Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0026837 (muscle rigidity)
 1,077 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. A technique was developed to generate 2-8 degrees C step temperature perturbations (T-jumps) in single muscle fibres to study the thermodynamics of muscle contraction. A solid-state pulsed holmium laser emitting at 2.065 microns heated the fibre and surrounding solution in approximately 150 mus. The signal from a 100 microns thermocouple fed back to a heating wire maintained the elevated temperature after the laser pulse. 2. Tension of glycerol-extracted muscle fibres from rabbit psoas muscle did not change significantly following T-jumps when the fibre was relaxed. 3. In rigor, tension decreased abruptly on heating indicating normal (not rubber-like) thermoelasticity. The thermoelastic coefficient (negative ratio of relative length change to relative temperature change) of the fibre was estimated to be -0.021 at sarcomere lengths of 2.5-2.8 microns. Rigor tension was constant after the temperature step and returned to the original value on recooling. 4. In maximal Ca2+ activation, tension transients initiated by T-jumps had several phases. An immediate tension decrease suggests that thermoelasticity during contraction is similar to that in rigor. Active tension then recovered to the value before the T-jump with an apparent rate constant of approximately 400 s-1 (at 10-20 degrees C). This rate constant did not have an appreciable dependence on the final temperature. Finally, tension increased exponentially to a new higher level with a rate constant of approximately 20 s-1 at 20 degrees C. This rate constant increased with temperature with a Q10 of 1.4. 5. At submaximal Ca2+ activation the tension rise was followed by a decay to below the value before the T-jump. This decline was expected from the temperature dependence of steady pCa-tension curves. The final tension decline occurred on the 1-5 s time scale. 6. The value and amplitude dependence of the rate constant for the quick recovery following T-jumps were similar to those of the quick recovery following length steps during active contractions. The enthalpy change associated with the quick tension recovery following temperature-step perturbations was estimated to be positive suggesting that the recovery process is an endothermic reaction. Slower reaction steps on the 10-30 ms timescale, as well as reactions corresponding to the quick recovery, may contribute to the cross-bridge power stroke.
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PMID:Transient tension changes initiated by laser temperature jumps in rabbit psoas muscle fibres. 344 91

We report a 71-year-old woman with progressive gait disturbance and dementia. The patient was well until 61 years of age (1980) when she noted a gradual onset of gait disturbance. A year later, she noted slurring of the speech and forgetfulness. In 1982, she noted difficulty in looking down and progression of her gait disturbance. In 1983, she became unable to walk alone unless supported. She was admitted to our service in 1984; neurological examination at that time revealed moderate dementia, limitation in the vertical gaze, slurred speech, and wide based ataxic gait. She was discharged for out patient follow up. Cranial CT scan in 1989 revealed cortical, brain stem, and cerebellar atrophies. On March 10, 1990, she fell down and hit her head. She developed headache on April 1, vomited on April 8, and was admitted to our service again. On admission, she was somnolent, she was unable to follow an object to any direction; oculocephalic response was elicited to horizontal directions, however, it was difficult to induce in the vertical direction. Rigidity was noted in the extremities except in the left lower extremity. Rapid alternating movement was difficult and dysmetria was noted in the finger-to nose test. Deep reflexes were exaggerated without clonus; the plantar response was extensor bilaterally. Cranial CT scan revealed bilateral subdural hematoma. She was treated with intravenous infusion of glycerol, and she became alert after this treatment; however, she was markedly demented. She was unable to walk alone. She was discharged to home, but she showed progressive loss of activities, and became bed ridden in December 1992. In January of 1993, she developed fever, dyspnea, and disturbance of consciousness, and was admitted again on January 26, 1993. On admission, her blood pressure was 70 mmHg by palpation and body temperature 38.5 degrees C. The lungs were clear. On neurologic examination, she was semicomatose; the optic fundi were unremarkable; only incomplete eye movements elicited by the oculocephalic reflex. She was passive supine in position; some spontaneous movements were observed in the extremities. Lead-pipe rigidity was noted in both upper extremities, but the muscle tone was decreased in the lower extremities. No abnormal involuntary movements were seen. Deep reflexes were exaggerated except for the ankle jerk which was diminished bilaterally. The plantar response was extensor on both sides.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[A 71-year-old woman with progressive gait disturbance and dementia]. 766 34

Clenbuterol is a beta2-adrenoceptor agonist primarily used for treating bronchospasm and alleviating the symptoms of chronic obstructive pulmonary disease (COPD) in the horse. In other species (rats, mice, sheep, and cattle), chronic high doses of clenbuterol (typically in the milligram per kilogram body weight range) has been shown to cause a muscle directed protein anabolic response. Clenbuterol can also modify muscle fibre composition and therefore potentially affect muscle function. This has implications for the performance of exercising horses being treated with therapeutic doses of clenbuterol (typically in the microgram per kilogram body weight range) for bronchospasm or COPD. It is not known whether clenbuterol treatment affects muscle fibre function in horses. The purpose of this study was to examine the effects of a therapeutic dose of clenbuterol, with and without exercise, on the contractile activation characteristics of single membrane permeabilized fibres prepared from muscle biopsies. We tested the hypothesis that therapeutic treatment with clenbuterol would not affect muscle fibre function. Unfit Standardbred mares were treated for 8 weeks with; clenbuterol (2.4 microg/kg twice/day, 5 days/week) plus exercise (20 min at 50% VO2(max) 3 d/wk; CLENEX), clenbuterol only (CLEN), or exercise only (EX). Muscle biopsies were taken from the gluteus medius muscle before and after treatment and stored in a glycerol-based solution to prepare permeabilized muscle fibres. The force-pCa relationship for fibres from CLEN horses was steeper (P < 0.05) indicative of greater cooperative interactions within the thin filament, however, fibre sensitivity to Ca2+ was unchanged. In contrast, the steepness of the force-pCa relationship was not changed in fibres from EX and CLENEX horses and Ca2+ sensitivity was also unaffected. Rigor force, activation in the absence of ATP, was not affected by any treatment indicating an approximately equivalent number of participating cross-bridges during activation. The results indicate that a therapeutic dose of clenbuterol to Standardbred horses does not affect the Ca(2+)-activated contractile characteristics of isolated muscle fibres.
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PMID:Therapeutic clenbuterol treatment does not alter Ca2+ sensitivity of permeabilized fast muscle fibres from exercise trained or untrained horses. 1467 50