Plantar flexion strengths were studied in 30 right-handed males. Static and dynamic maximum plantar flexion torques were recorded, knees fully extended (0 degrees) and in 90 degrees flexion. In five of the subjects the soleus and gastrocnemius muscle structure were studied by light microscopy and enzyme histochemistry. Specimens were obtained by needle biopsy, usually bilaterally. Intraindividual declines of force were found to be a function of angular motion velocity. Static and dynamic torques correlated significantly. Peak torques were significantly greater (mean 15%) at the 0 degrees than at the 90 degrees knee angle and left maximum plantar flexion torques at 0 degrees were greater (mean 10%) than right. Mean morphometric data on the m. soleus suggested right-left symmetry, which could not be demonstrated for the m. gastrocnemius. Fibres with low stainability for myofibrillar ATPase (Type 1 fibres) had smaller diameters, but constituted the major part of the cross-sectional areas. In these five non-athletes no significant correlation between data on plantar flexion strength and morphometric data on triceps surae structure could be demonstrated. On the other hand, strength covariated with calf circumference.

82 consecutive patients checked at the out-patient clinic of the Psychiatric Department of the Umeå University were typed for HL-A antigens. The patients belonged to the diagnostic subgroups: bipolar (manic-depressive) psychosis (n = 33), unipolar recurrent depressive psychosis (n = 29) and cycloid psychosis (n = 20) and all had been on lithium treatment for at least 6 months. By comparing the group of those who did not relapse on lithium therapy (n = 48) with the group of those who did relapse (n = 34) there was a significantly higher frequency of the HL-A A3 antigens among those who did relapse, and none of those who did not relapse were found to have the HL-A B18 antigens. The results suggest a possible interference between HL-A antigens and response to lithium treatment. However, a large number of antigens were tested and a small number of patients.

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We read with interest the review article by Komori et al. (Br J Surg 1991; 78: 1027-30). They emphasize the important role of the endothelium in modulating the underlying vascular smooth muscle by releasing endothelium-derived relaxing factor (EDRF), which is a potent vasodilator and inhibitor of platelet aggregation. In addition, they speculate on the possible relationship between decreased EDRF production by a functionally injured endothelium and the development of both vasospasm and intrinsic graft lesions.However, their article concentrates on reversed vein grafts where the effects of surgical preparation of the graft on EDRF production are well established', but they make no mention of the in situ technique. In femorodistal bypasses to below the knee this technique is the method of choice because it has the advantage of a better size-match between artery and vein graft at each anastomosis. Despite the fact that the vein is often fully mobilized' and a valvulotome is passed along its lumen to destroy the valves, it has been suggested that this technique leads to superior endothelial preservation when compared with the reversed method3.We have recently investigated endothelial and smooth muscle cell injury during preparation of both reversed and in situ vein grafts4. Whilst we agree that EDRF production is reduced after preparation of reversed vein grafts, it is absent after preparation of in situ grafts because of severe loss of endothelial cells and functional impairment of any remaining cells. In addition, preparation of reversed and in situ vein grafts also leads to injury to the smooth cells of the media.It is likely that cellular injury plays a role in the subsequent development of intrinsic lesions in infrainguinal vein grafts which are an important cause of failure in the first postoperative year. Recently a link has been established between endothelial and smooth muscle cell injury during preparation of reversed vein grafts and intimal hyperplasia in an organ culture system'. Therefore the importance of endothelial loss and absent EDRF production associated with the in situ technique warrants further study. . Surgical preparation impairs release of endothelium-derived relaxing factor from human saphenous vein. Ann Thorac Surg 1989; 48: 41 7-20. Beard JD. Wyatt M, Scott DJA, Baird RN, Horrocks M. The non-reversed vein femorodistal bypass graft: a modification of the standard in-situ technique. Eur J Vasc Sury 1989; 3: 55-60. Cambria RP, Megerman J, Abbott WM. Endothelial preservation in reversed and in-situ autogenous vein grafts. Ann Surg 1985; 4. Sayers RD, Watt PAC, Muller S, Bell PRF, Thurston H. Structural and functional smooth muscle injury after surgical 2. 3. 202: 50-5. preparation of reversed and non-reversed (in situ) saphenous vein bypass grafts. Br J Surg 1991; 78: 1256-8. Angelini GD, Soyombo AA, Newby AC. Smooth muscle cell proliferation in response to injury in an organ culture of human saphenous vein. Eur J Vasc Surg 1991; 5 : 5-12. 5.

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