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Platelets produce a range of bronchoconstrictor mediators. Measurements of plasma factors have implicated platelet activation in allergic asthma, and sensitised guinea pigs challenged with ovalbumin show pulmonary platelet aggregation accompanying bronchoconstriction. To investigate this further we injected autologous platelets labelled with indium 111 and red cells labelled with technetium 99m into three young volunteers with atopic asthma and three non-asthmatic volunteers and, after equilibration of platelets between blood and splenic pool, monitored lung 99mTc and 111In activities continuously. Comparison with the corresponding activities in blood samples allowed calculation of pulmonary platelet to red cell transit time ratio (tp/tr). This ratio was 0.9, 1.02, and 0.98 in the non-asthmatic subjects compared with 1.04, 0.97, and 1.17 in the asthmatic subjects. This argues against the existence of an intrapulmonary platelet pool in normal subjects; transpulmonary transit time was slightly prolonged in one asthmatic subject. Bronchial challenge with Dermatophagoides pteronyssinus was performed in the asthmatic subjects and monitoring continued for a further 30 minutes. Antigen induced falls in FEV1 of 20-50% were accompanied by small decreases in the 111In but not in the 99mTc lung signal. In line with this tp/tr fell to 0.89, 0.89, and 1.05. Antigen induced bronchoconstriction was therefore not accompanied by intrapulmonary platelet accumulation. Platelet survival was normal at 10.2 days in both groups of subjects.

The development of fluorescein angiography has stimulated a great deal of interest in the vascular physiology of the retina and choroid by providing a method for examining different aspects of the ocular circulation in vivo. Of particular interest is the role of the blood supply to the optic disc in the production of field defects in glaucoma, and its relationship to pathological disc cupping (Hayreh, I969, 1970; Blumenthal, Best, Galin, and Toyofuku, 1971; Goldmann and Blok, 197I). A number of experiments in animals and man have been carried out to demonstrate the influence of acute and chronic rises in the intraocular pressure on the choroidal supply to the disc and peripapillary region (Blumenthal, Gitter, Best, and Galin, I970; Swietliczko and David, 1970; Blumenthal, Best, and Galin, 197I). In these conditions of high intraocular pressure, whether pathological or experimental, several observations have been made on the accompanying reduction of blood velocity in the retinal arteries but, apart from the studies by Dollery, Henkind, Kohner, and Paterson (I968), little quantitative data exists on this relationship between altered perfusion pressure and retinal blood flow. The present series of experiments was designed as an extension of the work of Dollery and his co-workers to investigate the changes in retinal blood flow velocity and retinal blood flow at different intraocular pressures, and to study the effects of measures used to treat retinal artery obstructions in man.

Branch and hemisphere vein occlusion were produced in rhesus monkeys by argon laser photocoagulation. The following observations were made: (1) Immediately after occlusion there was venous dilatation, delayed filling of the artery, delayed drainage by the occluded vein, and capillary leakage. (2) Two patterns of evolution were identified within the first week. In some animals the fundus changes resolved and the retina returned to normal, while in others there was progressive retinal capillary closure. (3) Those animals destined to have capillary closure had diffuse or cluster retinal haemorrhages at 24 hours. (4) Capillary closure took place over 1 week and was usually complete over large areas of retina. (5) Retinal atrophy and major vessel changes occurred over several weeks. (6) Retinal revascularisation occurred in those areas of closure, though this was often limited. It was concluded that the early changes mimicked those seen in human retinal vein occlusion, though persistent retinal oedema and preretinal neovascularisation were not identified.

A self-administered symptom questionnaire was completed by 477 patients in a hypertension clinic. The complaints of the patients were analysed according to the type of therapy being given and the dose of drug taken. Methyldopa therapy was associated with sleepiness, weakness of the limbs, sleeping longer at night, and rising more frequently at night to pass urine. Diarrhoea, impotence, failure of ejaculation, blurred vision, depression, and the symptoms of postural hypotension were not related to methyldopa therapy. Bethanidine administration was related to postural hypotension, impotence, and failure of ejaculation but not to weakness of the limbs, blurred vision, depression, or diarrhoea. Patients receiving guanethidine complained of postural hypotension, failure of ejaculation, and had their bowels open more frequently. Similarly, patients receiving propranolol had an increased frequency of defaecation but also tended to complain of weakness of the limbs. Considering each drug individually, 5% of patients failed to take the prescribed dose of diuretic whereas

The possibility that enalapril might damage renal function was investigated in 1098 deaths recorded in a prescription-event monitoring study. Case notes for 913 patients were examined. In seventy five there was a rise in the urea or creatinine concentration of 50% or more above pretreatment values. Enalapril appeared to have contributed to a decline in renal function and subsequent death in 10 of these patients. Several characteristics were identified among these patients, including old age, the use of high dose or potassium sparing diuretics, and pre-existing renal disease. Adding a non-steroidal anti-inflammatory drug was also associated with a deterioration in patients with previously stable renal function. No death was encountered of a patient with uncomplicated hypertension. Enalapril infrequently contributed to a substantial decline in renal function in certain vulnerable patients, especially those receiving other drugs known to be capable of adversely affecting renal function. Awareness of the characteristics of these patients and of their concomitant treatment may serve to reduce the risk.