1 A prospective multicentre study of all acute poisonings among adults admitted to hospital (n = 1145) or dying outside hospital (n = 67) in Oslo was performed during 1980. 2 Of the 1212 episodes, 98.3% were self-poisonings, giving an annual incidence of 2.8 per 1000 inhabitants (%o), 3.1‰ in males and 2.6‰ in females. 3 The main toxic agents among the self-poisoned patients were ethanol (19.7%), benzodiazepines (17.8%), opiates (14.9%), neuroleptics (10.4%) and antidepressants (9.3%). In 58.9% of the episodes more than one toxic agent was taken. 4 Abuse among the self-poisoned patients was significantly ( p < 0.005) more common among males than females (64.2 v. 34.5%). 5 The rate of suicide attempts was significantly ( p < 0.005) higher among females than males (20.2 v. 12.9%), females showing increasing rate with age. However, when excluding abusers the rate of suicide attempts was similar in both sexes (27.6 v. 25.0%). 6 Compared to a reference population self-poisonings were most common in the lower middle and the lowest social classes. Patients in these social classes, however, showed a lower rate of suicide attempts than those in the two highest social classes. 7 Overall mortality was 6.0% ( n = 73), but 91.8% of all deaths occurred outside hospital indicating the importance of including these figures when self-poisonings are studied.

1 The clinical course in an unselected group of 1125 consecutively hospitalised self-poisonings was studied during 1 year in Oslo. 2 Mortality was 0.5%, but only 0.3% in those admitted without cardiac and respiratory arrest. Mortality among those in grade IV coma was 4.2%. 3 The deepest comas (grade III or IV) occurred in 25.1% of the admissions with a mean duration of the coma of 5.8 h (range 1-80). 4 Complications occurred in 21.7% of the admissions and 6.9% suffered more than one complication of which the most frequent were respiratory depression (13.5%), hypotension (5.3%), pneumonia (4.4%), and hypothermia (1.6%). The complication rate was highest in poisonings with opiates (60.7%), meprobamate (37.5%) and antihistamines (30.0%). 5 Arrhythmias and respiratory depression were closely associated with poisonings with antidepressants and opiates, respectively. Owing to frequent polydrug overdoses it was difficult to associate other complications with other main toxic agents. 6 Administration of antidotes (20.6%), cuffed intubation (4.4%) and forced alkaline diuresis (3.4%) were the most frequent special therapeutic measures taken. 7 The change in pattern of self-poisonings in Oslo focuses on antidote therapy and intensive care, especially outside hospital, but limits the need for haemodialysis and haemoperfusion which were performed in only 1.0% of the admissions.

Pharmacokinetics of lithium were studied in 4 females acutely intoxicated with lithium with maximal plasma concentrations of 8.7, 4.0, 3.4 and 1.3 mmol/l. Mean plasma dialysance values were 103, 105, 102 and 89 ml/min compared to mean renal clearance values of 13, 16, 20 and 30 ml/min, respectively. A rebound effect in plasma concentration suggested that the sum of the dialysance and renal clearance overestimated the total body clearance of lithium during hemodialysis. During hemodialysis the measured half-lives of the plasma lithium levels in three cases were 4.8, 3.4 and 2.3 hours compared to the corrected values of 12.0, 7.3 and 6.2 hours respectively, when this rebound effect was taken into consideration. These corrected half-lives were 30-66% of the control half-lives recorded later when each patient served as her own control, thus illustrating the effectiveness of hemodialysis in removing lithium. Forced diuresis with sodium chloride did not significantly increase renal lithium elimination.

Forty-year old men with untreated mild essential hypertension (n = 35) had decreased serum phosphate (P less than 0.001) concomitant with elevated resting plasma epinephrine (P less than 0.05) and heart rate (P less than 0.001) compared with age-matched, normotensive control men (n = 44). Blood pressure correlated negatively with serum phosphate (P less than 0.001) and positively with plasma epinephrine (P less than 0.01) and heart rate (P less than 0.01). Serum phosphate was significantly lowered during infusion of epinephrine, increasing arterial plasma epinephrine within the lower pathophysiological range corresponding to arousal reactions. Serum concentrations of immunoreactive parathyroid hormone were unchanged. Thus, hypophosphatemia in patients with mild essential hypertension appears to be inversely related to sympathetic adrenal tone and may be caused by increased plasma epinephrine within pathophysiologic arterial concentrations.

SUMMARY Baseline plasma vasopressin concentrations were measured in 48 men (all 50 years old) with decreased plasma renin concentration and untreated, sustained essential hypertension and in 29 healthy normotensive men. Mean hypertensive plasma vasopressin concentration was more than twice as high as the corresponding normotensive level (15.7 ± 2.2 [SE] vs 7.5 ± 1.0 pg/ml; p < 0.001). Plasma renin concentration in the hypertensive group was reduced compared with that in the normotensive group (0.28 ± 0.04 vs 0.46 ± 0.06 Goldblatt units X 10 4 /ml). These differences appeared despite virtually identical serum osmolality, creatinine clearance, and urinary sodium excretion in the two groups. In the first 38 hypertensive subjects, arterial plasma epinephrine concentrations were significantly increased over those of the first 28 control subjects (99 ± 12 vs 68 ± 6 pg/ml; p < 0.025). In contrast to those with low renin essential hypertension, 35 men with normal renin essential hypertension (all 40 years old) had normal plasma vasopressin levels that were not significantly different from those in a comparable normotensive control group (3.7 ± 0.8 vs 3.5 ± 0.4 pg/ml). Arterial epinephrine concentrations were not significantly different between normal renin subjects and the control group. After 6 weeks of treatment with the nonselective /3-adrenergic receptor blocker oxprenolol in 11 subjects with low renin hypertension, blood pressure was reduced and the plasma vasopressin concentration fell from 27.6 ±6.4 to 13.5 ±4.2 pg/ml (p < 0.01). After 6 weeks of treatment with the /3,-selective agent atenolol in another 11 men with low renin hypertension, plasma vasopressin level fell from 16.3 ± 3.3 to 13.1 ±3.1 pg/ml, but this reduction was not significant. In pooled groups treated with /3-adrenergic blockade, plasma vasopressin level decreased more the higher its initial concentrations (r= 0.79, p< 0.001, n = 22). These findings suggest that plasma vasopressin is increased in low renin essential hypertension and may be related to sympathetic adrenal overactivity. (Hypertension 8: 506-513, 1986) KEY WORDS • blood pressure • catecholamines • sodium • osmolality • /3-adrenergic blockade • pituitary • antidiuretic hormone A RGININE vasopressin (AVP) may increase /\ blood pressure primarily by volume reten-A. \. tion, but it is also a powerful vasoconstrictive agent, even more potent than angiotensin.1 It may also participate in cardiovascular regulation, both centrally 2 and peripherally, 3 and stimulate the gain of baroreceptor reflexes. 4 Potentiation of the vasoconstrictor effect of catecholamines has been established. with mineralocorticoid excess. 6 -9 "" Deoxycorticosterone-salt hypertension will not develop in the Brattleboro rat, which lacks AVP because of a genetic defect. Blockade by either specific antiserum or competitive antagonists of AVP substantially attenuates both the development and severity of preexisting deoxycorticosterone-salt hypertension. Most recently, observations by Hay wood et al.12 point to the sy...