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PubMed1980

Blockade of chlorpropamide-alcohol flushing by indomethacin suggests an association between prostaglandins and diabetic vascular complications.

Chlorpropamide/alcohol flushing (CPAF), found in many patients with non-insulin-dependent diabetes (NIDD), can be blocked by indomethacin in most patients who are free of vascular complications but not in those with such complications. Since indomethacin is a prostaglandin inhibitor this finding suggests that prostaglandins may be involved in the aetiology of vascular diseases in NIDD. All 6 pairs of identical twins with CPAF, of whom 2 pairs were disocrdant for diabetes, were concordant for indomethacin blocking, which suggests that the block has a genetic basis. The difference in the response of CPAF to indomethacin in diabetic patients with and without vascular complications is probably the first indication of a metabolic difference between these two types of patient.

Blood Vessels↗
PubMed1984

Prostacyclin and thromboxane in non-insulin dependent diabetes: the chlorpropamide alcohol flush reaction revisited.

Levels of immunoreactive 6-oxo-prostaglandin F1 alpha (6-oxo-PGF1 alpha) and thromboxane B2 (TXB2) were measured in peripheral venous plasma in a group of volunteers and non-insulin dependent diabetic patients (NIDDS). Levels of these eicosanoids were close to the limit of sensitivity of the radioimmunoassays and consequently data are reported as maximal values. Basal plasma levels of 6-oxo-PGF1 alpha did not exceed 5 pg/ml in either group and maximal levels of immunoreactive TXB2 were 125 +/- 14 and 128 +/- 8 pg/ml for volunteers and NIDDS respectively. Attempts to elicit peripheral vascular prostacyclin biosynthesis in volunteers by using forearm ischaemia produced no increase in plasma 6-oxo-PGF1 alpha levels. Measurement of the combined plasma levels of 6-oxo-PGF1 alpha, 13,14-dihydro-6-oxo-PGF1 alpha, 13,14-dihydro-6,15-dioxo-PGF1 alpha and 6-oxo-PGE1 indicated that these were also low (less than 5 pg/ml) and that failure to demonstrate increased 6-oxo-PGF1 alpha levels was unlikely to have arisen from metabolism of prostacyclin to one or more of these metabolites. Measurement of 6-oxo-PGF1 alpha and TXB2 in peripheral venous plasma before and during chloropropamide alcohol flushing (CPAF) did not provide evidence for a role for these eicosanoids in the etiology of this phenomenon. These findings point to the need for a reappraisal of studies that have described altered plasma levels of 6-oxo-PGF1 alpha and TXB2 in CPAF and other pathophysiological conditions in man.

6-Ketoprostaglandin F1 alpha↗