Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0026916 (MAC)
 5,226 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of iv succinylcholine (SCh) on cerebral blood flow (CBF), the electroencephalogram (EEG), muscle afferent activity (MAA), electromyographic activity (EMG), and PaCO2 were tested in six halothane-anesthetized dogs (1.0 MAC) more than 1 h after a 10-min period of complete cerebral ischemia. All dogs received treatments of both iv SCh (1.0 mg.kg-1) and saline placebo in a random sequence. Fasciculations and substantial increases in EMG activity were observed in all dogs following SCh administration. At the onset of fasciculations, there was an increase in MAA to a peak value of 353 +/- 74% of control (mean +/- SE; n = 5 for MAA; n = 6 for all other variables) at the 1-min measurement point. Thereafter, MAA gradually declined toward control values. There were delayed increases in PaCO2 throughout the 45-min study period, achieving values of 106 +/- 1% to 118 +/- 4% of control (an increase in PaCO2 of 2-7 mmHg). Despite the increases in MAA and PaCO2, there were no significant increases in CBF during the study. The control EEG 1-h after complete cerebral ischemia, but immediately before administering the drug treatments, consisted predominantly of a delta rhythm, denoting cerebral dysfunction. In one dog, SCh administration produced transient attenuation of the delta rhythm, a change consistent with cerebral stimulation. In the remaining five dogs, SCh had no effect on the EEG. Treatment with saline placebo did not affect any variable measured. The authors conclude that, in the electrically dysfunctioning brain (e.g., as occurs following resuscitation from complete cerebral ischemia), the cerebral (i.e., CBF and EEG) response to iv SCh is attenuated when compared to the previously reported response in normal brain.
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PMID:The effects of intravenous succinylcholine on cerebral function and muscle afferent activity following complete ischemia in halothane-anesthetized dogs. 239 33

The effects of iv succinylcholine (SCh) on cerebral blood flow (CBF), muscle afferent activity (MAA), electromyographic activity (EMG), visible fasciculations, and PaCO2 were tested in 12 dogs anesthetized with 0.87% end-expired halothane (1 MAC). Six dogs (group I) received treatments of both SCh 1.0 mg/kg iv and saline placebo 3.0 ml iv. Fasciculations and substantial increases in EMG activity were observed in all six dogs given SCh. At the onset of fasciculations, there were parallel increases in MAA and CBF to peak values of 466% +/- 77% of control (mean +/- SE) and 136% +/- 5% of control, respectively, at the 1-min measurement point. Thereafter, both MAA and CBF declined toward control values. An additional six dogs (group II) were prepared as above; however, they were pretreated with a defasciculating dose of pancuronium 0.01 mg/kg iv 5 min before being given SCh 1.0 mg/kg. These dogs were also given treatments of saline placebo 3.0 ml iv during another portion of the study. None of these six dogs had visible fasciculations following SCh, and only in one was slight EMG activity detected. Following iv SCh, there were parallel increases in both MAA and CBF. The peak MAA value of 255% +/- 56% of control occurred at the 1-min measurement point and was followed by a gradual decline in MAA. CBF increases were greatest during the periods of greatest MAA (i.e., the 1- to 3-min measurement points). The largest increase in CBF (128% +/- 9% of control) occurred at the 3-min measurement point.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cerebral function and muscle afferent activity following intravenous succinylcholine in dogs anesthetized with halothane: the effects of pretreatment with a defasciculating dose of pancuronium. 275 Nov 45

The effects of iv succinylcholine (SCh) on the electroencephalogram (EEG), cerebral blood flow (CBF), cerebral metabolic rate (CMRO2), intracranial pressure (ICP), central venous pressure (CVP), and mean arterial pressure (MAP) were tested in halothane-anesthetized dogs. Six dogs were maintained at 0.87 +/- 0.00% (mean +/- SE) expired halothane (1.0 MAC) and received both SCh 1.0 mg X kg-1 and lactated Ringer's solution placebo 0.05 ml X kg-1. Fasciculations began 24 +/- 4 s after iv SCh. Fasciculations were followed by immediate EEG arousal in five of six dogs and increases in CBF in all six. Average CBF was 151 +/- 14% of control for the 0-15 min measurement period and 127 +/- 7% of control for the 15-30 min period. Both were significantly greater than pre-SCh control values and placebo group values. Peak CBF of 177 +/- 19% of control occurred 3 min after iv SCh and was accompanied by a peak ICP of 435 +/- 131% of control. ICP values were significantly different between SCh and placebo treatments only during the periods of greatest CBF (1 to 5 min after iv SCh). Average PaCO2 values after iv SCh were significantly greater than pre-SCh control values and placebo values during each 15-min measurement interval. Average PaCO2 was 116 +/- 2% of control during the 0-15 min measurement period, 114 +/- 2% of control during the 15-30 min period, and 109 +/- 1% of control during the 30-45 min period. CVP, MAP, and CMRO2 did not significantly change after iv SCh.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cerebral stimulation following succinylcholine in dogs. 308 26