Arginine Vasopressin In Patients Research Articles

Change of Levels of NGF, ACTH, and AVP in the Cerebrospinal Fluid after Decompressive Craniectomy of Craniocerebral Injury and Their Relationship with Communicating Hydrocephalus.

In recent years, the incidence of craniocerebral trauma has increased, making it one of the important causes of death and disability in neurosurgery patients. The decompressive craniectomy (DC) after severe craniocerebral injury has become the preferred treatment for patients with severe craniocerebral injury, but the incidence of postoperative hydrocephalus has become a difficult problem in clinical treatment. This study observed the changes of nerve growth factor (NGF), adrenocorticotropic hormone (ACTH), and arginine vasopressin (AVP) levels in the CSF after DC in patients with craniocerebral injury and analyzed the relationship between the three indicators and communicating hydrocephalus. The results showed that the levels of NGF, ACTH, and AVP in patients with cranial injury after DC were significantly higher than those in healthy subjects, and subdural effusion, traumatic subarachnoid hemorrhage (tSAH), and the levels of NGF, ACTH, and AVP in the CSF were independent risk factors for communicating hydrocephalus. Monitoring the levels of NGF, ACTH, and AVP is of great significance for clinicians to judge the occurrence of traffic hydrocephalus, evaluate the prognosis of patients with craniocerebral injury after DC, and guide clinical treatment.

Psychoendocrinology: arginine vasopressin and resilience in patients with major depressive disorder.

There is a burgeoning body of evidence suggesting that arginine vasopressin (AVP) acts as a neuromodulator of the stress response. AVP stimulates the release of adrenocorticotropic hormone, synergistic to corticotropin-releasing hormone, which might explain AVP's role in resilience. Personal hardiness is the bedrock of resilience. Numerous studies have demonstrated elevated plasma levels of AVP in patients with major depressive disorder (MDD), suggesting an etiopathogenetic role as well as a novel therapeutic target. The aim of this study was to examine the relationship between AVP and resilience in patients with MDD and to determine AVP levels in serum of patients with MDD. Forty patients with MDD and 40 healthy control subjects were studied using the Dispositional Resilience (Hardiness) Scale by Barton, the Quality of Life Scale, the Social Readjustment Rating Scale, and the Beck Depression Inventory. Biochemical analysis of plasma levels of AVP, using the enzyme-linked immunosorbent assay (ELISA), was performed for all participants. Levels of AVP were statistically significantly elevated in patients with MDD compared with healthy controls. Psychological hardiness was decreased in patients with MDD compared with healthy controls, a finding also statistically significant. There was a negative correlation between plasma AVP level and psychological hardiness. AVP and psychological hardiness are negatively correlated, reflecting lower stress resilience. AVP levels are indeed higher in patients struggling with MDD.

What's New in Shock, February 2021?

What's New in Shock, February 2021?

Hemodynamic Response to Vasopressin Dosage of 0.03 Units/Min vs. 0.04 Units/Min in Patients With Septic Shock.

Arginine vasopressin (AVP) is suggested as an adjunct to norepinephrine in patients with septic shock. Guidelines recommend an AVP dosage up to 0.03 units/min, but 0.04 units/min is commonly used in practice based on initial studies. This study was designed to compare the incidence of hemodynamic response between initial fixed-dosage AVP 0.03 units/min and AVP 0.04 units/min. This retrospective, multi-hospital health system, cohort study included adult patients with septic shock receiving AVP as an adjunct to catecholamine vasopressors. Patients were excluded if they received an initial dosage other than 0.03 units/min or 0.04 units/min, or AVP was titrated within the first 6 hours of therapy. The primary outcome was hemodynamic response, defined as a mean arterial pressure ≥65 mm Hg and a decrease in catecholamine dosage at 6 hours after AVP initiation. Inverse probability of treatment weighting (IPTW) based on the propensity score for initial AVP dosage receipt was utilized to estimate adjusted exposure effects. Of the 1536 patients included in the observed data, there was a nearly even split between initial AVP dosage of 0.03 units/min (n = 842 [54.8%]) and 0.04 units/min (n = 694 [45.2%]). Observed patients receiving AVP 0.03 units/min were more frequently treated at the main campus academic medical center (96.3% vs. 52.2%, p < 0.01) and in a medical intensive care unit (87.4% vs. 39.8%, p < 0.01). The IPTW analysis included 1379 patients with achievement of baseline covariate balance. There was no evidence for a difference between groups in the incidence of hemodynamic response (0.03 units/min 50.0% vs. 0.04 units/min 53.1%, adjusted relative risk 1.06 [95% CI 0.94, 1.20]). Initial AVP dosing varied by hospital and unit type. Although commonly used, an initial AVP dosage of 0.04 units/min was not associated with a higher incidence of early hemodynamic response to AVP in patients with septic shock.

Regulation and Clinical Implication of Arginine Vasopressin in Patients with Severe Aortic Stenosis Referred to Trans-Catheter Aortic Valve Implantation.

Background and objectives: Plasma arginine vasopressin (P-AVP) is regulated by the non-osmotic pathway in patients with heart failure (HF) and reduced ejection fraction. However, the regulation of P-AVP in patients with severe aortic stenosis (AS) remains unknown. Materials and Methods: Consecutive patients with severe AS who received trans-catheter aortic valve implantation (TAVI) between Apr 2016 and Apr 2019 were enrolled in this prospective study. Clinical data including P-AVP were obtained just before TAVI, and the correlation between P-AVP and other variables was investigated. Results: In total, 159 patients with severe AS (85.3 ± 4.6 years, male 26%) were enrolled. P-AVP was 1.45 ± 1.13 ng/mL and cardiac index was relatively preserved (2.76 ± 0.54 L/min/m2). There was no significant correlation between cardiac index and P-AVP (p > 0.05), whereas plasma osmolality had a moderate positive correlation with P-AVP (r = 0.35, p < 0.01), predominantly due to blood urea nitrogen (r = 0.27, p < 0.01). Patients with diuretics had significantly higher P-AVP than those without diuretics (1.65 ± 1.43 vs. 1.22 ± 0.57 pg/mL, p < 0.01). Two-year survivals free from HF readmission were statistically comparable irrespective of the level of pre-procedural P-AVP (p = 0.44). Conclusion: In patients with severe high-gradient AS who received TAVI, the P-AVP level was dominantly regulated by plasma osmolality instead of arterial underfilling. The clinical implication of elevated P-AVP in the TAVI candidates is the next concern.

Incidence of Hypotension after Discontinuation of Norepinephrine or Arginine Vasopressin in Patients with Septic Shock: a Systematic Review and Meta-Analysis.

BackgroundThere has been no consensus regarding the discontinuation order of vasopressors in patients recovering from septic shock treated with concomitant norepinephrine (NE) and arginine vasopressin (AVP). The aim of this study was to compare the incidence of hypotension within 24 hours based on whether NE or AVP was discontinued first in order to determine the optimal sequence for discontinuation of vasopressors.MethodsA systematic literature search was conducted in MEDLINE, Embase, and the Cochrane Central Register. The primary end-point was incidence of hypotension within 24 hours after discontinuation of the first vasopressor.ResultsWe identified five studies comprising 930 patients, of whom 631 (67.8%) discontinued NE first and 299 (32.2%) discontinued AVP first. In pooled estimates, a random-effect model showed that discontinuation of NE first was associated with a significant reduction of the incidence of hypotension compared to discontinuing AVP first (31.8% vs. 54.8%; risk ratios, 0.35; 95% confidence interval, 0.16 to 0.76; P = 0.008; I2 = 90.7%). Although a substantial degree of heterogeneity existed among the trials, we could not identify the significant source of bias. In addition, there were no significant differences in intensive care unit (ICU) mortality, in-hospital mortality, 28-day mortality, or ICU length of stay between the groups.ConclusionDiscontinuing NE prior to AVP was associated with a lower incidence of hypotension in patients recovering from septic shock. However, our results should be interpreted with caution, due to the considerable between-study heterogeneity.

A PUZZLING DIAGNOSIS: UNUSUAL LARYNGEAL CARCINOMA PRESENTING AS PARANEOPLASTIC SYNDROME

SESSION TITLE: Wednesday Medical Student/Resident Case Report Posters SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: 10/23/2019 09:45 AM - 10:45 AM INTRODUCTION: The Syndrome of Inappropriate Antidiuretic Hormone (SIADH) is one of the most common causes of euvolemic hyponatremia. The most common malignancy associated with SIADH is small cell lung cancer. We present a case of a patient with SIADH secondary to well differentiated squamous cell carcinoma of the vocal cords. CASE PRESENTATION: A 62-year-old Caucasian male with a history of alcohol abuse and 80 pack-year smoking history presented with recurrent hyponatremia. He was initially admitted to the ICU for altered mental status due to hyponatremia of 111 which was thought to be a combination of beer potomania/SIADH/low solute intake. He required hypertonic saline boluses twice and a one dose of DDAVP to prevent overcorrection, along with fluid restriction with an improvement of Na to 132. (Image 1) Chest CT was obtained that did not reveal any malignancy. He was discharged with fluid restriction and follow up with his PCP. At his follow up, he was found to have again developed severe hyponatremia of 112. He was admitted again to the ICU for appropriate normalization of sodium, required isotonic saline and then fluid restriction. SIADH was confirmed by low Serum Osmolality at 245mosm/kg, high Urine osmolality of 502mosm/kg, Urine sodium of 41mEq/l,and normal serum Potassium of 4.3mEq/l along with low serum uric acid of 3.4mg/dl. Upon review of the CT chest with the radiologist he had some density on his left aryepiglottic fold. Upon closer discussion with him, he endorsed progressive hoarseness for the past year to the point of losing his voice. He also lost about 20 pounds over the last year, with a 10-pound weight loss over the past month. CT neck with IV contrast showed a 4.5cm laryngeal mass (Image 2) and direct laryngoscopy and microscopic laryngoscopy with biopsy of the tumor on the left vocal cord with multiple biopsies taken of the terminal vocal cords finally revealed squamous cell carcinoma. He is scheduled to follow up with oncology, ENT and radiation oncology after a PET scan for tumor staging to decide on further treatment with concurrent chemotherapy and radiation. DISCUSSION: There is a possible relationship between the tumor mass burden and the severity of the hyponatremia. This has been shown in another laryngeal carcinoma but was not seen with recurrence of the tumor.[1] The mechanisms leading to the associated hyponatremia could have been related to tumor ADH productions or other factors yet unknown.[2] CONCLUSIONS: SIADH is well known to occur with squamous cell lung cancer. Other types of squamous cell carcinomas are known to cause SIADH as a paraneoplastic syndrome, particularly squamous cell carcinoma of the tongue.[3] It has not been well documented to be from squamous cell carcinoma of vocal cords. Reference #1: Talmi YP, Hoffman HT, McCabe BF (1992) Syndrome of inappropriate secretion of arginine vasopressin in patients with cancer of the head and neck. Ann Otol Rhinol Laryngol 101:946-949 Reference #2: Roth Y, Lightman SL, Kronenberg J. (1994). Hyponatremia associated with laryngeal squamous cell carcinoma. Eur Arch Otorhinolaryngol 251: 183-185 Reference #3: Zohar Y, Talmi YP, Finkelstein Y, Nobel M, Gafter U (1991) Syndrome of inappropriate antidiuretic hormone secretion in cancer of the head and neck. Ann Otol Rhinol Laryngol 100:341-344 DISCLOSURES: No relevant relationships by Sofia Adamidi, source=Web Response no disclosure on file for Steven Lamontagne; No relevant relationships by Preeyanka Sundar, source=Web Response

Copeptin Levels in Patients With Treatment-Resistant Hypertension Before and 6 Months After Renal Denervation.

Copeptin, the C-terminal peptide of provasopressin, is released from the neurohypophysis and reflects the activity of the hormone arginine vasopressin in patients with hypertension. Elevated copeptin levels are associated with increased cardiovascular and all-cause mortality. The aim of this study is to compare copeptin levels in patients with treatment-resistant hypertension (TRH) before and 6 months after renal denervation (RDN). Copeptin was measured in 34 patients with TRH and 30 patients with primary hypertension stage 1 or 2 (HT). In addition, copeptin levels were measured in patients with TRH at 6-month follow-up visit after RDN. RDN was performed by an experienced interventionalist applying at least 4 ablations longitudinally and rotationally within the lengths of each renal artery to cover a full 4-quadrant ablation. In patients with TRH 24-hour ambulatory blood pressure (BP) decreased from 154 ± 15/87 ± 12 mm Hg to 146 ± 13/83 ± 7.9 mm Hg after RDN (systolic: P = 0.001, diastolic: P = 0.034). There was no significant change in copeptin levels in these 34 patients with TRH before vs. 6 months after RDN (median 8.4 [interquartile range 3.6-14] vs. 8.5 [4.5-13] pmol/l, P = 0.334). Patients with TRH had higher copeptin levels (P = 0.024) than patients with HT (24-hour ambulatory BP: 142 ± 11/91 ± 8.3 mm Hg, copeptin: 4.2 [2.8-6.3] pmol/l). Patients with TRH showed 2-fold higher copeptin levels than patients with HT. RDN did not lead to any change of copeptin levels in patients with TRH 6 months after procedure despite significant fall in BP. NCT01318395, NCT01687725.

Effect of Low-Dose Supplementation of Arginine Vasopressin on Need for Blood Product Transfusions in Patients With Trauma and Hemorrhagic Shock

Current therapies for traumatic blood loss focus on hemorrhage control and blood volume replacement. Severe hemorrhagic shock, however, is associated with a state of arginine vasopressin (AVP) deficiency, and supplementation of this hormone may decrease the need for blood products in resuscitation. To determine whether low-dose supplementation of AVP in patients with trauma (hereinafter referred to as trauma patients) and with hemorrhagic shock decreases their need for transfused blood products during resuscitation. This randomized, double-blind placebo-controlled clinical trial included adult trauma patients (aged 18-65 years) who received at least 6 U of any blood product within 12 hours of injury at a single urban level 1 trauma center from May 1, 2013, through May 31, 2017. Exclusion criteria consisted of prehospital cardiopulmonary resuscitation, emergency department thoracotomy, corticosteroid use, chronic renal insufficiency, coronary artery disease, traumatic brain injury requiring any neurosurgical intervention, pregnancy, prisoner status, or AVP administration before enrollment. Data were analyzed from May 1, 2013, through May 31, 2017, using intention to treat and per protocol. After administration of an AVP bolus (4 U) or placebo, participants received AVP (≤0.04 U/min) or placebo for 48 hours to maintain a mean arterial blood pressure of at least 65 mm Hg. The primary outcome was total volume of blood product transfused. Secondary end points included total volume of crystalloid transfused, vasopressor requirements, secondary complications, and 30-day mortality. One hundred patients underwent randomization (49 to the AVP group and 51 to the placebo group). Patients were primarily young (median age, 27 years [interquartile range {IQR}, 22-25 years]) and male (n = 93) with penetrating trauma (n = 79). Cohort characteristics before randomization were well balanced. At 48 hours, patients who received AVP required significantly less blood products (median, 1.4 [IQR, 0.5-2.6] vs 2.9 [IQR, 1.1-4.8] L; P = .01) but did not differ in requirements for crystalloids (median, 9.9 [IQR, 7.9-13.0] vs 11.0 [8.9-15.0] L; P = .22) or vasopressors (median, 400 [IQR, 0-5900] vs 1400 [IQR, 200-7600] equivalent units; P = .22). Although the groups had similar rates of mortality (6 of 49 [12%] vs 6 of 51 [12%]; P = .94) and total complications (24 of 44 [55%] vs 30 of 47 [64%]; P = .37), the AVP group had less deep venous thrombosis (5 of 44 [11%] vs 16 of 47 [34%]; P = .02). Low-dose AVP during the resuscitation of trauma patients in hemorrhagic shock decreases blood product requirements. Additional research is necessary to determine whether including AVP improves morbidity or mortality. ClinicalTrials.gov identifier: NCT01611935.

Vasopressin and oxytocin in CSF and plasma of patients with aneurysmal subarachnoid haemorrhage

ObjectiveClinicopathological studies on patients succumbing to subarachnoid haemorrhage (SAH) demonstrated hypothalamic lesions. The implication of the hypothalamic neuropeptides arginine-vasopressin (AVP) and oxytocin (OXT) has not been linked to aneurysmal SAH yet. This study investigates AVP and OXT in CSF and plasma of patients with spontaneous aneurysmal SAH and their association with outcome. MethodsCSF and plasma samples of 12 patients with aneurysmal SAH were prospectively studied for 2weeks. AVP and OXT were measured by radioimmunoassay. Outcome was assessed on Glasgow-Outcome-Scale. Twenty-nine patients without neuropsychiatric disturbances served as controls. Differences in neuropeptide concentration time courses were assessed by regression models. Group comparisons were performed by Kruskal–Wallis and correlations by Spearman tests. ResultsRegression of CSF levels between patients with poor and good outcome revealed significantly lower levels of AVP in patients with poor outcome (p=0.012) while OXT showed a trend towards lower levels (p=0.063). In plasma, no significant differences between outcome groups were found. Group comparisons between poor outcome patients and controls revealed significant differences in CSF for AVP (p=0.001) and OXT (p=0.015). In plasma, AVP yielded significantly different results while OXT did not. No differences were found between the good outcome group and controls. Plasma and CSF concentrations showed no significant correlation. ConclusionPatients with poor outcome after aneurysmal SAH have lower AVP and OXT levels in CSF than patients with good outcome while neuropeptide levels in plasma failed to reflect differences in outcome. The data indicate hypothalamic damage as an aetiologic factor for outcome after aneurysmal SAH.

Suprachiasmatic Nucleus Neuropeptide Expression in Patients with Huntington's Disease

To study whether sleep and circadian rhythm disturbances in patients with Huntington's disease (HD) arise from dysfunction of the body's master clock, the hypothalamic suprachiasmatic nucleus. Postmortem cohort study. Eight patients with HD and eight control subjects matched for sex, age, clock time and month of death, postmortem delay, and fixation time of paraffin-embedded hypothalamic tissue. Using postmortem paraffin-embedded tissue, we assessed the functional integrity of the suprachiasmatic nucleus in patients with HD and control subjects by determining the expression of two major regulatory neuropeptides, vasoactive intestinal polypeptide and arginine vasopressin. Additionally, we studied melatonin 1 and 2 receptor expression. Compared with control subjects, the suprachiasmatic nucleus contained 85% fewer neurons immunoreactive for vasoactive intestinal polypeptide and 33% fewer neurons for arginine vasopressin in patients with HD (P = 0.002 and P = 0.027). The total amount of vasoactive intestinal polypeptide and arginine vasopressin messenger RNA was unchanged. No change was observed in the number of melatonin 1 or 2 receptor immunoreactive neurons. These findings indicate posttranscriptional neuropeptide changes in the suprachiasmatic nucleus of patients with HD, and suggest that sleep and circadian rhythm disorders in these patients may at least partly arise from suprachiasmatic nucleus dysfunction.

Changes of VE-cadherin andarginine vasopressin in patients with acute brain injuries

：Objective To observe thechanges of serum vascular endothelium-cadherin (VE-cadherin) and plasma argininevasopressin (AVP) in patients with acute brain injury, and to investigate the VE-cadherinand plasma AVP related to brain edema and prognosis following acute brain injury. MethodELISA was used to measure the serum VE-cadherin level and radioimmunoassay was used tomeasure serial concentration of AVP in plasma of 110 patients with acute brain injury 12hours and 3 and 5 days after brain injury. The outcome was estimated in combination ofclinical manifestation, iconographic findings and Glasgow Outcome Scale (GOS). Results Thelevels of VE-cadherin and AVP increased significantly over 12 hours after brain injurywith reduction of GCS. The severer brain injury resulted in higher levels of VE-cadherinand AVP, and prolongation of peak brain edema (P < 0.01). VE-cadherin levels showedpositive correlation with severity of brain edema (r = 0.69, P < 0.01) and prolongationof brain edema (r = 0.70.P < 0.01). AVP levels had positive correlation with severityof brain edema (r = 0.65, P < 0.01) and prolongation of brain edema (r = 0.64, P <0.01). Furthermore, there were significant increases in VE-cadherin and AVP levels inpatients with low GOS groups (P < 0.01). The VE-cadherin and AVP leveb in poor outcomegroup persistently increased for 5 days after brain injury and were higher than those ingood outcome group and normal control group. There were a correlation between VE-cadherinand AVP in patients with acute brain injury (r = 0.75, P < 0.01). ConclusionsVE-cadherin and AVP leveb are closely associated with the prognosis of patients afteracute brain injury. VE-cadherin and AVP may play pivotal roles in the pathogenesis ofbrain edema after acute brain injury.

Arginine vasopressin in vasodilatory shock: effects on metabolism and beyond

To describe the effects of arginine vasopressin other than its vasoconstrictive and antidiuretic potential in vasodilatory shock. Arginine vasopressin influences substrate metabolism by stimulation of hepatic glucose release, gluconeogenesis, ureogenesis and fatty acid esterification. Although arginine vasopressin is a secretagogue of different hormones, only prolactin increases during arginine vasopressin therapy. Plasmatic and cellular coagulation are affected by arginine vasopressin, resulting in thrombocyte aggregation. Therefore, platelet count typically decreases following arginine vasopressin infusion in critically ill patients. In addition, arginine vasopressin reduces bile flow and may increase bilirubin concentrations. Despite its potential to decrease serum sodium, no change in electrolytes was observed in critically ill patients receiving arginine vasopressin. Although arginine vasopressin is an endogenous antipyretic, body temperature is not decreased by central venous arginine vasopressin infusion. In addition, arginine vasopressin modulates immune function through V1 receptors. Compared with norepinephrine, arginine vasopressin may have protective effects on endothelial function. Net arginine vasopressin effects on gastrointestinal motility seem to be inhibitory and are dose dependent. Except for its antidiuretic and vasoconstrictive actions, the effects of arginine vasopressin in patients with vasodilatory shock have so far only been partially examined. Potential influences of arginine vasopressin on metabolism and immune, liver and mitochondrial function remain to be assessed in future studies.

Vasopressin impairs brain, heart and kidney perfusion: an experimental study in pigs after transient myocardial ischemia

IntroductionArginine vasopressin (AVP) is increasingly used to restore mean arterial pressure (MAP) in low-pressure shock states unresponsive to conventional inotropes. This is potentially deleterious since AVP is also known to reduce cardiac output by increasing vascular resistance. The effects of AVP on blood flow to vital organs and cardiac performance in a circulation altered by cardiac ischemia are still not sufficiently clarified. We hypothesised that restoring MAP by low dose, therapeutic level AVP would reduce vital organ blood flow in a setting of experimental acute left ventricular dysfunction.MethodsCardiac output (CO) and arterial blood flow to the brain, heart, kidney and liver were measured in nine pigs using transit-time flow probes. Left ventricular pressure-volume catheter and central arterial and venous catheters were used for haemodynamic recordings and blood sampling. Transient left ventricular ischemia was induced by intermittent left coronary occlusions resulting in a 17% reduction in cardiac output and a drop in MAP from 87 ± 3 to 67 ± 4 mmHg (p < 0.001). A low-dose therapeutic level of AVP (0.005 U/kg/min) was used to restore MAP to pre-ischemic values (93 ± 4 mmHg).ResultsAVP further impaired systemic perfusion (CO and brain, heart and kidney blood flow reduced by 29, 18, 23 and 34%, respectively) due to a 2.0-, 2.2-, 1.9- and 2.1-fold increase in systemic, brain, heart and kidney specific vascular resistances. The hypoperfusion induced by AVP was associated with an increased systemic oxygen extraction. Oxygen saturation in blood drawn from the great cardiac vein fell from 29 ± 1 to 21 ± 3% (p = 0.01). Finally, these effects were reversed 40 min after AVP was withdrawn.ConclusionLow dose AVP induced a pronounced reduction in vital organ blood flow in pigs after transient cardiac ischemia. This indicates a potentially deleterious effect of AVP in patients with heart failure or cardiogenic shock due to impaired coronary perfusion.

Author’s reply to the correspondence letter from Dr. S. Meyer et al. entitled arginine-vasopressin as a rescue therapy in children and neonates for catecholamine-resistant shock

We appreciate the interest in our study and the comments by Dr. Meyer and would like to respond to them. Our study reported the retrospectively analysed data of 17 neonates, who developed systemic inflammatory response syndrome (SIRS) with catecholamineresistant vasodilatory shock following open-heart surgery and were treated with lowdose continuous infusion of arginine-vasopressin (AVP). Despite the use of modified ultrafiltration uncontrolled release of proinflammatory cytokines may lead to SIRS after cardiopulmonary bypass. Especially neonates who undergo cardiac surgery with long bypass duration are at high risk to develop post bypass SIRS [2, 7]. This syndrome is not necessarily associated with cardiac dysfunction or cardiogenic shock. Both septic as well as post cardiopulmonary bypass-induced severe vasodilatation are associated with inappropriately low vasopressin plasma levels; so this vasopressin deficiency may contribute to the hypotension of vasodilatory shock [3, 4, 6]. Low dose continuous infusions of vasopressin have been successfully used in several trials in adults and children with vasodilatory shock secondary to open-heart surgery [1, 5, 6]. In accordance with these findings, our study showed that in neonates with vasodilatory shock refractory to traditional vasopressors after cardiac surgery vasopressin seems to be a potent agent to increase blood pressure and avoid end-organ failure. Because vasopressin is less appropriate for neonates with ventricular dysfunction [6], we took care not to use AVP in patients with cardiac dysfunction. One major limitation of our study was that we did not measure endogenous vasopressin levels prior to the initiation of AVP. We fully agree with the suggestion of Dr. Meyer that future clinical studies should assess endogenous vasopressin levels prior to the administration of exogenous AVP.

Decrease in nocturnal urinary levels of arginine vasopressin in patients with nocturnal polyuria

Objectives To elucidate whether heart function and endocrine levels of arginine vasopressin (AVP) or solute diuresis is associated with the nocturnal voided volume, and whether the urinary AVP could be a parameter for screening for nocturnal polyuria caused by AVP insufficiency. Methods A total of 50 patients were enrolled in this study. The blood and urine samples were obtained every 6 hours at 6 pm, 12 am, 6 am, and 12 pm. Atrial natriuretic peptide and brain natriuretic peptide were measured at admission. All voided urine samples were collected every 6 hours for examination. The evaluation items were AVP, osmolarity, sodium, potassium, chloride, and creatinine in blood and urine. Results The patients were classified into a group with nocturnal polyuria (n = 21) and a group without nocturnal polyuria (n = 25). There was no significant difference in atrial natriuretic peptide, brain natriuretic peptide, electrolytes in blood and urine, and plasma AVP of each sample between the two groups, but urinary AVP/urinary creatinine and urine osmolarity at 12 am and 6 am in the group with nocturnal polyuria were significantly lower than those in the group without nocturnal polyuria. The nocturnal voided volume correlated with urinary AVP/urinary creatinine level in the urine samples obtained at 12 am and 6 am. Conclusions The present data have demonstrated that the significant decrease in urinary AVP/urinary creatinine level at 6 am may contribute to the increased nocturnal voided volume followed by nocturia and that the circadian rhythm disorder of AVP can be predicted by a noninvasive test measuring urinary AVP/urinary creatinine in the urine voided early in the morning.

Urinary excretion of aquaporin-2 water channel exaggerated dependent upon vasopressin in congestive heart failure

Impaired water excretion occurs in patients with congestive heart failure. The present study was undertaken to determine whether urinary excretion of aquaporin-2 (AQP-2) water channel is exaggerated in patients with congestive heart failure dependent upon arginine vasopressin (AVP). Sixty-five patients with congestive heart failure and eight age- and gender-matched control subjects were examined. The patients were divided into four groups according to the criteria of New York Heart Association (NYHA). Plasma AVP levels, urinary excretion of AQP-2, and cardiac index were determined. Plasma AVP levels were progressively increased following the severity of NYHA class in the patients with congestive heart failure. Cardiac index was inversely decreased, and there was a negative correlation between plasma AVP levels and cardiac index (r=-0.430, P < 0.02). Urinary excretion of AQP-2 was 187.3 +/- 50.2 fmol/mg creatinine in the control subjects. It was markedly increased in the patients. Urinary excretion of AQP-2 was elevated to 1144.4 +/- 257.5 and 990.5 +/- 176.0 fmol/mg creatinine in the patients with NYHA class III and class IV, respectively, values significantly greater than the control subjects (P < 0.05). Urinary excretion of AQP-2 had a positive correlation with plasma AVP levels (r= 0.280, P < 0.02). The present study indicates that exaggerated urinary excretion of AQP-2 is dependent on baroreceptor-mediated release of AVP in patients with congestive heart failure.

Resistance to vasopressin action on the kidney in patients with Cushing's disease.

To assess the plasma levels and action of arginine vasopressin (AVP) in patients with Cushing's disease. There are many reports that patients with Addison's disease have increased AVP levels associated with hyponatraemia and hypoosmolality, but none on the dynamics of secretion of this neurohormone during osmolality-based stimulation in patients with chronic hypercortisolism. The plasma AVP concentration and the urinary and plasma osmolality after a 7.5-h water deprivation test (WDT) were evaluated in 13 patients with Cushing's disease and 15 normal (control) individuals. In patients with Cushing's disease we also assessed the urinary osmolality in response to 10 micrograms i.v. desmopressin (DDAVP) administered at the end of the WDT. At the end of the WDT, urinary osmolality was significantly lower in patients with Cushing's disease (511.5 +/- 148.5 mOsm/l) than in the normal subjects (981.1 +/- 107.1 mOsm/l, P < 0.001), whereas plasma osmolality did not differ between the two groups. Consequently, the urine/plasma osmolality ratio (Uosm/Posm) was lower in patients with Cushing's disease than in normal individuals (1.8 +/- 0.5 compared with 3.4 +/- 0.4, P < 0.001). The AVP concentration also was greater (7.3 +/- 3.1 pmol/l) in those with Cushing's disease than in the controls (3.9 +/- 2.3 pmol/l, P < 0.005). After administration of DDAVP to the hypercortisolaemic patients, the urinary osmolality attained (718.0 +/- 200.0 mOsm/l) was still lower than that in the normal group at the end of WDT (P < 0.005). Patients with Cushing's disease presented higher AVP levels and smaller Uosm/Posm ratios than normal subjects. After DDAVP, the patients with Cushing's disease were unable to concentrate the urine adequately. These data suggest that the kidney shows resistance to the action of both endogenous and exogenous AVP in patients with Cushing's disease.

Plasma levels of β-endorphin, leucine enkephalin and arginine vasopressin in patients with essential hypertension and the effects of clonidine

In order to investigate the changes of endogenous opiate systems in hypertension and their possible role in the pathogenesis in hypertension, we measured plasma concentrations of β-endorphin, leucine-enkephalin, neurotension, arginine vasopressin, plasma renin activity and angiotensin II by radioimmunoassay in 60 normal persons and 120 patients with essential hypertension. The results showed that the patient group had lower levels of β-endorphin and leucineenkephalin ( P < 0.001), higher levels of arginine vasopressin, plasma renin activity and angiotensin II ( P < 0.01, P < 0.05 and P < 0.05, respectively), and normal level of neurotensin, as compared with those in normal group. Plasma levels of leucine-enkephalin was correlated negatively to the mean artery pressure ( r = −0.196, P < 0.05). Plasma level of arginine vasopressin was correlated to the duration of the hypertension ( r = 0.216, P < 0.05). After 150 min and 14 days of treatment with clonidine, plasma levels of β-endorphin, leucine-enkephalin increased significantly (< 0.01) and correlated negatively with the decrease of the mean artery pressure ( r = − 0.340 and r = − 0.436 at 150 min, r = − 0.369 and r = − 0.441 on the 14th day, respectively, P < 0.01). Plasma renin activity and angiotensin II decreased significantly ( P < 0.05 and P < 0.01). Arginine vasopressin and neurotensin did not change significantly. After intravenous administration of opiate antagonist-naloxone, the blood pressure and heart rate increased significantly ( P < 0.01). The results suggested that the changes of endogenous opioids may be involved in the pathogenesis of hypertension and in the antihypertensive action of clonidine.

Association of fluoxetine treatment with reductions in CSF concentrations of corticotropin-releasing hormone and arginine vasopressin in patients with major depression.

The authors measured CSF concentrations of corticotropin-releasing hormone (CRH) and arginine vasopressin in nine depressed patients before and after fluoxetine treatment. They found significant decreases in CSF CRH, CSF arginine vasopressin, and Hamilton depression ratings. Thus, the therapeutic effect of this serotonin-uptake inhibitor may be related to diminution of these arousal-promoting neuropeptides.