Disease relevance of DAZMEGREL

• The ultimate establishment of severe hypertension was not prevented by UK-38,485 [1].
• In a canine model of global brain ischemia, six dogs received a selective thromboxane A2 synthetase inhibitor, UK 38,485 (dazmagrel) before the ischemic event; six received a saline placebo [2].
• Since the highly metastatic variant M4 of the mFS6 fibrosarcoma has the peculiar feature of generating larger amounts of immunoreactive thromboxane B2 (TxB2) than the non-metastatic variant (M9), we used the thromboxane synthase inhibitor dazmegrel (UK-38,485) in an effort to influence its metastatic potential [3].
• Oral administration of UK-38,485 for six days to nephrotic rats did not result in a statistically significant reduction of proteinuria despite 85% inhibition of glomerular TxB2 [4].
• Dazoxiben, UK 38,485 and aspirin: duration of effect for preventing thrombotic sudden death in rabbits [5].

High impact information on DAZMEGREL

• The rationale and potential uses of UK-38,485 in the in vivo prevention of platelet aggregation and for the therapy of cerebrovascular disease are discussed [6].
• The mean forced expiratory volume in one second (FEV1) after UK-38,485 was 2.55 l, compared to 2.56 l after treatment with placebo (p = 0.74) [7].
• The geometric mean provocative dose of methacholine producing a 20% fall in FEV1 (PD20) before and after UK-38,485 was 23.9 and 32.2 micrograms, respectively, compared to 25.1 and 26.3 micrograms respectively, before and after placebo (p = 0.31) [7].
• Pulmonary vasoconstriction was inhibited by the cyclooxygenase blocker meclofenamate (10 mg/kg) and the thromboxane synthase inhibitor Dazmegrel (UK-38,485) (2 mg/kg) [8].
• However, the TXA2 mimetic, U46619, did not stimulate TNF alpha release by AM either in the absence or presence of UK 38,485 [9].

Chemical compound and disease context of DAZMEGREL

• Effects of thromboxane synthetase inhibitor (UK 38,485) and thromboxane receptor antagonist (ICI 185,282) on digoxin-induced arrhythmias in anaesthetized guinea-pigs [10].

Biological context of DAZMEGREL

• UK 38,485 did not influence the baseline perfusion pressure, the mean arterial blood pressure or the potentiation of neurotransmission by angiotensin II [11].
• The effect of the thromboxane synthetase inhibitor Dazmegrel (UK-38,485) on wound healing, dermal ink perfusion and skin blood flow measurements in deep partial thickness burns [12].
• Rabbit epigastric skin flaps were subjected to 4 h of body temperature ischaemia, then infused with either the TXA2 synthetase inhibitor UK-38,485, the free radical scavenger superoxide dismutase (SOD), or both immediately prior to reperfusion [13].

Anatomical context of DAZMEGREL

• These data indicate that in the in situ rat mesentery UK 38,485 attenuates the release of neurotransmitter from sympathetic nerve terminals [11].
• Ten piglets were infused with GBS, and all animals developed a significant increase in pulmonary artery pressure (to 39 +/- 5 and 36 +/- 5 mmHg for DAZ and BW755C animals respectively) [14].

Associations of DAZMEGREL with other chemical compounds

• Some of these flaps were treated at the time of reperfusion with the free-radical scavenger superoxide dismutase (EC 1.15.1.1) and/or the thromboxane synthetase inhibitor UK-38,485 [15].
• Inhibition of thromboxane synthase by UK 38,485 also reduced TNF alpha release by active miners' AM but had no effect on PGE2, LTB4 production, or IL-1 beta release [16].

References