Harm minimisation for drug misusers.
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Biomedical subjects
Publications and source records attributed to N Payne.
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Measurements of plasma atrial natriuretic peptide concentrations at 8 AM showed raised levels in 21 patients with cirrhosis and ascites (10.5 +/- 0.8 pmol/L) compared with levels in 10 age-matched controls (4.1 +/- 0.64 pmol/L; p less than 0.0001). In eight patients and 10 controls, atrial natriuretic peptide, plasma renin activity, plasma aldosterone and urinary sodium excretion were measured every 4 hr for 24 hr. Subjects were mobile between 8 AM and 11 PM and supine from 11 PM to 8 AM. In controls, urinary sodium excretion was highest between 4 PM and 11 PM (19.34 +/- 3.74 mumol/min) and lowest between midnight and 8 AM (7.06 +/- 1.23 mumol/min; p less than 0.001). In patients, urinary sodium excretion was 0.63 +/- 0.14 mumol/min between 4 PM and midnight and 1.85 +/- 0.71 mumol/min (p less than 0.08) between midnight and 8 AM. In patients during the day, mean plasma atrial natriuretic peptide concentration did not change despite large individual variation, but large, sustained rises in plasma renin activity and plasma aldosterone were seen. Correlations were noted between atrial natriuretic peptide and urinary sodium excretion between midnight and 8 AM (r = 0.65; p less than 0.02) and 4 PM and midnight (r = 0.54; p less than 0.05) but not between 8 AM and 4 PM. Plasma renin activity dropped from 12.54 +/- 2.49 at midnight to 7.41 +/- 0.88 pmol/hr/ml at 8 AM (p less than 0.05); plasma aldosterone decreased from 1,032 +/- 101 to 798 +/- 56 pmol/L (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
We studied 86 primiparous women with uncomplicated pregnancy and labour requesting extradural analgesia in labour. All the women were over 36 weeks of gestation with a cephalic-presenting singleton fetus. The women were allocated randomly to two groups: group A, who received an extradural infusion of lignocaine 0.75%, after an initial dose of 10 ml of lignocaine 1.5%, and group B, who received an infusion of bupivacaine 0.125% after an initial dose of 10 ml of bupivacaine 0.25%. All the women had their labour actively managed. Assessment of analgesia during labour and delivery, and the requirements for additional top-ups were noted, as were mode of delivery, requirement for oxytocic augmentation and incidence of fetal distress. Maternal and umbilical cord plasma concentrations of lignocaine were measured at delivery in 12 women receiving extradural lignocaine. There were no statistically significant differences between the two groups in terms of the mode of delivery, incidence of fetal distress, fetal heart rate abnormalities, or Apgar scores of the babies. Women in the bupivacaine group had a significantly better quality of analgesia during both the first and second stages of labour (p = 0.0005) and required fewer top-ups than those in the lignocaine group. However, the requirement for oxytocin augmentation during the first and second stages of labour was significantly less in the lignocaine group (p = 0.004). Similarly, the duration of the second stage was shorter compared with the bupivacaine group. In spite of high plasma concentrations of lignocaine, no side effects were noted in either mothers or babies.
Hydrocephalus can occur in conjunction with large acoustic neuromas. Cerebral tentorial herniation and brainstem compression can be a complication of surgical excision. Three cases of hydrocephalus and acoustic neuroma are presented and therapeutic options are discussed. Ventriculoperitoneal shunting 1 to 2 weeks before translabyrinthine or suboccipital excision of acoustic neuroma is recommended.
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1. Azumolene sodium is a new water-soluble derivative of dantrolene sodium that also acts as a skeletal-muscle relaxant. 2. Azumolene (6 mumol/L) inhibited the hypercontractility induced separately by 3% halothane, 2 mmol/L caffeine and 80 mmol/L potassium chloride in isolated malignant hyperpyrexia (MH)-susceptible muscle. Azumolene was equipotent with dantrolene in inhibiting the abnormal responses. 3. Like dantrolene, azumolene (6 mumol/L) not only prevented but reversed the abnormal contractures induced by halothane and caffeine. Contracture responses to caffeine were also modified by azumolene in control preparations. 4. In the presence of maximal effective concentrations of dantrolene, azumolene failed to further relax caffeine-induced contractures, and the converse was also true. This was observed in both MH-susceptible and control preparations. 5. Sarcoplasmic reticulum Ca(2+)-dependent ATPase activity from MH-susceptible and control muscle was not affected by azumolene. 6. Like dantrolene, azumolene may inhibit Ca2+ release directly from the sarcoplasmic reticulum and be of therapeutic value for the treatment of MH.
It has been postulated that deficiency of a putative natriuretic factor, or resistance to such a factor, may contribute to sodium retention in fulminant hepatic failure. Levels of plasma human atrial natriuretic factor (h-ANF), plasma renin activity, and aldosterone concentration were measured in 33 patients with fulminant hepatic failure due to paracetamol overdose, and 12 healthy control subjects. Levels of h-ANF were raised only in patients with evidence of severe renal impairment (serum creatinine greater than 300 mumol/l and urine output less than 100 ml/24 hours). h-ANF values were median 4.15, range 2-9 pmol/l and 10.1, 1-25 pmol/l for the control and severe renal impairment groups respectively (p less than 0.001). In the latter plasma renin activity was raised compared to that in control subjects (median 19.8, range 1.04-41.7 and 2.86, 1.87-5.9 pmol/l/h respectively, p less than 0.02). Plasma aldosterone concentration was also raised in patients (2176, 199-6894 pmol/l compared to 368, 133-578 pmol/l in control subjects, p less than 0.01). Haemodialysis induced changes in circulating h-ANF which correlated with volume and right atrial pressure changes (p less than 0.001 and p less than 0.05 respectively). In six patients with no or mild renal failure infusion of 900 ml 5% human albumin solution caused a significant increase in plasma h-ANF (p less than 0.05) without natriuresis or diuresis, a finding compatible with the hypothesis that there may be resistance to h-ANF in this group. The present findings indicate that there is no deficiency of h-ANF in fulminant hepatic failure and that known mechanisms of h-ANF release are not impaired.
The acute natriuretic effect of human atrial natriuretic peptide (ANP) has been well described in man. We have now studied possible hormonal mediators of this effect. We studied six healthy volunteers on two occasions when they received either an infusion of ANP of 1.5 pmol X kg-1 X min-1 for 30 min followed by 15 pmol X kg-1 X min-1 for a further 30 min, or matching vehicle infusions in a randomized single-blind fashion. On the placebo day, plasma renin activity (PRA) rose from 1.26 +/- 0.08 to 1.57 +/- 0.14 ng A1 X ml-1 X h-1, while on the ANP study day PRA fell from 1.45 +/- 0.15 to 1.28 +/- 0.05 ng A1 X ml-1 X h-1 (p less than 0.01). No significant changes were found in plasma aldosterone concentrations or in urinary dopamine excretion. These results provide evidence that ANP suppresses renin release in man.
1. Fourteen mildly hydropenic normal volunteers were slowly tilted at a constant rate from the horizontal to the 85 degrees head-up position in order to study the interrelationship between plasma arginine vasopressin concentration, plasma renin activity and the change of plasma volume. 2. Nine subjects did not develop vaso-vagal symptoms and were studied for 45-60 min. Arginine vasopressin rose biphasically in all subjects: a small initial rise, which was seen at 3 min and persisted for 30 min, was followed by a striking rise between 30 and 45 min, when the fall of plasma volume had reached its maximum (17%). 3. Plasma renin activity reached a maximum at 30 min but fell by 45 min, as plasma concentration of arginine vasopressin rose. 4. Five subjects developed vaso-vagal symptoms 4-24 min after reaching 85 degrees when the study was terminated. A striking increase of arginine vasopressin concentration was seen within 4 min of syncope, but there was no change of plasma osmolality, cortisol concentration or renin activity.