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

The authors investigated the hemodynamic, metabolic, electroencephalographic (EEG), and electromyographic (EMG) characteristics of narcotic-induced rigidity during induction of anesthesia with alfentanil (175 micrograms/kg) in 10 patients. Thiopental (4 mg/kg) was administered to a ten-patient control group. Rigidity was quantified in eight muscle groups (sternocleidomastoid, deltoid, biceps, forearm flexors, intercostal, rectus abdominus, vastus medialis/lateralis, and gastrocnemius). Marked rigidity was observed in all muscle groups in all patients receiving alfentanil and in none receiving thiopental. Central venous pressure increased with onset of rigidity, while mean arterial pressure and cardiac index remained unchanged. Manual ventilation was extremely difficult during alfentanil-induced rigidity. Arterial oxygen tension decreased more rapidly during rigidity than during the same time interval in the control group, while patients experiencing rigidity were more acidotic, as reflected by greater increases in base deficit. The EEG demonstrated an anesthetic state without seizure activity. The immediate increase in central venous pressure with the onset of rigidity, along with occasional simultaneous parallel variations in central venous pressure and the EMG, strongly suggest a mechanical mechanism for the change in central venous pressure. The metabolic changes during rigidity may be partly related to the absence of the normal cardiovascular reflexes that are reported to occur during voluntary isometric muscle contractions. A neurochemical mechanism of narcotic-induced rigidity is briefly reviewed.
 ...
PMID:Physiology of alfentanil-induced rigidity. 300 95

The safety of etomidate for induction of anesthesia in malignant hyperthermia-susceptible (MHS) pigs was evaluated in a two-phase experiment. Two litters of Purebred Poland China pigs, one MHS (n = 4) and the other malignant hyperthermia-resistant (MHR) (n = 4) were used. Phase I compared MHS vs MHR animals in terms of cardiovascular, metabolic, and skeletal muscle rigidity responses to etomidate and fentanyl anesthesia and to a subsequent malignant hyperthermia (MH) challenge with halothane-succinylcholine. When three of the four criteria for the diagnosis of MH occurred (rigidity, tachycardia, or increases in temperature or end-tidal CO2) in an animal, phase I was terminated. In phase II, only the MHS animals were used and experimental procedures were as in phase I except thiopental replaced etomidate. In phase I, evidence was inadequate to support the diagnosis of MH based upon responses of MHS pigs to the infusion of etomidate even though the infusion of etomidate in MHS pigs was associated with statistically significant increases in body temperature and plasma lactate levels above those observed in MHR pigs. Heart rate and bicarbonate levels were lower in MHS than in MHR pigs during etomidate infusion. With discontinuation of etomidate and a subsequent challenge with halothane-succinylcholine, all four pigs developed the MH syndrome within 15-30 min. Thiopental replacement of etomidate in the phase II experiment resulted in a twofold greater time (45-75 min) for halothane-succinylcholine to trigger MH in the susceptible pigs.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Malignant hyperthermia: is etomidate safe? 398 91