Agonists, Narcotic

Table 19-1 identifies the responses in the body associated with each of these receptors. The narcotic agonists... 

Administration of a narcotic agonist-antagonist may result in symptoms of narcotic witiidrawal in those addicted to narcotics. Other adverse reactions associated widi die administration of a narcotic agonist-antagonist... 

When monitoring a patient receiving a narcotic agonist-antagonist, the nurse must be aware that... 

The narcotic agonist/antagonist nalbuphine (8.88) is poorly bioavailable in humans (ca. 10%), mostly due to extensive first-pass metabolism. Two prodrugs were examined, namely the acetylsalicylate (8.89) and the anthran-ilate (8.90) [125]. The hydrolysis of these compounds in rat plasma was fast (tU2 values of some minutes and 1 - 2 h, respectively), while it was slow in dog plasma (lW2 ca. 3 h and 15 h, respectively) and in human plasma (t1/2 ca. 7-10 h and 50-60 h, respectively). Hydrolysis in dog tissue homogenates was also markedly slower than in rat. The dog was, thus, considered to be a fair animal model, and it is of interest that, in this species, the oral bioavailability of 8.88, 8.89, and 8.90 were ca. 6, 20, and 50%, respectively. 

Cross-tolerance - Cross-tolerance is not complete. Switching to another narcotic agonist, starting with half the predicted equianalgesic dose, may circumvent the cross-tolerance. 

Pharmacology Nalbuphine is a potent analgesic with narcotic agonist and antagonist actions. Its analgesic potency is essentially equivalent to that of morphine on a milligram basis. 

Mechanism of Action A narcotic agonist-antagonist that binds with opioid receptors in the CNS. May displace opioid agonists and competitively inhibit their action may precipitate withdrawal symptoms. Therapeutic Effect Alters the perception of and emotional response to pain. 

Nalbuphine (Nubain) [Analgesic/Narcotic Agonist-Antagonist1]... 

Chemical and structural specificity Any alteration in the structure of a compound alters its pharmacologic properties. For example, nalorphine, a narcotic antagonist, differs from morphine, a narcotic agonist, by the replacement of the CH3 group on the morphine s nitrogen with the allyl radical -CH2CH=CH2. 

Cho TM, Law PY, Loh HH. A proposed mode of action for narcotic agonists and antagonists. In Loh HH, Ross DH, eds. Neurochemical Mechanisms of Opiates and Endorphins. New York Raven Press, 1979 69-102. 

Note. For a review of the pharmacokinetics of narcotic agonists-antagonists, see R. E. S. Bullingham etal., Clin. Pharmacokinet., 1983,, 332-343. 

The most serious side effect of the opioids is respiratory depression.The narcotic agonists suppress the brainstem respiratory centers and thus alter tidal volume, respiratory rate, rhythmicity, and responsiveness to CO2. When used in equianalgesic doses, the opioids, with the exception of pentazocine, produce similar degrees of respiratory depression.Therapeutic doses of opioid analgesics are unlikely to produce significant respiratory depression in most healthy patients.The opioids must be used with caution, however, in patients with preexisting pulmonary disease, especially patients with airway compromise such as chronic obstructive pulmonary disease. 

Loperamide is a narcotic agonist acting on opioid JL receptors. Loperamide has mild antisecretory effects but its primary effects are to increase segmental intestinal contractions and slow the propulsion of intestinal contents (Ruppin 1987). Loperamide has been associated with reduction in diarrhea in many clinical studies in humans but has minimal impact on the patient s fluid and electrolyte balance because the secreted fluid remains in the bowel lumen. Loperamide can have dose-dependent CNS depressant effects. Loperamide also has been shown to promote intestinal bacterial overgrowth because of promoting the retention of fluid within bowel segments (Duval-Iflah et al 1999), which may favor the proliferation of enteropathogenic bacteria. 

Xylazine (0.5 mg/kg i.v.) alone had minimal effects on gastroduodenal motility, but when combined with the narcotic agonist-antagonist butorphanol there is pronounced suppression of antroduode-nal myoelectric activity (Merritt et al 1998). Interestingly, butorphanol alone had minimal effects on antroduodenal myoelectric activity. However, detomidine, at 0.0125 mg/kg, markedly depressed duodenal motility and would be expected to affect gastric motility similarly. 

Cardiopulmonary effects of narcotic agonists and a partial agonist in horses. American Journal of Veterinary Research 39 1632-1635... 

In experimental horses, a-methylfentanyl induces locomotive responses (as quantified by counting the number of footsteps taken per unit of time), indicating that it is a morphine-like narcotic agonist in horses. The maximum effect can be seen 10 min after treatment of horses with greater than 4 pg kg body weight. 

Narcotic analgesics (narcotic agonists) such as opioids act on the central nervous system to treat moderate and severe pain, suppress respiration and coughing by acting on the respiratory and cough centers in the medulla of the brain stem. All narcotic analgesics relieve pain. All except meperidine (Demerol) are also antitussive (cough suppression) and antidiarrheal. 

Naloxone (Narcan) is a narcotic agonist and is prescribed to reverse the effects of narcotic analgesics. Naloxone (Narcan) is also used to determine if a patient s unconsciousness is caused by an overdose of narcotic analgesics. If the patient regains consciousness after administering Naloxone (Narcan) IV, then it can be assumed that the patient s unconsciousness is caused by an overdose of narcotic analgesics... 

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