Phaeochromocytoma is rare and usually presents as paroxysmal or sustained hypertension; none the less, it can also cause severe acute pulmonary oedema in normotensive individuals.Six patients with phaeochromocytoma presenting in Cornwall and West Devon between 1982 and 1986 bilateral scattered crepitations. The chest x ray showed a slightly enlarged cardiac shadow and pulmonary oedema. The electrocardiogram showed sinus tachycardia, poor R wave progression in the chest leads, and non-specific T wave changes. Full blood count and electrolytes were normal and analysis of arterial blood gases showed Po2 9-8 kPa, Pco2 3-2 kPa, and pH 7-2. She deteriorated rapidly and despite resuscitative measures she died within two hours of admission.At necropsy the heart weighed 285 g (normal 250-400 g) with minimal dilatation of both ventricles. No significant lesions were found in the coronary arteries and histological examination of the heart showed patchy muscle fibre necrosis with phagocytosis. Severe haemorrhagic oedema was found in both lungs, which showed no evidence of acute pulmonary infarction. A tumour 4 cm in diameter was found in the right adrenal gland and histology showed this to be a phaeochromocytoma.PATIENT 2 A 63 year old woman was admitted with a history of chest pain and breathlessness for two hours. The week before she had presented to the local cottage hospital with malaise, pedal oedema, and non-specific chest discomfort. She had had no other significant problems in the past and had never had hypertension. On admission she was pale with sinus tachycardia of 146 beats/min and blood pressure of 110/70 mm Hg. Jugular venous pressure was 3 cm above the sternal angle and auscultation showed a gallop rhythm. She had widespread crepitations in both lung fields. The electrocardiogram showed no evidence of myocardial infarction or left ventricular hypertrophy and the chest x ray was consistent with pulmonary oedema. She was treated with frusemide, amoxycillin, and dobutamine but she did not respond to these measures and died within eight hours of admission.At necropsy the heart weighed 350 g (normal 250-400 g) and was macroscopically normal. Histological examination of the myocardium showed vacuolar and focal necrosis with an inflammatory reaction. The coronary arteries were normal. The airways contained frothy liquid and the lungs were moist on section with microscopic changes consistent with acute pulmonary oedema. The right adrenal gland was replaced by a phaeochromocytoma weighing 70 g with typical histology. PATIENT 3 This 39 year old woman with long standing 234

IThe effects of ,-adrenoceptor blockade on the metabolic responses to isoprenaline have been studied in an in vitro system of isolated fat cells and in six normal subjects. 2 The inhibitory effects of varying concentrations of acebutolol, practolol and propranolol on free fatty acid (FFA) release produced by isoprenaline (10-7 M) were compared in isolated fat cells prepared from rat epididymal adipose tissue. Acebutolol and practolol, at equimolar concentrations, showed a similar inhibitory effect whilst propranolol was approximately 100 times more potent then either drug. At 10-SM concentration of propranolol, lipolysis was virtually abolished whilst at the same molar concentration, acebutolol and practolol halved the response.3 Six healthy volunteers received three successive 15 min intravenous isoprenaline challenges (0.03 ,g kg-' min-' ) per individual experiment. The first acted as a control whilst the following two were given either after single oral doses of placebo, acebutolol or practolol. The mean (± s.e. mean) basal FFA level was 0.77 ± 0.06 mEq/1 and subsequent resting values after the administration of placebo or ,-adrenoceptor blocker were not significantly different. 4 Acebutolol inhibited the respective mean rises in FFA, produced by both post-control isoprenaline challenges, by (mean ± s.e. mean) 70 ± 4% and 84 ± 5%. The comparable figures for practolol were 33 ± 15% and 24 ± 20%. The higher serum concentration of acebutolol produced greater inhibition but correlation of log serum concentration of the drug with percentage inhibition of FFA rise did not achieve significance. 5 Administration of isoprenaline, acebutolol or practolol did not significantly alter serum glucose, triglyceride or cholesterol levels. 6 Acebutolol and practolol effectively blocked the isoprenaline-induced tachycardia. The degree of blockade produced by practolol was greater than its inhibitory effect on FFA release. The diastolic fall in blood pressure in response to isoprenaline was abolished by acebutolol suggesting that its ,-adrenoceptor blocking action encompasses peripheral vascular sites. The comparable effect with practolol was a partial inhibition of the diastolic fall.

No abstract

brain damage and continued excessive drinking represents a particularly serious threat to the lives of other road users, and if we are to take this threat seriously the assessment of convicted drunken drivers with the Halstead-Reitan test battery and the EMI-Scanner deserves our careful consideration not only as a possible index of current disability but also as a possible prognostic guide.I hope shortly to produce a six-year followup of our series of 33 alcoholics which may tell us whether the likelihood of relapse is related to objective indices of the extent of brain damage.