain in both thighs, inability to walk, loss of bladder control, and brown urine following a strenuous soccer practice 3 days earlier. Physical examination revealed exquisite tenderness in each quadriceps, and her urine was positive for blood, protein, and myoglobin. Upon hospital admission, extracorporeal hemodyalisis was carried out every other day for 3 weeks and her renal function gradually returned to normal. Enzyme assays of a muscle biopsy eventually revealed a type 2 carnitine palmitoyltransferase deficiency (CPTD 2).
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PMID:Acute Muscle Pain in an Adolescent Athlete. 1035 81

Carnitine palmitoyltransferase II (CPT II) deficiency is the most common lipid myopathy in adults and is characterized by exercise-induced pain, stiffness, and myoglobinuria. Retrospective analysis of patients with CPT II deficiency has made it possible to correlate the presence of disease-causing mutations in the CPT2 gene with residual CPT activity in muscle. We present evidence that the ratio of CPT II activity to citrate synthase activity in the skeletal muscle of patients presumed to have CPT II deficiency is important for predicting whether the patient has one, two, or no mutations in the CPT2 gene. This finding will assist in the future correlation of the phenotype with the genotype and in identifying manifesting heterozygotes.
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PMID:Biochemical and molecular correlations in carnitine palmitoyltransferase II deficiency. 1039 18

The aim of this study was to evaluate the results of complex hip revision using a cemented, collarless and polished femoral stem design (CPT, Zimmer, Warsaw, In.) within a tightly impacted morselized allograft. We have now been using the impaction grafting technique in combination with the CPT stem (Zimmer) for 10 years in complex cases of severe bone loss. In this study we have elected to report only those patients who have been revised at least once before revision using the impaction grafting technique. All the patients in the study group have a minimum follow-up of 5 years after the impaction grafting revision. In total, 43 consecutive hips in 40 patients, 22 men and 18 women, with a follow-up time of between 5 and 7 years are included in the study. The complications related to the revised hip consist of three early dislocations managed by closed reduction. Two patients suffered from periprosthetic fracture, both managed with plate osteosynthesis. Two cementless sockets were revised due to aseptic socket loosening. The Endoklinik rating of preoperative bone loss for the revised hips was 2 in 13 hips, 3 in 23 hips, and 4 in 7 hips. During the first year 29 stems subsided 2-4 mm within the cement mantle. In 8 cases, a subsidence of 5-9 mm was measured. The subsidence was nonprogressive, and no subsidence occurred after the 1st year. The Charnley, D'Aubigne, Postel scoring (maximum 6 points) for pain improved from 2.2 points preoperatively to 4.4 postoperatively, function from 2.3 to 4.3, and movement from 2.3 to 4.1. In conclusion, the concept of impaction grafting in THR revision in our study has so far proven to be successful with good clinical results at 5 years despite the relatively high early subsidence of the femoral component.
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PMID:Complex cemented revision using polished stem and morselized allograft. Minimum 5-years' follow-up. 1044 25

We report a case of a patient with carnitine palmityl deficiency in active labour. We discuss the metabolic and energetic implications of obstetrical labour in regard with the mitochondrial myopathy and we propose an optimal management. Neuroaxial analgesia and glucose infusion are indicated in early labour because it is necessary to alleviate stress and pain in order to avoid rhabdomyolysis associated with CPT deficiency. Combined spinal epidural analgesia using intrathecal opioid alone then epidural naropein should be a relevant choice because of a minimal motor blockage. Monitoring of myolysis using serum creatinine phosphokinase levels must take in account CK and MB fractions releases to the circulation during obstetrical labour.
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PMID:[Anesthetic management of obstetrical labor in a parturient with muscular carnitine palmitoyl transferase deficiency]. 1109 24

Capsaicin, the pungent ingredient in hot pepper, activates nociceptors to produce pain and inflammation. However, repeated exposures of capsaicin will cause desensitization to nociceptive stimuli. In cultured trigeminal ganglion (TG) neurons, we investigated mechanisms underlying capsaicin-mediated inhibition of action potentials (APs) and modulation of voltage-gated sodium channels (VGSCs). Capsaicin (1 microM) inhibited APs and VGSCs only in capsaicin-sensitive neurons. Repeated applications of capsaicin produced depolarizing potentials but failed to evoke APs. The capsaicin-induced inhibition of VGSCs was prevented by preexposing the capsaicin receptor antagonist, capsazepine (CPZ). The magnitude of the capsaicin-induced inhibition of VGSCs was dose dependent, having a K(1/2) = 0.45 microM. The magnitude of the inhibition of VGSCs was proportional to the capsaicin induced current (for -I(CAP) < 0.2 nA). Capsaicin inhibited activation of VGSCs without changing the voltage dependence of activation or markedly changing channel inactivation and use-dependent block. To explore the changes leading to this inhibition, it was found that capsaicin increased cAMP with a K(1/2) = 0.18 microM. At 1 microM capsaicin, this cAMP generation was inhibited 64% by10 microM CPZ, suggesting that activation of capsaicin receptors increased cAMP. The addition of 100 microM CPT-cAMP increased the capsaicin-activated currents but inhibited the VGSCs in both capsaicin-sensitive and -insensitive neurons. In summary, the inhibitory effects of capsaicin on VGSCs and the generation of APs are mediated by activation of capsaicin receptors. The capsaicin-induced activation of second messengers, such as cAMP, play a part in this modulation. These data distinguish two pathways by which neuronal sensitivity can be diminished by capsaicin: by modulation of the capsaicin receptor sensitivity, since the block of VGSCs is proportional to the magnitude of the capsaicin-evoked currents, and by modulation of VGSCs through second messengers elevated by capsaicin receptor activation. These mechanisms are likely to be important in understanding the analgesic effects of capsaicin.
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PMID:Capsaicin inhibits activation of voltage-gated sodium currents in capsaicin-sensitive trigeminal ganglion neurons. 1116 May 9

Research has demonstrated that exposure to acute stress may attenuate pain perception. Mechanisms of this effect in humans have not been determined. This study was conducted to determine the extent to which psychophysiological and adrenocortical responses to acute stress predict subsequent pain perception. One hundred and fifty-two healthy participants (80 women) were assigned to one of two conditions: rest followed by the cold pressor test (CPT; N=76) or stress followed by CPT (N=76). The stress protocol consisted of a public-speaking challenge. Participants rated their pain every 15 s during a 90-s hand CPT (0-4 degrees C), and they completed the short form of the McGill Pain Questionnaire. Salivary cortisol, mood, blood pressure (BP), and impedance cardiography measures were collected in both conditions. Women had lower BP and reported greater pain than men in both conditions (ps<0.01). Participants in the stress condition reported less pain during CPT than those in the rest condition (p=0.02). Regression analyses demonstrated that the stress effect on pain ratings was mediated by systolic BP level during stress; however, cortisol responses did not affect this relationship. Mood changes were independent predictors of pain. The study demonstrates that BP changes in response to stress mediate the stress-induced attenuation of pain perception.
Pain 2003 Dec
PMID:Blood pressure but not cortisol mediates stress effects on subsequent pain perception in healthy men and women. 1465 11

Glutamate (which facilitates peripheral nociception) releases adenosine (which inhibits peripheral nociception via adenosine A(1) receptors) when injected locally into the rat hindpaw. The present study determined whether this locally released adenosine could modulate spontaneous pain behaviors produced by a local injection of 1.5% formalin, by determining the effect of 8-cyclopentyl-theophylline (CPT; selective adenosine A(1) receptor antagonist) on flinching produced by formalin/glutamate combinations. Experiments were performed following a prior conditioning injection of 2.5% formalin into the contralateral hindpaw 3-4 days earlier. CPT augmented flinching behaviors produced by 1.5% formalin/1 micromol glutamate, but had no effect on behaviors produced by formalin or glutamate alone. CPT also augmented flinches generated by formalin/alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) and formalin/kainic acid, but not by formalin/N-methyl-D-aspartate (NMDA) combinations. The conditioning leads to a clearer expression of the peripheral inhibitory effect of adenosine (inhibitory effect of an inhibitor of adenosine kinase on flinching also was observed), rather than an increased release of adenosine (no enhanced release observed by microdialysis). Microglia appear to be involved in the conditioning, as microglia are activated in the dorsal spinal cord 3 days following injection of 2.5% formalin, and augmentation of formalin/glutamate-induced flinching by CPT is inhibited by the glial metabolic inhibitor fluorocitrate. The augmentation of flinching by CPT is also eliminated following a spinal pretreatment with MK-801 (NMDA receptor antagonist), cyclohexyladenosine (adenosine A(1) receptor agonist), N(G)-nitro-L-arginine methyl ester HCl (nitric oxide synthetase inhibitor), and chelerythrine (protein kinase C inhibitor). The conditioning pretreatment with 2.5% formalin does not lead to a generalized chemical or thermal hypersensitivity in the contralateral hindpaw. This study demonstrates that prior exposure to 2.5% formalin in the contralateral hindpaw reveals an inhibitory effect of adenosine on peripheral nociception in the presence of glutamate; this conditioning involves microglia and other mechanisms involved in central sensitization.
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PMID:Glutamate-evoked release of adenosine and regulation of peripheral nociception. 1521 63


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