Pharmacological and clinical importance of narcotic antagonists and mixed antagonists‐use in cardiology.

Coltart, D J; Malcolm, A D

doi:10.1111/j.1365-2125.1979.tb04705.x

Cited by 8 publications

(4 citation statements)

References 25 publications

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“…It probably relates primarily to the concentration of the drug achieved at mast cell membrane (1 7). Coltart & Malcolm (19) reported that "buprenorphine does not seem to cause histamine release", but this statement was not supported by clinical or experimental observations. Therefore, we can assume that buprenorphine, which is 30-40 times as potent an analgesic as morphine (18), may not cause histamine release since very low amounts (0.2-0.4 mg) are required to achieve clinically useful effects.…”

Section: Discussionmentioning

confidence: 96%

“…Therefore, we can assume that buprenorphine, which is 30-40 times as potent an analgesic as morphine (18), may not cause histamine release since very low amounts (0.2-0.4 mg) are required to achieve clinically useful effects. Coltart & Malcolm (19) reported that "buprenorphine does not seem to cause histamine release", but this statement was not supported by clinical or experimental observations. Buprenorphine, which is a derivative of thebain, bears a close structural resemblance to morphine (Fig.…”

Section: Discussionmentioning

confidence: 96%

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No cutaneous histamine release with buprenorphine?

Girotra

Atray

Mittal

1990

Acta Anaesthesiol Scand

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Most narcotics cause histamine release, both systemic and cutaneous. Whether buprenorphine causes histamine release is not yet known. We conducted intradermal tests on 11 healthy adults with buprenorphine in dilutions of 1:10,000, 1:1000, 1:100 and 1:10 and with 0.9% saline and histamine 10(-3) mol/l. The size of dermal reaction was noted after 15 and 30 min. None of the volunteers showed any cutaneous reaction suggestive of histamine release with buprenorphine. The absence of histamine-releasing activity of buprenorphine may be due to the structure of the drug resulting in its decreased basicity or to the insufficient concentration of the drug achieved at mast cell membrane.

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Section: Discussionmentioning

confidence: 96%

Section: Discussionmentioning

confidence: 96%

No cutaneous histamine release with buprenorphine?

Girotra

Atray

Mittal

1990

Acta Anaesthesiol Scand

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“…14 Because of its apparent lack of cardiovascular effects, buprenorphine has been suggested as a preferred treatment for severe pain control in patients with unstable hemodynamic parameters. 15 Buprenorphine inhibits the human ether-a-gogo-related gene (HERG) I Kr in vitro. 4 However, to our knowledge, no cases of cardiac arrhythmia related to this compound have been documented.…”

Section: Discussionmentioning

confidence: 99%

Effects of Buprenorphine on Cardiac Repolarization in a Patient with Methadone-Related Torsade de Pointes

2005

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Torsade de pointes is a rare but potentially fatal ventricular arrhythmia that is often triggered by drugs that prolong the rate-corrected QT (QTc) interval. This arrhythmia has been attributed to levacetylmethadol and methadone, synthetic opioids used to treat heroin addiction. Levacetylmethadol, a derivative of methadone, is being withdrawn from the United States market because its use waned after a black box warning was issued to require electrocardiographic monitoring. Therefore, methadone and buprenorphine are the only opioids available for the treatment of heroin addiction. To our knowledge, the cardiac safety of buprenorphine in patients with methadone-related QTc prolongation has not been described. We report a patient who developed torsade de pointes while receiving high-dose methadone and was successfully inducted onto buprenorphine under close medical supervision. No clinically important QTc prolongation was observed in the acute setting or during follow-up. This observation suggests that buprenorphine may be a safe alternative to oral methadone in patients with opioid addiction who develop torsade de pointes.

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“…Nevertheless, attention must be paid to dosage and speed of administration, particularly where a preexisting pathological condition may affect cardiovascular competence, that is, in acute or chronic shock or in cardiac insufficiency. The cardiovascular effects of agonist and antagonist analgesics (including pentazocine and buprenorphine) are reviewed elsewhere in these Proceedings (Coltart & Malcolm, 1979).…”

Section: Cardiovascular Effectsmentioning

confidence: 99%

Side‐effects of mixed agonist‐antagonist analgesics used in sequential anaesthesia.

Devaux¹,

Schoepffler²,

Jp³

1979

Brit J Clinical Pharma

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1 Mixed agonist‐antagonist analgesics have analgesic action but also possess a range of side‐effects. 2 Narcotic antagonists do not reverse the non‐specific effects of opiates. 3 Under certain circumstances the effects of agonists and mixed agonist‐antagonists can be additive. 4 Chronic dosage of mixed agonist‐antagonists leads to a lower level of dependence than that observed with the standard narcotics. 5 Mixed agonist‐antagonists may not antagonize the respiratory effects of narcotics and may result in potentiation of such depression.

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Pharmacological and clinical importance of narcotic antagonists and mixed antagonists‐use in cardiology.

Cited by 8 publications

References 25 publications

No cutaneous histamine release with buprenorphine?

No cutaneous histamine release with buprenorphine?

Effects of Buprenorphine on Cardiac Repolarization in a Patient with Methadone-Related Torsade de Pointes

Side‐effects of mixed agonist‐antagonist analgesics used in sequential anaesthesia.

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