Chlorpropamide alcohol flush and circulating met-enkephalin: a positive link.

Medbak, S.; Wass, Jah; Clement‐Jones, Vicky; Cooke, E. D.; Bowcock, S.A.; Cudworth, A G; Rees, Lesley

doi:10.1136/bmj.283.6297.937

Cited by 46 publications

(18 citation statements)

References 16 publications

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“…This last effect involves both endogenous prostaglandins and a naloxone-sensitive component (Medbak et al, 1981) and we are currently investigating whether the PGI2 flush is also naloxone-sensitive.…”

Section: Discussion and Literature Review Flushingmentioning

confidence: 99%

Side effects occurring during administration of epoprostenol (prostacyclin, PGI2), in man.

Pickles¹,

O’Grady²

1982

Brit J Clinical Pharma

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1 Fifty infusions of epoprostenol (PGI2) were made, usually increasing the infusion rate until adverse effects were encountered. The volunteers were appraised that they might experience headache and facial flushing. 2 Facial flushing, headache, tachycardia and decrease in diastolic blood pressure were seen in almost all subjects. Erythema over the venous infusing site was also encountered in 13 infusions. Less common effects were sudden bradycardia, pallor and sweating-the vagal reflex-(seven times) and chest pain (twice). Other complaints included restlessness, abdominal discomfort, nausea and drowsiness.3 The literature on side effects reported during PGI2 infusion is reviewed and recommendations are made concerning administration of PGI2.

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Section: Discussion and Literature Review Flushingmentioning

confidence: 99%

Side effects occurring during administration of epoprostenol (prostacyclin, PGI2), in man.

Pickles¹,

O’Grady²

1982

Brit J Clinical Pharma

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“…ap <0.05, significance of difference between CPAF-positive and CPAF-negative subjects hyde [8]. In addition, there are data suggesting that endogenous opiates such as metenkephalins may be implicated in CPAF [15] either directly or indirectly by interference with the rise in blood acetaldehyde.…”

Section: Discussionmentioning

confidence: 99%

Roles of chlorpropamide, alcohol and acetaldehyde in determining the chlorpropamide-alcohol flush

et al. 1984

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Summary. The value and reproducibility of the chlorpropamide-alcohol flush (CPAF) have been questioned, and objective measures of the test are required. Recording of facial skin temperature, measurement of chlorpropamide, ethanol and acetaldehyde concentrations have been proposed for this purpose. The present study was designed to evaluate the relative contributions of these variables in determining CPAF. Twenty-one Type 2 (non-insulin-dependent) diabetic patients (11 CPAF-positive and 10 CPAF-negative according to previous tests with standard amounts of alcohol and chlorpropamide) were investigated in a random fashion with either chlorpropamide or placebo given on three subsequent evenings before a two-step alcohol challenge with increasing body-weightmatched amounts of alcohol. Higher rises in facial skin temperature and heart rate, higher flush-score and higher acetaldehyde levels resulted from chlorpropamide therapy than followed placebo. After smaller alcohol challenges (with chlorpropamide pretreatment) there were positive intercorrelations between flush-score, rise in facial skin temperature, and plasma concentrations of chlorpropamide and blood acetaldehyde. The increased alcohol dose abolished most of these correlations and a minimum temperature rise of 1.8 ~ appeared in all but two subjects regardless of previous CPAF classification. During the current experimental conditions, the previously-classified CPAF-positive and CPAF-negative patients did not differ with respect to flush-score, rise in skin temperature, heart rate, blood acetaldehyde or ethanol concentrations, whereas they differed with respect to chlorpropamide concentrations. The present results support the view that CPAF is associated with elevated blood acetaldehyde levels due to inhibition of aldehyde dehydrogenase by chlorpropamide. Thus both alcohol and chlorpropamide concentrations are critical in determining the CPAF. Furthermore, body weight matching in applying the CPAF test is essential.

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“…However, recently we have shown that circulating MLI levels rise following oral ethanol in chlorpropamide pretreated human subjects (Medbak et al, 1981) and dogs (Medbak et al, 1983). Moreover plasma MLI levels rise in greyhounds during insulininduced hypoglycaemia (Medbak et al, 1985) and artificial hyperventilation (Mason & Medbak, 1986).…”

Section: Discussionmentioning

confidence: 99%

Circulating [Met]enkephalin and catecholamine responses to acute hypotension and hypertension in anaesthetized greyhounds

Mason

Medbak

Rees

1987

British J Pharmacology

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4 Intravenous hexamethonium (2.5 mg kg-') provoked a fall in blood pressure which was not associated with any changes in plasma MLI. However, it produced a fall in plasma noradrenaline and a rise in plasma adrenaline. Thus it appears that neural mechanisms are required, at least in part, for the release of MLI. 5 Angiotensin 11 (1.25 jig kg-' min ') and noradrenaline (8 pg kg-' min ') infusions produced an elevation in blood pressure without altering the circulating MLI levels. 6 Study of the molecular forms of circulating MLI, before and during hypotension, revealed that the large molecular weight enkephalin-containing peptides with approximate molecular sizes of 1 8kD and 8kD were the predominant forms both in the basal and stimulated states. 7 It is concluded that circulating [Metlenkephalin is not involved in the tonic control of blood pressure but it may modulate catecholamine release following hypotension as part of the stress response.

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Chlorpropamide alcohol flush and circulating met-enkephalin: a positive link.

Cited by 46 publications

References 16 publications

Side effects occurring during administration of epoprostenol (prostacyclin, PGI2), in man.

Side effects occurring during administration of epoprostenol (prostacyclin, PGI2), in man.

Roles of chlorpropamide, alcohol and acetaldehyde in determining the chlorpropamide-alcohol flush

Circulating [Met]enkephalin and catecholamine responses to acute hypotension and hypertension in anaesthetized greyhounds

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