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Biomedical subjects

M L Forsling

Publications and source records attributed to M L Forsling.

At least 163 records · Page 9Linked to original sources

Effects of the opiate antagonist naloxone and the enkephalin analog DAMME on the vasopressin response to a hypertonic stimulus in man.

Experiments were performed to study the effects of opioids on both the plasma arginine vasopressin and renal responses to hypertonic saline. Neither the opiate antagonist naloxone nor the enkephalin agonist DAMME [D-Ala2, MePhe4, Met (0)-ol)enkephalin] altered the vasopressin response to the same hypertonic stimulus, although DAMME increased free water clearance. In man, opioids do not seem to be important mediators of the vasopressin response to osmolar change.

Adult↗

Conversion of triglycylvasopressin to lysine-vasopressin in man.

The concentrations in plasma of triglycl-8-lysine-vasopressin (TGLVP), determined by radioimmunoassay, and lysine-vasopressin, determined by bioassay, have been monitored in five subjects after intravenous (7.5 micron/kg) or intranasal (5 mg) administration of TGLVP. The level of excretion in urine was also measured. The TGLVP concentration in plasma fell rapidly after the intravenous injection, the mean half-time of disappearance being 24.2 +/- 1.9 (S.E.M.) min (d.f. 4). Biologically active lysine-vasopressin reached a peak between 60 and 120 min. A similar pattern was seen following intranasal instillation but only a small proportion of the administered dose appeared in the plasma and the concentration of lysine-vasopressin was relatively higher. Less than 1% of the TGLVP injected appeared in the urine. Intravenous TGLVP had no effect on systolic blood pressure but produced an increase in diastolic blood pressure of 1.7 +/- 0.19 kPa (d.f. 4) and a fall in heart rate of 9 +/- 2.3 beats/min. Creatinine clearance and sodium excretion remained relatively constant in all subjects throughout the study but intravenous injection of TGLVP resulted in an antidiuresis which was evident within the first hour of observation and was maintained for a further 4 h. It was concluded that TGLVP is converted to lysine-vasopressin in man and after an intravenous injection of 7.5 micron/kg sufficiently high concentrations of lysine-vasopressin may be maintained for 2 h to produce sustained vasoconstriction. Tryglycylvasopressin may therefore be of value in controlling haemorrhage.

Administration, Intranasal↗

Plasma antidiurectic hormone during hypoxia and anaesthesia in pigs.

The level of antidiuretic hormone (ADH) in the plasma of pigs was studied during hypozia, anaesthesia and a combination of the two conditions. Hypoxia, caused by making conscious pigs breathe nitrogen, elicited a rise in the level of ADH without change in plasma osmolality; the hypoxia was accompanied in some cases by a slight lowering of arterial pressure which quickly returned to its original level after the period of hypoxic breathing. Pentobarbitone anaesthesia had no significant effect on the level of ADH but halothane anaesthesia elicited a rise in ADH. Transient high levels of ADH were seen in animals which were exposed to hypoxia during halothane or pentobarbitone anaesthesia. These high levels of ADH were sometimes, but not invariably, accompanied by a fall in arterial pressure. No consistent changes in plasma osmolality or haematocrit were associated with the raised plasma ADH.

Anesthesia↗

Effect of the exercise of seven consecutive days hill-walking on fluid homeostasis.

1. The effect of 7 consecutive days of strenuous exercise, hill-walking, on water balance and distribution was studied in five subjects. The exercise was preceded and followed by 3 control days. The diet was fixed throughout but water was allowed ad libitum. 2. Packed cell volume was measured daily. Serum electrolytes and arginine vasopressin were measured twice daily. Daily water, sodium and potassium balances were calculated. 3. During exercise there was a fall in packed cell volume, reaching a maximum of 11% by day 5 and a retention of sodium reaching a cumulative maximum of 358 mmol by day 6. During and immediately after exercise there was a retention of potassium, reaching a total of 120 mmol by day 3 after stopping exercise. 4. There was a loss of 650 ml of water on day 1 of exercise, followed by a modest retention reaching a cumulative maximum of 650 ml on day 5 of exercise. 5. Neither arginine vasopressin nor serum electrolyte concentrations were affected by exercise. 6. From the packed cell volume, sodium and water balances it was calculated that by day 5 of exercise there was an increase in plasma volume of .068 litre (22%), an increase in interstitial fluid volume of 2.0 litres (17%) and a decrease in intracellular fluid volume of 1.8 litres (8%). 7. These changes, together with the clinical observation of facial and ankle oedema during the experiemnt, suggest that continuous exercise may cause oedema and thus may be a factor in the aetiology of high-altitude oedema.

Adult↗

Plasma oxytocin and steroid concentrations during late pregnancy, parturition and lactation in the miniature pig.

Plasma oxytocin concentrations were measured during late pregnancy, parturition and lactation in the miniature pig. Measurements were made of plasma oestradiol, oestrone and progesterone to determine whether there was any relationship between the concentrations of oxytocin and these steroids in the circulation. Plasma oxytocin concentrations were low or undetectable in late pregnancy. Rises of up to 68.8 mum./ml were seen at the time of delivery of the foetuses and at the expulsion of the placenta. The only steroid that seemed to relat to oxytocin release was progesterone. Oxytocin release was consistently seen when progesterone concentrations had fallen to below 10 ng/ml but no increase in concentration was observed while oestrone and oestradiol increased to their maximum concentrations of 3.86--11.6 and 0.43--0.70 ng/ml respectively. During lactation, when both oestrogen and progesterone concentrations were low, suckling caused the levels of oxytocin to increase to 7.4 muu./ml. These increases were greater during the first 2 weeks of lactation than later.

Animals↗

Blockade of the Ferguson reflex by lumbar epidural anaesthesia in the parturient sheep: effects on oxytocin secretion and uterine venous prostaglandin F levels.

The role of oxytocin in the increase in utero-ovarian venous prostaglandin F (PGF) level caused by vaginal distension was investigated by using lumbar epidural anaesthesia to block the oxytocin secretion reflex. Whereas vaginal distension raised jugular venous oxytocin and utero-ovarian venous PGF levels in untreated sheep, neither response occurred after lumbar anaesthesia. Lumbar anaesthesia had no effect on the rise in utero-ovarian venous PGF level caused by administered oxytocin. These findings support the suggestion that a reflex release of oxytocin is involved in the elevation of utero-ovarian venous PGF observed after vaginal distension in parturient sheep.

Anesthesia, Epidural↗

Oxytocin release following osmotic activation of oxytocin neurones in the paraventricular and supraoptic nuclei.

1. Recordings were made from a total of 35 antidromically identified neurones in the paraventricular (PV) and supraoptic (SO) nuclei of urethane-anaesthetized lactating rats. During recording plasma osmotic pressure was raised by 12 m-osmole/kg by injection of hypertonic solutions of NaCl, LiCl, or mannitol.2. Nine PV neurones (mean firing rate 4.2 +/- 1.0 (S.E.) spikes/sec) were classified as oxytocin cells because they gave a burst of activity before reflex milk-ejections. None of these showed a bursting (phasic) firing pattern. Ten PV neurones (mean firing rate 1.8 +/- 0.2 spikes/sec) fired phasically either before or after injection of hypertonic NaCl and were classified as vasopressin cells. The remaining six PV cells (mean firing rate 1.6 +/- 0.9 spikes/sec) showed no bursts of firing related to milk ejection and did not fire phasically.3. Increasing plasma osmotic pressure by injection of hypertonic NaCl increased the mean firing rate of PV oxytocin cells to 7.0 +/- 1.0 spikes/sec. Vasopressin cells in the PV nucleus were much less responsive and the mean firing rate after injection was 2.9 +/- 0.4 spikes/sec. The third group of PV neurones was unresponsive.4. Plasma oxytocin concentration (determined by radioimmunoassay) increased from 2.1 +/- 0.3 muu./ml. in the control period to 10.9 +/- 2.8 muu./ml. 30 min after I.P. injection of 1 ml. 1.5 M-NaCl and to 14.8 +/- 2.8 muu./ml. following injection of a second 1 ml. 1.5 M-NaCl.5. The responses of oxytocin and vasopressin neurones in the SO nucleus to an increase in plasma osmotic pressure following injections of hypertonic solutions of LiCl or mannitol were similar to those observed when plasma osmotic pressure was raised by NaCl.6. It may be concluded that both oxytocin and vasopressin cells in the neurohypophysical system are responsive to the osmotic pressure of the blood plasma rather than to Na(+) or Cl(-) concentration, that osmotic activation of oxytocin cells releases sufficient oxytocin to increase its plasma concentration, and that there may be a functional difference between the SO and PV nuclei.

Action Potentials↗

The interrelationship between the release of renin and vasopressin as defined by orthostasis and propranolol.

The concentration of both plasma renin and plasma arginine vasopressin rose in normal subjects after an 85 degrees head-up tilt. Plasma renin activity, which increased 70-80% above the supine value, was maximal at 15 or 30 min, whereas the six- to seven-fold increase of plasma arginine vasopressin concentration was observed between 30 and 45 min. Intravenous propranolol administered just before tilt was used to investigate the possibility that the delayed rise of arginine vasopressin was stimulated by renin. Although the response of plasma renin was completely abolished by propranolol, the response of vasopressin was unaffected. These findings suggest that the release of vasopressin that follows isosmolar hypovolemia achieved by orthostasis may occur independently of changes in the renin-angiotensin system in the presence of propranolol.

Adult↗