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PubMed2005

Coronary effects of endothelin-1 and vasopressin during acute hypotension in anesthetized goats.

Coronary effects of endothelin-1 and vasopressin during acute hypotension, and the role of NO and prostanoids in these effects were examined in anesthetized goats. Left circumflex coronary artery flow was measured electromagnetically, and hypotension was induced by constriction of the caudal vena cava in animals non-treated (7 goats) or treated with the inhibitor of NO synthesis N(w)-nitro-L-arginine methyl esther (L-NAME, 5 goats), the cyclooxygenase inhibitor meclofenamate (5 goats) or both drugs (5 goats). Under normotension (22 goats), mean arterial pressure averaged 93 +/- 3 mm Hg and coronary vascular conductance (CVC) 0.37 +/- 0.025 ml/min/mm Hg. Endothelin-1 (0.01-0.3 nmol) and vasopressin (0.03-1 nmol), intracoronarily injected, dose-dependently decreased CVC by up to 56% for endothelin-1 and 40% for vasopressin. During hypotension in every condition tested, mean arterial pressure decreased to approximately 60 mm Hg, and CVC only decreased during hypotension pretreated with L-NAME (23%) or L-NAME + meclofenamate (34%). Under non-treated hypotension, the decreases in CVC by endothelin-1 were augmented approximately 1.5 fold, and those by vasopressin were not modified. This increase in CVR by endothelin-1 was not affected by L-NAME and was reversed by meclofenamate or L-NAME + meclofenamate. The coronary effects of vasopressin were not modified by any of these treatments. Therefore, acute hypotension increases the coronary vasoconstriction in response to endothelin-1 but not to vasopressin. This increased response to endothelin-1 may be related to both inhibition of NO release and release of vasoconstrictor prostanoids.

Acute Disease↗
PubMed2005

Inhibitory effect of gaseous neuromodulators in vasopressin and oxytocin release induced by endotoxin in rats.

Nitric oxide (NO) and carbon monoxide (CO) are endogenously synthesized gaseous molecules that act as neurotransmitters in central nervous system. In this study we investigated the modulatory role of NO and CO in lipopolysaccharide (LPS)-induced vasopressin and oxytocin secretion. Intracerebroventricular (i.c.v.) injection of N omega-L-nitro-arginine methyl ester (L-NAME), 3-morpholino-sydnonimine (SIN-1), zinc deuteroporphyrin 2,4-bis glicol (ZnDPBG) or hemin did not change the basal vasopressin and oxytocin plasma levels. After endovenous LPS administration, plasma vasopressin and oxytocin increased, reaching a peak at 60 min, and returning to basal levels afterwards. LPS administration induced a higher vasopressin and oxytocin plasma levels in rats previously treated with L-NAME and ZnDPBG (P<0.05) compared to rats pre-treated with vehicle. On the other hand, in rats previously treated with SIN-1 or hemin, there was a significant reduction in the vasopressin and oxytocin secretion. These findings confirm the inhibitory role of NO and CO in the LPS-induced vasopressin and oxytocin secretion.

Animals↗
PubMed2004

Temporal dissociation of the feedback effects of dendritically co-released peptides on rhythmogenesis in vasopressin cells.

Vasopressin neurones fire action potentials in a rhythmic 'phasic' pattern, characterised by alternating periods of activity and silence. Vasopressin and dynorphin are co-packaged in neurosecretory vesicles that are exocytosed from vasopressin cell dendrites and terminals and both have been implicated in the generation of phasic activity patterning through autoregulatory mechanisms. Here, identified supraoptic nucleus vasopressin cells exhibiting spontaneous phasic activity were recorded from urethane-anaesthetised rats administered the V1 vasopressin receptor antagonist, OPC 21268, or the kappa-opioid receptor antagonist, nor-binaltorphimine. OPC 21268 elevated firing rate throughout each burst whereas nor-binaltorphimine excitation emerged over the course of each burst, indicating a progressive activation of kappa-opioid receptor mechanisms during bursts. To determine whether changes in post-spike excitability could account for these effects, we plotted the probability of action potential firing with time after the preceding action potential (hazard function) and found that, similarly to firing rate, this too was elevated by OPC 21268 throughout each burst whilst the excitatory effects of nor-binaltorphimine progressively increased over the course of each burst. Thus, the temporal organisation of the feedback effects of these co-released peptides is different, with vasopressin effectively causing an immediate reduction in overall excitability whilst dynorphin causes a progressive decrease in post-spike excitability over the course of each burst.

Action Potentials↗
PubMed2005

Haploinsufficiency of the arginine-vasopressin gene is associated with poor spatial working memory performance in rats.

Behavioral pharmacological studies have implicated a role for the neurophysin arginine-vasopressin in learning and memory. Vasopressin, and its analogues, can produce either improvements or impairments in mnemonic functions, effects that depend upon the agent administered, the memory process measured and the task employed. As recent data have implicated vasopressin in regulating the cognitive functions of the prefrontal cortex, we sought to determine whether changes in vasopressinergic tone would affect a form of memory that is dependent upon this brain region. To that end, we used a genetic approach to examine how haploinsufficiency of the vasopressin gene affects working memory performance. Specifically, we tested a naturally occurring null-mutant rat on an operant delayed-non-match-to-position task. Male and female heterozygous and wild-type rats were trained to perform this working memory task, and the effects of varying the delay across which they had to maintain task information were systematically varied. Although vasopressin-deficient rats omitted fewer trials and completed trials more quickly, they exhibited delay-dependent deficits of choice accuracy. The genotype effects were not modified by sex. Collectively, these data indicate that even partial vasopressin deficiency can trigger deficits of spatial working memory performance and add to the growing body of results supporting a regulatory control of neocortical-dependent cognitive functions by this neurohormone.

Analysis of Variance↗
PubMed1996

Treatment of oligohydramnios with maternal 1-deamino-[8-D-arginine] vasopressin-induced plasma hypoosmolality.

OBJECTIVE: Maternal 1-deamino-[8-D-arginine] vasopressin (a selective antidiuretic agonist) and oral water loading decrease maternal and fetal plasma osmolality and markedly increase fetal urine flow in sheep. We hypothesized that a titrated reduction in maternal plasma osmolality would increase human amniotic fluid volume. STUDY DESIGN: Pregnant women (n = 5) with oligohydramnios at term were administered oral water loading (20 ml/kg) and intravenous 1-deamino-[8-D-arginine] vasopressin (2 micrograms) to induce antidiuresis. Maternal plasma and urine osmolality and urine production were measured hourly, and water replacement was titrated for 8 hours to reduce plasma osmolality by 15 to 20 mOsm/kg. The amniotic fluid index determined by ultrasonography was measured at baseline, 8 hours, and 24 hours. A control group of pregnant women (n = 5) with oligohydramnios at term was observed for 8 hours with maintenance intravenous hydration. RESULTS: In 1-deamino-[8-D-arginine] vasopressin-treated women, maternal urine flow increased with oral water loading, decreased with 1-deamino-[8-D-arginine] vasopressin administration, and remained reduced for 8 hours. Maternal plasma osmolality significantly decreased (285 +/- 4 to 265 +/- 4 mOsm/kg) and the amniotic fluid index significantly increased (4.1 +/- 0.6 to 8.2 +/- 1.5 cm) at 8 hours. Although maternal urine osmolality returned to basal values at 24 hours, plasma osmolality was reduced and the amniotic fluid index remained significantly increased (8.2 +/- 1.3 cm). There was no change in the amniotic fluid index (4.3 +/- 0.4 to 4.7 +/- 0.7 cm) in control patients observed with maintenance intravenous hydration. CONCLUSIONS: Maternal 1-deamino-[8-D-arginine] vasopressin and oral water administration can reduce and stabilize plasma osmolality and increase amniotic fluid volume. 1-Deamino-[8-D-arginine] vasopressin therapy has potential for the prevention and treatment of oligohydramnios.

Adult↗
PubMed1996

1-Deamino-[8-D-arginine] vasopressin-induced maternal plasma hypoosmolality increases ovine amniotic fluid volume.

OBJECTIVE: Maternal 1-deamino-[8-D-arginine] vasopressin (a selective antidiuretic agonist) and oral water loading decrease maternal and fetal plasma osmolality and markedly increase fetal urine flow in sheep over 24 hours. We hypothesized that a sustained reduction in plasma osmolality would increase the amniotic fluid volume. STUDY DESIGN: Pregnant sheep (130 +/- 1 days, n = 6) were given oral water loading (2000 ml) and intravenous 1-deamino-[8-D-arginine] vasopressin (20 microgram injection followed by 4 micrograms/hr) to induce maternal urinary antidiuresis and to maintain a maternal plasma osmolality decrease of approximately 20 mOsm/kg for 48 hours. Fetal plasma osmolality, electrolytes, atrial natriuretic factor, and arginine vasopressin levels, fetal swallowing activity, and fetal urine flow and composition were measured each study day, and amniotic fluid volume was measured by tracer dilution before and at 48 hours of plasma hypoosmolality. RESULTS: In response to 1-deamino-[8-D-arginine] vasopressin and water loading, maternal plasma osmolality decreased (298 +/- 1 to 275 +/- 3 mOsm/kg), mirrored by fetal plasma hypoosmolality (293 +/-1 to 271 +/- 3 mOsm/kg). Fetal urine osmolality (155 +/- 16 to 117 +/- 10 mOsm/kg) and amniotic fluid osmolality significantly decreased (281 +/- 3 to 269 +/- 5 mOsm/kg). Fetal urine flow rate significantly increased (0.33 +/- 0.06 to 0.51 +/- 0.04 ml/min), whereas fetal swallowing activity decreased (56 +/- 7 to 33 +/-5 swallows per hour). In response to alterations in fetal fluid dynamics, amniotic fluid volume significantly increased from 493 +/- 80 to 839 +/- 160 ml. CONCLUSION: Chronic maternal 1-deamino-[8-D-arginine vasopressin-induced plasma hypoosmolality induces a sustained reduction in fetal swallowing activity and an increase in fetal urine production, which results in a marked increase in amniotic fluid volume. Use of maternal 1-deamino-[8-D-arginine] vasopressin and oral fluid loading has the potential for manipulation of amniotic fluid volume homeostasis and may prove useful in the treatment of oligohydramnios.

Amniotic Fluid↗
PubMed1988

Vasopressin is the only component of serum-free medium that stimulates phosphatidylcholine hydrolysis and accumulation of diacylglycerol in cultured REF52 cells.

Vasopressin stimulates phosphatidylcholine hydrolysis in REF52 cells, and this phosphatidylcholine hydrolysis results in increases in choline containing metabolites in the culture medium (2.3 x control levels) and accumulation of cellular diacylglycerol (6.5 x control levels). Vasopressin is the only component of a 6-component mixture of the serum-free medium for REF52 cells that induces the phosphatidylcholine hydrolysis response. The effect of vasopressin is both time- and concentration-dependent. Maximal levels of both phosphatidyl-choline hydrolysis and accumulation of diacylglycerol are observed between 10 and 20 min after treatment with vasopressin. Effects are maximal at vasopressin concentrations of 100 ng/ml; the ED50 for vasopressin-stimulated phosphatidyl-choline hydrolysis is approximately 0.7 ng/ml. The evolution of diacylglycerol occurs in a time frame that is consistent with the diacylglycerol activating protein kinase C in a "second phase" agonist response.

Animals↗
PubMed1994

Hemorrhage-induced vasopressin release in the paraventricular nucleus measured by in vivo microdialysis.

Experiments were carried out, using the technique of in vivo microdialysis in conscious rats, to determine whether hemorrhage, a potent stimulus for the release of vasopressin from the posterior pituitary into the circulation, would also result in a local release of vasopressin from the paraventricular nucleus (PVN), and whether this release is affected by gender. Male and non-estrous female rats were prepared with a microdialysis probe adjacent to the PVN and femoral arterial and venous catheters the day before the experiment. On the day of the experiment, rats was bled either 20% or 30% of blood volume. The concentration of vasopressin in the dialysate increased significantly in the males following both hemorrhages and in the females following the 30% hemorrhage. There were no statistically significant differences in the post-hemorrhage dialysate vasopressin concentration with respect to either gender or magnitude of the hemorrhage. The plasma vasopressin concentration increased markedly in response to the hemorrhage and this response was greater in females following the 30% hemorrhage. There were no gender differences in the reduction in arterial pressure following either hemorrhage. It is concluded that physiological stimuli for the release of vasopressin into the circulation also result in intrahypothalamic release of this hormone.

Animals↗
PubMed2003

Vascular reactivity to vasopressin during diabetes: gender and regional differences.

The isometric response to vasopressin of 2-mm-long segments of basilar, coronary, renal and tail arteries from male and female, control (normoglycemic) and streptozotocin-induced diabetic rats was studied. Vasopressin (10(-12)-3 x 10(-8) M) produced arterial concentration-dependent contraction, with a lower potency in coronary arteries from female than from male rats, and was similar for both genders in basilar, renal and tail arteries. This contraction was reduced by diabetes in basilar and coronary arteries, increased in renal arteries, and not modified in tail arteries, in both genders. Inhibition of nitric oxide synthesis with N(W)-nitro-L-arginine methyl ester (L-NAME, 10(-4) M) increased the contraction to vasopressin in coronary arteries from control female and diabetic female rats; as well as in renal arteries from control male and control female rats, but not in any other experimental group. Inhibition of cyclooxygenase with meclofenamate (10(-5) M) reduced the contraction to vasopressin in basilar arteries from diabetic female rats and in renal arteries from diabetic male rats, but not in any other experimental group. These results suggest that the response to vasopressin (a) has lower potency in female coronary arteries due to higher nitric oxide production; (b) is reduced by diabetes in basilar and coronary arteries from both genders, by mechanisms independent of nitric oxide and prostanoids; and (c) is increased by diabetes in renal arteries due to reduced production of nitric oxide in females, and to both reduced production of nitric oxide and increased production of prostanoids in males. Therefore, the effects of diabetes on vascular reactivity to vasopressin may differ between vascular beds, and the mechanisms underlay these effects may be distinct between genders.

Animals↗
PubMed2001

Altered osmotic thresholds for arginine vasopressin secretion and thirst during superovulation and in the ovarian hyperstimulation syndrome (OHSS): relevance to the pathophysiology of OHSS.

OBJECTIVE: To test the hypothesis that decreases in and maintenance of a new steady state in plasma osmolality and sodium level in ovarian hyperstimulation syndrome (OHSS) are due to altered osmoregulation of arginine vasopressin secretion and thirst. DESIGN: Prospective study. SETTING: IVF-ET program in a university-based assisted reproductive treatment center. PATIENT(S): Eight women undergoing superovulation for IVF-ET and five women with normal menstrual cycles. INTERVENTION(S): Two-hour infusion of 5% saline on day 3 or 4 after hCG administration in patients undergoing IVF or in the early luteal phase in controls. A 5% saline infusion test was done on day 10 after hCG administration in one patient with OHSS and one patient without OHSS, both of whom were undergoing IVF. MAIN OUTCOME MEASURE(S): Comparison of changes in thresholds for thirst and plasma vasopressin to plasma osmolality. Changes in urine osmolality, plasma electrolytes, hemoglobin level, and hematocrit were assessed at baseline and during infusion of 5% saline. RESULT(S): The sensitivity of the changes in arginine vasopressin secretion and thirst after 5% saline infusion was similar in IVF patients on day 3 or 4 after hCG and controls. However, the osmotic threshold was significantly lower by 6 mOsm/kg in IVF patients. By day 10 after hCG, the lower osmotic thresholds for arginine vasopressin secretion and thirst persisted in OHSS, although the sensitivity to arginine vasopressin secretion was markedly reduced. CONCLUSION(S): The osmotic thresholds for arginine vasopressin secretion and thirst are reset to lower plasma osmolality during superovulation for IVF-ET. This new lower body tonicity is maintained until at least day 10 after hCG in OHSS. Decreases in plasma osmolality and plasma sodium levels in OHSS are due to altered osmoregulation rather than electrolyte losses; correction of apparent "electrolyte imbalance" in OHSS is therefore inappropriate.

Adult↗
PubMed1997

The effect of dilute vasopressin solution on the force needed for cervical dilatation: a randomized controlled trial.

OBJECTIVE: To assess the force needed to mechanically dilate the cervix of a nonpregnant woman after intracervically injecting dilute (0.05 U/mL) vasopressin solution. METHODS: In a randomized, double-blind study, equal amounts of either a dilute vasopressin solution or placebo (normal saline) were injected into the intracervical stroma at 4- and 8-o'clock positions, just beneath the mucosal surface, in 52 women immediately before cervical dilatation in preparation for operative hysteroscopy. When vasopressin solution was used, 20 mL of a dilute solution (4 U of 0.05 U/mL of vasopressin in 80 mL of normal saline) was injected. An electronic strain gauge and load cell were used to measure the peak linear force needed to dilate the cervix from 3 mm to 11 mm, using half-size metal dilators. RESULTS: The mean (+/- standard error of the mean) total peak linear force needed to dilate the cervix from 3 to 11 mm in the treated (vasopressin) and control (placebo) groups was 20.29 +/- 1.22 lb (range 5.54-40.82) and 37.05 +/- 2.55 lb (range 6.11-52.2), respectively, a statistically significant difference. The mean total peak linear force needed to dilate the cervix in the treated group and in the control group in 0.5-mm increments from 3 to 11 mm was 1.14 +/- 0.07 lb (range 0.81-1.69) and 2.08 +/- 0.07 lb (range 1.64-2.43), respectively, also a statistically significant difference. With increasing parity, significantly less force was needed to dilate the cervix from 3 to 11 mm in the treated group than in the control group (P < .001). CONCLUSIONS: Administration of dilute vasopressin solution (0.05 U/mL) to the cervical stroma significantly reduces the force needed to dilate the cervix.

Adult↗
PubMed1982

Controlled trial of terlipressin ('Glypressin') versus vasopressin in the early treatment of oesophageal varices.

In a randomised controlled trial the effect of intermittent bolus injection of triglycyl lysine vasopressin (terlipressin 'Glypressin') (2 mg that 6-hourly), an analogue of vasopressin, was compared with that of a constant peripheral intravenous infusion of vasopressin (0.4 units/Min) in the initial management of bleeding oesophageal varices in nineteen patients. Failure of vasopressin therapy was defined as continued bleeding of sufficient severity to necessitate the passage of a Sengstaken tube. Bleeding was controlled in 70% of patients treated with glypressin but in only 9% of patients given vasopressin. The glypressin group required significantly less blood after randomisation than the vasopressin group. Because of its efficacy, lack of side-effects, and ease of administration, glypressin appears to be valuable in the management of bleeding varices.

Adult↗
PubMed1987

Mecamylamine prevents the enhancement of retention induced by lysine vasopressin in mice.

Lysine vasopressin (0.03 microgram/kg, sc) enhanced retention of a one-trial, step-through inhibitory avoidance task when injected into male Swiss mice immediately post-training, as indicated by retention performance 48 h later. A low dose of the vasopressin antagonist, AAVP (0.01 microgram/kg, sc), did not significantly affect retention, whereas a higher dose (0.03 microgram/kg, sc) impaired retention. Neither lysine vasopressin nor AAVP modified latencies to step-through of mice that had not received a footshock during training. The simultaneous injection of AAVP (0.01 microgram/kg, sc) prevented the enhancement of retention induced by lysine vasopressin. The influence of lysine vasopressin on retention was antagonized by the simultaneous administration of mecamylamine (5 mg/kg, sc) but not by hexamethonium (5 mg/kg, sc), atropine (0.5 mg/kg, sc), or methylatropine (0.5 mg/kg, sc). A modulatory role of vasopressin on the activity of central cholinergic nicotinic mechanisms which participate in memory formation is suggested.

Animals↗
PubMed1997

Idazoxan and the effect of intracerebroventricular oxytocin or vasopressin on sodium intake of sodium-depleted rats.

The alpha2-adrenergic agonist clonidine and the neuropeptide oxytocin, inhibit sodium intake when injected intracerebroventricularly (i.c.v.). The present work investigates whether (1) vasopressin also inhibits sodium intake when injected i.c.v., and (2) the effect of oxytocin and of vasopressin on sodium intake is affected by i.c.v. injection of idazoxan, an alpha2-adrenergic antagonist. Clonidine (30 nmol), oxytocin (40, 80 nmol) and vasopressin (40, 80 nmol) were injected i.c.v. 20 min prior to a 1.5% NaCl appetite test, in rats depleted of sodium for 24 h by a combination of a single s.c. injection of furosemide (10 mg/rat) and removal of ambient sodium. Every dose of clonidine, oxytocin and vasopressin inhibited the 1.5% NaCl intake. Seizures were observed with the higher dose of vasopressin, but not with either dose of oxytocin. The effect of i.c.v. injection of clonidine (30 nmol), oxytocin (80 nmol) or vasopressin (40 nmol) was partially inhibited by prior i.c.v. injection of idazoxan (160, 320 nmol). The results suggest that the inhibition of 1.5% NaCl intake induced by i.c.v. injection of neuropeptides in sodium-depleted rats depends, in part, on the activation of central alpha2-adrenoceptors.

Adrenergic alpha-Agonists↗
PubMed1998

Ontogeny of the vasopressin and oxytocin RNAs in the mouse hypothalamus.

The single-copy genes encoding the vasopressin and oxytocin prepropeptides are closely linked in mouse genome, being separated by an intergenic region of only 3 kbp. These genes are expressed in anatomically defined hypothalamic neurons--in the adult rodent, vasopressin is synthesised in the paraventricular nucleus and the supraoptic nucleus, and in the dorsomedial region of the suprachiasmatic nucleus, whilst oxytocin is expressed in the supraoptic nucleus and paraventricular nucleus, but not in the suprachiasmatic nucleus. The molecular mechanisms that mediate the cell-specific and developmental expression patterns of the two transcription units within the vasopressin-oxytocin locus remain to be elucidated. As a first step in this process, we have used in situ hybridisation to study the expression of the RNAs encoded by the linked vasopressin and oxytocin genes during the development of the mouse hypothalamus. We have revealed a hierarchy of gene activation events, with vasopressin first being observed in presumptive supraoptic nucleus at day 13.5, and in the paraventricular at day 14.5. Oxytocin is seen first in the paraventricular at day 15.5; expression in the supraoptic nucleus is clearly seen at day 18.5. As early as day 15.5, the vasopressin and oxytocin RNAs are expressed in different groups of neurons.

Animals↗
PubMed1992

A randomized controlled trial comparing octreotide and vasopressin in the control of acute esophageal variceal bleeding.

This randomized controlled trial was conducted to compare the efficacy of intravenous infusion of octreotide (a synthetic long-acting somatostatin analogue) with vasopressin in 48 cirrhotic patients with endoscopically proven bleeding esophageal varices. Twenty-four patients received a continuous infusion of octreotide 25 micrograms/h for 24 h after an initial bolus of 100 micrograms and another 24 patients received a continuous infusion of vasopressin 0.4 U/min for 24 h. Bleeding was initially controlled after 6 h of drug infusion in 88% (21/24) and 54% (13/24) of the patients treated with octreotide and vasopressin respectively (p = 0.03). Complete control of bleeding after 24 h of drug infusion was achieved in 15 (63%) patients receiving octreotide and in 11 (46%) patients receiving vasopressin (p > 0.05). Side effects during drug infusion such as headache, chest pain and abdominal pain were significantly lower in the octreotide group (3/24) than in the vasopressin group (11/24). Serum gastrin and insulin levels fell significantly following octreotide infusion, but plasma glucose levels remained unchanged. Mortality related to bleeding esophageal varices was no different between the two groups. This report showed that octreotide infusion was more effective and had fewer side effects than vasopressin in initial controlling of acute esophageal variceal bleeding until an elective endoscopic sclerotherapy could be performed.

Aged↗
PubMed1986

Circulatory actions of vasopressin in anaesthetized rats with portal hypertension subjected to haemorrhage.

To assess the influence of vasopressin on splanchnic and renal circulatory changes induced by haemorrhage in portal hypertension, we studied 4 groups of 7 rats with chronic portal vein stenosis. Two groups received saline (C and H) and two groups vasopressin, 0.01 IU/kg/min (VP and VP-H). Ten minutes after starting drug infusion, group H and VP-H animals were allowed to bleed from the superior mesenteric vein. Both haemorrhage and vasopressin alone, decreased portal venous tributary blood flow and pressure but their association was not additive (as reflected by comparable bleeding rate in groups H and VP-H). By contrast, vasopressin increased renal perfusion in bleeding and non-bleeding animals whereas haemorrhage alone decreased renal perfusion. These results indicate that the effects of vasopressin on the splanchnic circulation in bleeding anaesthetized animals differ from the effects observed when blood volume is normal. Therefore, in patients with cirrhosis the effects of vasopressin during bleeding might also differ from those observed in patients in stable condition.

Anesthesia↗
PubMed1996

Effect of vasopressin on esophageal varices blood flow in patients with cirrhosis: comparisons with the effects on portal vein and superior mesenteric artery blood flow.

BACKGROUND/AIMS: Vasopressin reduces portal pressure which may be due to decreased portal inflow. However, it remains unclear whether vasopressin is able to selectively reduce esophageal varices blood flow. The aim of this study was to address this question. METHODS: Fifteen patients with cirrhosis and esophageal varices were included in this prospective study. Portal vein and superior mesenteric artery flow velocity were measured with a percutaneous echo-Doppler. Esophageal varices flow velocity was measured using a transesophageal echo-Doppler technique. Mean arterial pressure and heart rate were also recorded. These measurements were performed at baseline condition and 15 min after observer blind drug administration. In this study, two groups, six patients receiving placebo and nine patients receiving 0.3 U/min of vasopressin, were randomized according to the coded number. RESULTS: Placebo administration had no effect on systemic and splanchnic circulation. In contrast, vasopressin administration increased mean arterial pressure (p < 0.05) associated with a bradycardia (p < 0.01). In splanchnic circulation, vasopressin decreased portal vein (-32 +/- 3%, p < 0.01), superior mesenteric artery (-30 +/- 2%, p < 0.01), and esophageal varices flow velocity (-48 +/- 5%, p < 0.01). When the magnitude of these reductions was compared, ANOVA showed a significant difference (p < 0.01). Furthermore, the reduction in esophageal varices flow velocity was significantly higher than that in portal vein flow velocity (p < 0.01) and that in superior mesenteric artery flow velocity (p < 0.01). CONCLUSIONS: These data support the view that vasopressin is able to selectively reduce esophageal varices blood flow. This effect, in addition to its well-established portal pressure reducing action, may play a role in its therapeutic efficacy in the treatment of variceal bleeding.

Aged↗