Chronic hypernatraemia and hypothermia following subarachnoid haemorrhage

Nussey, S. S.; Ang, V. T. Y.; Jenkins, Janis H.

doi:10.1136/pgmj.62.728.467

Cited by 9 publications

(5 citation statements)

References 17 publications

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“…Apomorphine-induced nausea caused a marked rise in plasma AVP in normal subjects similar to that seen in other studies (Rowe et al, 1979;Baylis et al, 198,l;Sorensen & Hammer, 1985;Grant et al, 1986). We have previously demonstrated that the immunoreactive AVP released in response to this stimulus is chromatographically identical to synthetic peptide and is bioactive (Nussey et al, 1986b). In the present study we show that in normal subjects there is also a significant, though much smaller, increase in plasma OXT in response to the same stimulus.…”

Section: Discussionsupporting

confidence: 90%

Responses of Plasma Oxytocin and Arginine Vasopressin to Nausea Induced by Apomorphine and Ipecacuanha

Nussey

Hawthorn

Page

et al. 1988

Clinical Endocrinology

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Apomorphine, a centrally-acting emetic, was administered subcutaneously (50 micrograms/kg) to nine normal subjects (four male, five female; aged 22-36 years) and four patients with idiopathic diabetes insipidus (DI) (one male, three female; aged 24-49 years). In the normal subjects this stimulus caused nausea (and vomiting in seven of nine) with a latency of 9.5 +/- 0.9 min which was followed by a large increase in plasma arginine vasopressin (AVP) concentration (from 0.9 +/- 0.2 pmol/l to 249 +/- 104 pmol/l at 15 min after the onset of symptoms; mean +/- SEM, P less than 0.01). There was a small but significant increase in plasma oxytocin (OXT) concentration (from 1.6 +/- 0.4 pmol/l to 6.2 +/- 3.4 pmol/l; P less than 0.05). Mean arterial pressure (MAP) fell slightly (from 87 +/- 1.9 mm Hg to 71 +/- 4.4 mm Hg; P less than 0.05) 15 min after the onset of nausea; there was no change in blood haematocrit or plasma osmolality and sodium concentration. In the DI patients apomorphine produced nausea (with vomiting in three of four) with a latency of 10.0 +/- 1.4 min but failed to cause an increase in either plasma AVP or OXT. In the DI patients the fall in MAP did not reach statistical significance (83 +/- 4 mm Hg to 71 +/- 11 mm Hg); there was also no change in haematocrit, osmolality or sodium concentration. Ipecacuanha, an emetic with both peripheral and central actions, was administered orally to seven normal subjects (three male, four female; aged 22-36 years) six of whom also underwent apomorphine tests.(ABSTRACT TRUNCATED AT 250 WORDS)

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Section: Discussionsupporting

confidence: 90%

Responses of Plasma Oxytocin and Arginine Vasopressin to Nausea Induced by Apomorphine and Ipecacuanha

Nussey

Hawthorn

Page

et al. 1988

Clinical Endocrinology

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“…Plasma cortisol was assayed using Amerlex kits (Amersham International plc) with an intra-assay CV of 6.3% and an inter-assay CV of 10.5%. Plasma GH and prolactin were assayed as described (Nussey et al, 1986) using standard RIAs. The detection limits, intra-assay CV and inter-assay CV were 0.5 mU/l, 8% and 11% respectively for the GH assay and 20 mU/l, 8.5% and 11 % for the prolactin assay.…”

Section: Materials a N D Methodsmentioning

confidence: 99%

The Effect of Oxytocin Infusion on Adenohypophysial and Adrenal Cortical Responses to Insulin‐induced Hypoglycaemia

Nussey

Page

Ang

et al. 1988

Clinical Endocrinology

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The responses of plasma adrenocorticotrophin (ACTH), cortisol, growth hormone (GH) and prolactin to insulin-induced hypoglycaemia were studied in six lean male subjects (age 22-29 years). Intravenous insulin tests were performed with and without oxytocin infusion. Blood sugar nadir occurred at the onset of symptoms (time S) with no significant differences between oxytocin and saline infusion. During the oxytocin infusion mean plasma oxytocin increased from 1.9 pmol/l to 138 pmol/l. Peak increase in plasma ACTH (oxytocin 266 +/- 54 ng/l; saline 281 +/- 43 ng/l, mean +/- SEM) was at S + 10 min while peak plasma cortisol (oxytocin 680 +/- 47 nmol/l: saline 656 +/- 40 nmol/l) was measured at S +/- 60 min, peak GH (oxytocin 96 +/- 17.8 mU/l; saline 106 +/- 18.6 mU/l) at S + 60 min and prolactin (oxytocin 1332 +/- 239 mU/l; saline 1242 +/- 273 mU/l) at S + 30 min. There were no significant differences in plasma concentrations of ACTH, cortisol, GH or prolactin between saline and oxytocin infusion. The results indicate that oxytocin has no effect on plasma ACTH, cortisol, GH and prolactin responses to insulin-induced hypoglycaemia. In particular they fail to support previous studies which suggested an inhibitory role for oxytocin in ACTH secretion.

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“…26 The association between raised plasma osmolality and reduced survival may have reflected stroke severity, stroke subtype, increasing age, or coexisting infection. There is evidence 19 that lesions around the hypothalamus and, in particular, intracranial hemorrhage may alter plasma osmolality through vasopressin release. However, after adjustment for age, sex, subtype, and stroke severity, we demonstrated that raised plasma osmolality, defined as Ͼ296 mOsm/kg on admission, was independently related to mortality.…”

Section: Discussionmentioning

confidence: 99%

Influence of Raised Plasma Osmolality on Clinical Outcome After Acute Stroke

Bhalla

Sankaralingam

Dundas

et al. 2000

Stroke

186

135

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Background and Purpose-Abnormal physiological parameters after acute stroke may induce early neurological deterioration. Studies of the effect of dehydration on stroke outcome are limited. We examined the association of raised plasma osmolality on stroke outcome at 3 months and the change of plasma osmolality with hydration during the first week after stroke. Methods-Acute stroke patients had their plasma osmolality measured at admission and at days 1, 3, and 7. Maximum plasma osmolality and the area under curve (AUC) were also calculated during the first week. Patients were stratified according to how they were hydrated: orally, intravenously, or both. Outcome included survival at 3 months after stroke. Logistic regression was performed to examine the association between raised plasma osmolality (Ͼ296 mOsm/kg) and survival, adjusting for stroke severity. Linear regression was performed to examine the pattern of plasma osmolality across hydration groups. Results-One hundred sixty-seven patients were included. Mean admission (300 mOsm/kg, SD 11.4), maximum (308.1 mOsm/kg, SD 17.1), and AUC (298.3 mOsm/kg, SD 11.7) plasma osmolality were significantly higher in those who died compared with survivors (293.1 mOsm/kg [SD 8.2], 297.7 mOsm/kg [SD 8.7], and 291.7 mOsm/kg [SD 8.1], respectively; PϽ0.0001). Admission plasma osmolality Ͼ296 mOsm/kg was significantly associated with mortality (OR 2.4, 95% CI 1.0 to 5.9). In patients hydrated intravenously, there was no significant fall in plasma osmolality compared with patients hydrated orally (Pϭ0.68). Conclusions-Raised plasma osmolality on admission is associated with stroke mortality, after correcting for case mix.Correction of dehydration after stroke requires a more systematic approach. Trials are required to determine whether correcting dehydration after stroke improves outcome.

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Chronic hypernatraemia and hypothermia following subarachnoid haemorrhage

Cited by 9 publications

References 17 publications

Responses of Plasma Oxytocin and Arginine Vasopressin to Nausea Induced by Apomorphine and Ipecacuanha

Responses of Plasma Oxytocin and Arginine Vasopressin to Nausea Induced by Apomorphine and Ipecacuanha

The Effect of Oxytocin Infusion on Adenohypophysial and Adrenal Cortical Responses to Insulin‐induced Hypoglycaemia

Influence of Raised Plasma Osmolality on Clinical Outcome After Acute Stroke

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