Myocardial bridging is recognized as an anatomical variation of the human coronary circulation in which an epicardial artery lies in the myocardium for part of its course. Thus, the vessel is 'bridged' by myocardium. The anterior interventricular branch of the left coronary artery has been reported as the most common site of myocardial bridges but other locations have been reported. The purpose of this study was to provide more definitive information on the vessels with myocardial bridges, the length and depth of the bridged segment, and the relationship between the presence of bridges and coronary dominance. Two hundred formalin-fixed human hearts were examined.Myocardial bridges were found in 69 (34.5%) of the hearts with a total of 81 bridges. One bridge was found in 59 of these hearts and multiple bridges were observed in ten (eight with double bridges and two with triple bridges).Bridges were most often found over the anterior interventricular artery (35 hearts). Bridges were also found over the diagonal branch of the left coronary artery (14), over the left marginal branch (five) and over the inferior interventricular branch of the left coronary artery (six). Bridges were also found over the right coronary artery (15 hearts), over the right marginal branch (four) and over the inferior interventricular branch of the right coronary artery (two). The presence of bridges appeared to be related to coronary dominance, especially in the left coronary circulation. Forty-six (66.6%) of the hearts with bridges were left dominant. Forty-two of these had bridges over the left coronary circulation and four over the right coronary circulation. Seventeen hearts (24.6%) were right dominant. Eleven of these had bridges over the right coronary circulation and six over the left coronary circulation.The remaining six hearts were co-dominant with four having bridges over the left coronary circulation and two over the right coronary circulation. The mean length of the bridges was 31 mm and the mean depth was 12 mm.The possible clinical implications of myocardial bridging may vary from protection against atherosclerosis to systolic vessel compression and resultant myocardial ischaemia.

Prolonged exposure to hand-transmitted vibration can cause debilitating neural and vascular dysfunction in humans. It is unclear whether the pathophysiology involves simultaneous or sequential injury of arteries and nerves. The mechanism of vibration injury was investigated in a rat tail model, containing arteries and nerves structurally similar to those in the human hand. Tails were selectively vibrated for 1 or 9 days with the remainder of the animal at rest. One vibration bout of 4 h/day, 60 HZ, 5 g (49 m/s(2)) acceleration, injured endothelial cells. Injury was signaled by elevated immunostaining for NFATc3 transcription factor. Electron microscopy revealed that vibration for 9 days produced loss and thinning of endothelial cells, with activated platelets coating the exposed subendothelial tissue. Endothelial cells and arterial smooth muscle cells contained double membrane-limited, swollen processes indicative of vasoconstriction-induced damage. Laser doppler surface recording demonstrated that 5 min of vibration significantly diminished tissue blood perfusion. These findings indicate that early injury involves vasoconstriction and denuding of the arterial endothelium.

Pure antiandrogens, like flutamide, antagonize androgen action both peripherally and centrally at the hypothalamic-pituitary axis, which leads to an increase in LH and testosterone secretion. A new non-steroidal antiandrogen ICI 176,334 [2RS)-4'-cyano-3-(4-fluorophenylsulphonyl)-2-hydroxy-2-methyl-3'- trifluoromethyl)propion-anilide) has now been discovered which causes regression of the accessory sex organs but does not increase serum concentrations of LH and androgens. ICI 176,334 binds to rat prostate androgen receptors with an affinity around fourfold that of hydroxyflutamide. When administered s.c. concurrently with testosterone propionate (200 micrograms/kg) for 7 days to immature castrated rats, ICI 176,334 (10 mg/kg) significantly (P less than 0.001) inhibited growth of the seminal vesicles and ventral prostate gland. Oral administration of ICI 176,334 at doses of 1, 5 and 25 mg/kg for 14 days to adult rats caused a dose-related reduction in accessory sex organ weights but had no effect on the testes. None of these doses caused a significant increase in serum LH and testosterone. Flutamide was around fourfold less potent and significantly increased serum LH and testosterone at the higher doses. ICI 176,334 was well tolerated. ICI 176,334 should, therefore, prove useful for the treatment of androgen-responsive benign and malignant diseases.

Increased tolerance to ischemia exhibited by chronically hypoxic rabbit hearts is associated with increased activation of the KATP channel. This increased KATP activity may be the result of increased intracellular concentrations of lactate.

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