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Biomedical subjects

J Warberg

Publications and source records attributed to J Warberg.

At least 145 records · Page 8Linked to original sources
PubMed1986

Influence of central venous pressure change on plasma vasopressin in humans.

After overnight food and fluid restriction, nine healthy males were examined before, during, and after lower body positive pressure (LBPP) of 11 +/- 1 mmHg (mean +/- SE) for 30 min and before, during, and after graded lower body negative pressure (LBNP) of -10 +/- 1, -20 +/- 2, and -30 +/- 2 mmHg for 20 min each. LBPP and LBNP were performed with the subject in the supine position in a plastic box encasing the subject from the xiphoid process and down, thus including the splanchnic area. Central venous pressure (CVP) during supine rest was 7.5 +/- 0.5 mmHg, increasing to 13.4 +/- 0.8 mmHg (P less than 0.001) during LBPP and decreasing significantly at each step of LBNP to 2.0 +/- 0.5 mmHg (P less than 0.001) at 15 min of -30 +/- 2 mmHg LBNP. Plasma arginine vasopressin (AVP) did not change significantly in face of this large variation in CVP of 11.4 mmHg. Mean arterial pressure increased significantly during LBPP from 100 +/- 2 to 117 +/- 3 Torr (P less than 0.001) and only at one point during LBNP of -30 +/- 2 mmHg from 102 +/- 1 to 115 +/- 5 mmHg (P less than 0.05). Heart rate did not change during LBPP but increased slightly from 51 +/- 3 to 55 +/- 3 beats/min (P less than 0.05) only at 7 min of LBNP of -30 +/- 2 mmHg. Plasma osmolality, sodium, and potassium did not change during the experiment. Hemoglobin concentration increased during LBPP and LBNP, whereas hematocrit only increased during LBNP.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1986

Histaminergic stimulation of prolactin secretion mediated via H1- or H2-receptors: dependence on routes of administration.

Controversy exists regarding the involvement of H1- or H2-receptors in the PRL-releasing activity of histamine (HA). This could be due to differences in the route of administration of HA and histaminergic compounds. Therefore, we studied the effect on PRL secretion of HA and HA-agonists infused intracerebroventricularly (ICV) or systemically (IA) either alone or in combination with HA-antagonists in male rats. HA administered ICV as well as IA stimulated PRL secretion dose dependently. The stimulatory effect of ICV-infused HA was blocked by the H2-receptor antagonist cimetidine (CIM) and mimicked by the H2-receptor agonists 4-methylhistamine (4-MeHA) and dimaprit (DIM). In contrast, the H1-receptor antagonist mepyramine (MEP) enhanced the PRL-releasing effect of HA while the H1-receptor agonist 2-thiazolylethylamine (2-TEA) had no significant effect. The stimulatory effect of IA-infused HA was blocked by the H1-receptor antagonist MEP and mimicked by the H1-receptor agonist 2-TEA, whereas the H2-receptor antagonist CIM enhanced the PRL-stimulatory effect of HA and the H2-receptor agonist DIM was without effect. 4-MeHA stimulated PRL secretion, but this effect was unrelated to stimulation of H2-receptors. The effect of ICV administered HA was unaffected by IA infused antagonists and the effect of IA administered HA was not altered by ICV infused antagonists. HA had no effect on the PRL release from isolated adenohypophyses, and HA did not stimulate PRL secretion in pituitary stalk-sectioned rats following IA infusion. The findings indicate that HA administered ICV exerts its PRL releasing activity via H2-receptors while HA administered IA stimulates PRL secretion via H1-receptors.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

Effect of prostaglandin D2 on the release of luteinizing hormone and prolactin in castrated and intact male rats.

One, 5 or 20 micrograms of prostaglandin D2 (PGD2) was infused into a lateral ventricle of the brain of anaesthetized intact or castrated male rats, and the response of luteinizing hormone (LH) and prolactin (Prl) was determined. PGD2 stimulated the release of LH in both groups of rats. The greatest LH-response was observed in the castrated rats, where the lowest dose of PGD2 (1 microgram) caused the greatest LH response. This dose was ineffective in the non-castrated animals. PGD2 had no effect on the release of Prl neither in intact nor in orchidectomized rats. It is concluded that PGD2 is capable of stimulating the release of LH in male rats and that the stimulating effect is intensified by removal of the gonadal negative feedback effect on the hypothalamo-pituitary unit.

Animals↗
PubMed1986

Haemodynamic and humoral effects of lower body negative pressure in normal, sodium-replete man during angiotensin-converting enzyme inhibition with captopril.

The significance of the renin-angiotensin system (RAS) for circulatory homeostasis during gravitational stress (10 min of lower body negative pressure, LBNP, at -40 mmHg) was investigated in eight men on liberal sodium intake. The function of RAS was inhibited by a single oral dose of 100 mg captopril, an angiotensin-converting enzyme inhibitor. Plasma concentrations of renin and angiotensin I were normal before and increased after captopril and during LBNP. Plasma concentration of angiotensin II was normal before captopril, increased during LBNP, and fell to low values after captopril. Systolic blood pressure decreased more during LBNP after captopril than in the control situation. In three cases, the LBNP experiment after captopril had to be interrupted due to marked hypotension. Heart rate and plasma concentration of adrenaline increased above pre-captopril levels. In six subjects, plasma concentration of noradrenaline increased more during LBNP after captopril, less in two subjects, whereas the arginine vasopressin concentration increased more after captopril in all five subjects where measurements were available. The results demonstrate that RAS participates in blood pressure homeostasis also in sodium-replete, normal man. The enhanced increases in heart rate and plasma catecholamines after captopril do not suggest that sympathetic reflex activity during gravitational stress is blunted after captopril, in contrast to the evidence from animal experiments.

Adult↗
PubMed1985

Central venous pressure and plasma arginine vasopressin during water immersion in man.

The influence of increased central venous pressure (CVP) on the plasma concentration of arginine vasopressin (pAVP) was examined in 7 healthy males subjected to water immersion (WI) up to the neck following overnight food- and fluid restriction. During WI the subject sat upright in a pool (water temperature = 35.0 degrees C) for 6 h. In control experiments the subject assumed the same position outside the pool wearing a water perfused garment (water temperature = 34.6 degrees C). CVP increased markedly during WI and after 20 min of immersion it attained a level which was significantly higher than the control value (10.9 +/- 1.5 (mean +/- SE) vs. 2.2 +/- 1.3 mm Hg, p less than 0.01). This increase was sustained throughout the 6 h WI period. Simultaneously, after 20 min pAVP during WI was significantly lower than control values (1.8 +/- 0.3 vs. 2.2 +/- 0.3 pg X ml-1, p less than 0.05) and sustained throughout WI. Systolic arterial pressure increased significantly by 7-10 mm Hg (p less than 0.05) after 2 h of WI, while diastolic arterial pressure was unchanged. Heart rate was decreased by 10 bpm throughout immersion. There was no change in plasma osmolality when comparing control with immersion. A pronounced osmotic diuresis, natriuresis and kaliuresis occurred during WI, counteracting an acute significant increase in plasma volume of 6.5 +/- 1.9% (P less than 0.01 within 20 min of immersion). We conclude that an increase in CVP due to WI is accompanied by suppressed pAVP.

Adult↗
PubMed1984

Impermeability of the blood-cerebrospinal fluid barrier to 1-deamino-8-D-arginine-vasopressin (DDAVP) in patients with acquired, communicating hydrocephalus.

The passage of the vasopressin analogue, 1-deamino-8-D-arginine-vasopressin (DDAVP) into the cerebrospinal fluid (CSF) following intravenous (i.v.) administration was studied in human subjects. After i.v. injection of DDAVP, resulting in plasma levels exceeding normal plasma concentrations of vasopressin (AVP) by 100-fold, serial blood and ventricular CSF specimens were sampled during 2 h. Plasma and CSF were analysed by radioimmunoassay using two different AVP antisera: one specific against natural AVP and another cross-reacting 100% with DDAVP. No changes in the joint concentrations of DDAVP + AVP in CSF were found following i.v. infusion of DDAVP when compared with the concentration before the infusion. Neither was any difference between CSF concentrations of AVP and DDAVP + AVP observed at any sampling time following the i.v. DDAVP administration. Hence, it is concluded that no measurable amounts of DDAVP can be found in the CSF for up to 2 h after i.v. administration of the peptide, and that for all practical purposes a blood-CSF barrier to DDAVP exists.

Adult↗
PubMed1984

Renal effects of overhydration during vasopressin infusion in conscious dogs.

The antidiuretic and possibly natriuretic effects of small doses of vasopressin (AVP) were investigated in conscious dogs. Plasma composition and renal excretion of water, Na+, and K+ were measured after overhydration by 20 ml/kg performed during infusion of AVP at rates of 50, 100, 150, 200, or 400 pg X min-1 X kg body wt-1 or of 1-desamino-8-D-arginine vasopressin (DDAVP) 50 pg X min-1 X kg body wt-1. Hydration lowered plasma osmolality and sodium concentration by 4.2 +/- 0.3 and 3.8 +/- 0.2%, respectively; plasma protein showed a larger decrease, 8.5 +/- 0.4% (P less than 0.01). Urine osmolality during hydration was 52 +/- 3 mosmol/kg H2O. AVP infusion at 100 pg X min-1 X kg-1 elevated plasma vasopressin by 1.7 +/- 0.3 pg/ml and urine osmolality by 1,049 +/- 152 mosmol/kg H2O and elicited marked natriuresis and kaliuresis but no change in osmolar clearance. During DDAVP infusion urine osmolality was 1,365 +/- 134 mosmol/kg H2O, but electrolyte excretion was indistinguishable from control. It is concluded that 1) AVP is associated with marked natriuresis and kaliuresis even in doses required to prevent water diuresis, 2) DDAVP--although strongly antidiuretic--does not affect electrolyte excretion, and 3) the water load causes disproportionate dilution of plasma protein and osmolality, probably due to protein redistribution.

Animals↗
PubMed1984

Cyclic and diurnal alterations in the response of luteinizing hormone and prolactin to prostaglandin E2 during the rat oestrous cycle.

Two micrograms of prostaglandin E2 (PGE2) was infused into a lateral ventricle of the brain of female rats at 09.00 or 13.00 h on the different days of the oestrous cycle and the effect on luteinizing hormone (LH) and prolactin (Prl) release was determined. At 09.00 h PGE2 caused a pronounced release of LH in pro-oestrous, oestrous and metoestrous rats whereas the LH response in dioestrous rats was moderate. The secretion of Prl was only stimulated in rats from the pro-oestrous phase. When infused at 13.00 h PGE2 had a marked stimulatory effect on the release of LH in all groups of rats. The response was almost the same in oestrous, metoestrous and dioestrous rats but pro-oestrous rats a 2-fold higher LH response was observed. On each day of the oestrous cycle it was found that the LH-releasing activity of PGE2 was greater at 13.00 h than at 09.00 h. Thus, the overall greatest responsiveness of LH to PGE2 was noted at 13.00 h on pro-oestrus i.e. at a time which was prior to the onset of the spontaneous LH surge. At 13.00 h - as at 09.00 h - PGE2 was only capable of stimulating Prl release in pro-oestrous rats. Resembling the LH response it was found that PGE2-induced Prl release was greater at 13.00 h than at 09.00 h. In adult male rats the stimulatory effect of PGE2 on LH and Prl release was independent of the time of administration. It is concluded that the neuroendocrine elements of the hypothalamo-pituitary unit in mature female rats exhibit cyclic as well as diurnal alterations in the responsiveness to PGE2.

Animals↗
PubMed1984

Bradycardia during severe but reversible hypovolemic shock in man.

Severe bleeding and hypovolemic shock causing hypotension are most often associated with tachycardia. In response to passive head-up tilt, five healthy men exhibited an increase in heart rate (HR) from 62 to 79 beats X min-1 and a gradual increase in the plasma concentration of aldosterone and protein. The increase in HR was followed by a decrease of 29 beats X min-1 (range 11-46) at the time when blood pressure decreased 38 mmHg (6-73). When tilted back to 0 degree, blood pressure immediately reversed while HR remained unchanged. Hypotension was associated with large but variable increases in plasma vasopressin (86 +/- 28 pg X ml-1) accompanied by peripheral vasoconstriction. In two cases where patients with internal bleeding presented with a moderate HR of 96 beats X min-1, the ensuing fall in blood pressure was associated with a decrease in HR to 68 and 76 beats X min-1, respectively. Administration of albumin solution and blood normalized cardiovascular function. Two other patients showing initial HR of 130 and 100 beats X min-1, respectively, also developed relative bradycardia in conjunction with a decrease in blood pressure. Administration of ephedrine and atropine increased HR temporarily from 56 to 90 and from 36 to 110 beats X min-1, respectively. The latter two patients died in extreme bradycardia and autopsies revealed severe internal bleeding. It is concluded that although hypovolemic shock is most often associated with an increase in HR, the increase is modest and a paradoxical bradycardia develops in severe but potentially reversible hypotensive hypovolemic shock.

Adult↗
PubMed1983

Effects on intravascular pressures of vasopressin and angiotensin II in dogs.

The effects of 30-min intravenous infusions of 8-arginine vasopressin (AVP) and angiotensin-(1,8)-octapeptide (ANG II) to conscious dogs were studied by measurements of systolic (SABP), mean (MABP), and diastolic arterial blood pressures, central venous pressure (CVP), heart rate (HR), and plasma concentrations of vasopressin (pAVP). Infusion of AVP at six rates (0.4-12.8 ng X min-1 X kg-1) raised mean pAVP by 5-490 pg/ml and increased CVP by 2-10 cmH2O. HR decreased and arterial pressures increased with infusion rates of 1.6-12.8 ng X min-1 X kg-1. However, the increase in SABP was only transient. ANG II increased all arterial pressures; however, it barely changed CVP and did not change HR or pAVP. It is concluded that 1) AVP can elevate MABP without changes in SABP, 2) the effects of AVP on arterial pressures are buffered within 5-15 min, 3) CVP can be increased by doses of AVP that do not affect arterial pressures, and 4) the pressor activity is independent of the presence of ANG II. The results confirm that the cardiovascular response to vasopressin is qualitatively different from that elicited by ANG II.

Angiotensin II↗
PubMed1981

Internal K+ and Na+ concentrations and the volume of hypothalamic synaptosomes.

Hypothalamic synaptosomes, prepared by discontinuous sucrose density gradient centrifugation, were suspended in media of varying osmolarity and ionic composition and the internal concentrations of K+ and Na+ were measured. The intrasynaptosomal volume was determined using [14C]inulin, 35SO4 or [14C]sucrose as extracellular markers. When the synaptosomes were suspended in 0.32 M sucrose the distribution volume of [14C]inulin and 35SO4 were similar. However, when the medium contained 140 mM NaCl and 5 mM KCl the 35SO4 space was equal to the total water space while the distribution volume of [14C]inulin corresponded to 35-51% of the total water space. [14C]sucrose distributed in a larger volume than did [14C]inulin, presumably due to intracellular permeation of sucrose. Using inulin as an extracellular marker the synaptosome volume was found to be inversely proportionate to the tonicity of the medium. [14C]inulin was considered a suitable marker of the extrasynaptosomal space and was used when determining intrasynaptosomal K+ and Na+ concentrations. The internal concentration of K+ was considerably higher than the external indicating that the synaptosomes were able to retain K+ against a concentration gradient. The synaptosomes gained Na+ when transferred to media containing 140 mM NaCl. The internal concentrations of K+ and Na+ were unaffected by glucose and elevated temperature and was only moderately changed during 90 min of incubation. The equilibrium potentials for K+ and Na+ were -68 and 13 mV respectively when the medium consisted of 0.03 M sucrose containing 140 mM NaCl, 5 mM KCl. It is concluded that hypothalamic synaptosomes can maintain a high transmembrane concentration gradient for K+ whereas the membrane is rather easily penetrated by Na+.

Animals↗
PubMed1981

Potentiation of prostaglandin E2-induced release of LH by the prostaglandin analogue, 7-oxa-13-prostynoic acid.

The prostaglandin (PG) analogue 7-oxa-13-prostynoic acid (7-OPA) was infused into a lateral ventricle of the brain of adult male rats and the effect of the analogue on the subsequent stimulation of LH release by intraventricular infusion of PG's was determined. Pretreatment of the animals with 44- 132 micrograms of 7-OPA potentiated the stimulatory effect of 2 micrograms PGE2 on the release of LH but the analogue alone had no effect on the hormone secretion. The minimal effective dose of PGE2 was determined to be within the range 0.01-0.05 micrograms and it was found that priming with 132 micrograms of 7-OPA caused a formerly sub-threshold dose (0.01 micrograms) of PGE2 to become an effective stimulus for the release of LH. In contrast to its potentiating effect on PGE2-induced LH release 7-OPA did not alter the stimulatory action of PGF2 alpha (2 micrograms) on the secretion of LH. 7-OPA had no effect on LRH-induced release of LH indicating that PG analogue acts at a suprapituitary site to enhance PGE2-induced LH release. The potentiating effect of 7-OPA may be exerted at a binding site for PGE2 in the brain and the results suggest the existence of a different binding site for PGF2 alpha. The possibility also exists that 7-OPA inhibit metabolic inactivation of PGE2.

Animals↗
PubMed1979

Release of immunoreactive alpha-MSH by synaptosome-enriched fractions of homogenates of hypothalami.

Immunoreactive alpha-melanocyte-stimulating hormone (alpha-MSH) was found to be concentrated in a synaptosome-enriched fraction prepared by differential centrifugation of rat hypothalamic homogenates. The release of the hormone from this preparation was investigated. After incubation, the synaptosomes were isolated by ultrafiltration and alpha-MSH in the ultrafiltrate was determined by radioimmunoassay. Particle-bound alpha-MSH, recovered by extraction with acid ethanol, and alpha-MSH released from the synaptosome preparation, were immunologically similar to synthetic alpha-MSH and had an accompanying melanotropic activity. Less than 10% of the particle-bound alpha-MSH was released during incubation in 0.32 M sucrose. However, in the presence of 2 mM Ca2+, alpha-MSH release increased with increasing concentrations (30-150 mM) of K+. The stimulatory effect of 60 mM K+ was complete within 2 min and was potentiated by increasing Ca2+ concentrations over the range of 0 to 2 mM. K+-induced release of alpha-MSH was independent of temperature from 1 to 30 degrees C, and neither glucose (10 mM) nor dopamine (10(-10)-10(-2) M) had any effect on the release of the peptide. It is concluded that a synaptosome-enriched fraction from the hypothalamus contains a releasable pool of immunoreactive alpha-MSH that is mobilized by depolarizing concentrations of K+ in a Ca2+-dependent manner.

Animals↗