Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0020672 (hypothermia)
 17,327 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Clonidine, an alpha2-adrenergic agonist, has been demonstrated to produce significant analgesia and potentiate morphine analgesia. Endothelin (ETA) receptor antagonists have also been found to potentiate the antinociceptive response to morphine. Clonidine and ET have been reported to have cardiovascular interactions involving the sympathetic nervous system, but it is not known whether ETA receptor antagonist affects clonidine analgesia. This study examined the influence of sulfisoxazole (ETA receptor antagonist) on clonidine analgesia. Male Swiss Webster mice were used to determine antinociceptive response of drugs by measuring tail-flick latency. The effect of clonidine (0.3, 1.0, and 3.0 mg/kg, i.p.) alone or in combination with sulfisoxazole (25, 75, and 225 mg/kg, p.o.) on analgesia and body temperature was determined. Clonidine produced a dose-dependent analgesia and hypothermia. Sulfisoxazole (25, 75, and 225 mg/kg), when administered with clonidine (0.3 mg/kg), significantly potentiated (31% increase in area under the curve (AUC)) the analgesic effect of clonidine. Yohimbine (alpha2-adrenergic receptor antagonist) did not affect analgesic effect of clonidine plus sulfisoxazole. Idazoxan (I1-imidazoline and alpha2-adrenergic receptor antagonist) reduced (47% decrease in AUC) the analgesic effect of clonidine plus sulfisoxazole. Treatment with naloxone reduced (46% decrease in AUC) the analgesic effect of clonidine plus sulfisoxazole. The effect of another ETA receptor antagonist, BMS-182874 (2, 10, and 50 microg, i.c.v.) was studied, and it was found that the dose of 10 microg significantly potentiated (26% increase in AUC) the analgesic effect of clonidine. These results indicate that sulfisoxazole, an ETA receptor antagonist, potentiates the analgesic effect of clonidine, which could be mediated through I1-imidazoline receptors and opioid receptors.
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PMID:Involvement of imidazoline and opioid receptors in the enhancement of clonidine-induced analgesia by sulfisoxazole. 2055 23

The ring of the red notification phone breaks the relative calm of an otherwise typical Monday morning and heralds the arrival of a critically ill patient. The dispatcher announces that EMS is on the way with a 57-year-old man in cardiac arrest, with an ETA of 3 minutes. Shortly after preparations for their arrival are complete, EMS personnel enter with CPR in progress and the patient already intubated. As monitor/defibrillator attachment, ETT placement confirmation, additional IV access, and complete exposure of the patient occur, you hear more about the clinical scenario from EMS. Mr. I.C. is a 57-year-old male who was moving furniture when, as described by witnesses, he complained of difficulty catching his breath and a slight tightness in his chest. He began coughing violently, vomited once, gasped, and collapsed. Emergency medical services personnel state that they arrived approximately 20 minutes after the patient had collapsed, with CPR in progress. The patient was intubated in the field, and EMS reports that the initial rhythm was PEA. Upon the patient's arrival in the ED, the rhythm is noted to be ventricular fibrillation. Defibrillation is attempted twice over the next 4 minutes, with concomitant administration of medications. During the next rhythm check, QRS complexes are noted on the monitor and a pulse is palpated. The patient has had a return of spontaneous circulation, apparently 50 minutes from onset of the arrest. As you initiate postresuscitation care, you consider the patient's prognosis and wonder if he qualifies for therapeutic hypothermia; ie, will therapeutic hypothermia make a difference in his outcome?
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PMID:Current evidence in therapeutic hypothermia for postcardiac arrest care. 2216