Continuous Infusion Of Hypertonic Saline Research Articles

Effect of continuous hypertonic saline infusion on clinical outcomes in patients with traumatic brain injury.

Osmotic therapy has been recognized as an important treatment option for patients with traumatic brain injury (TBI). Nevertheless, the effect of hypertonic saline (HTS) remains unknown, as findings are primarily based on a large database. This study aimed to elucidate the effect of HTS on the clinical outcomes of patients with TBI admitted to the intensive care unit (ICU). We retrospectively identified patients with moderate-to-severe TBI from two public databases: Medical Information Mart for Intensive Care (MIMIC)-IV and eICU Collaborative Research Database (eICU-CRD). A marginal structural Cox model (MSCM) was used, with time-dependent variates designed to reflect exposure over time during ICU stay. Trajectory modeling based on the intracranial pressure evolution pattern allowed for the identification of subgroups. Overall, 130 (6.65%) of 1955 eligible patients underwent HTS. MSCM indicated that the HTS significantly associated with higher infection complications (e.g., urinary tract infection (HR 1.88, 95% CI 1.26-2.81, p = 0.002)) and increased ICU LOS (HR 2.02, 95% CI 1.71-2.40, p < 0.001). A protective effect of HTS on GCS was found in subgroups with medium and low intracranial pressure. Our study revealed no significant difference in mortality between patients who underwent HTS and those who did not. Increased occurrence rates of infection and electrolyte imbalance are inevitable outcomes of continuous HTS infusion. Although the study suggests slight beneficial effects, including better neurological outcomes, these results warrant further validation.

Early and prolonged continuous hypertonic saline infusion in patients with acute liver failure

PurposeTo study patient characteristics, physiological changes, and outcomes associated with prolonged continuous hypertonic saline (HTS) infusion in acute liver failure (ALF). Materials and methodsRetrospective observational cohort study of adult patients with ALF. We collected clinical, biochemical, and physiological data six hourly for the first week, daily until day 30 or hospital discharge, and weekly, when documented, until day 180. ResultsOf 127 patients, 85 received continuous HTS. Compared with non-HTS patients they were more likely to receive continuous renal replacement therapy (CRRT) (p < 0.001) and mechanical ventilation (p < 0.001). Median HTS duration was 150 (Interquartile range (IQR): 84–168) hours, delivering a median 2244 (IQR: 979–4610) mmol sodium load. Median peak sodium concentration was 149 mmol/L vs 138 mmol/L in non-HTS patients (p < 0.001). The median rate of sodium increase with infusion was 0.1 mmol/L/h and median rate of decrease during weaning was 0.1 mmol/L every 6 h. Median lowest pH value was 7.29 vs. 7.35 in non-HTS patients. Survival of HTS patients was 72.9% overall and 72.2% without transplantation. ConclusionsIn ALF patients, the prolonged administration of HTS infusion was not associated with severe hypernatremia or rapid shifts in serum sodium upon commencement, delivery, or weaning.

Comparison of intermittent versus continuous infusion of 3% hypertonic saline on intracranial pressure in traumatic brain injury using ultrasound assessment of optic nerve sheath

ABSTRACT Background The employment of hypertonic saline (HTS) in intracranial hypertension treatment has been effective when administered as a continuous infusion or bolus. However, the best route and concentration are undecided because of insufficient randomized controlled trials. This study aims to function the optic nerve sheath diameter (ONSD) ultrasonographic measurements to compare the effectiveness of 3% HTS continuous infusion and intermittent boluses in reducing elevated intracranial pressure (ICP) in traumatic brain injuries (TBIs). Methods This randomized study comprised 50 patients with TBI. In all patients examined by ultrasound, we employed a cutoff value of 5.5 mm for the ONSD to predict an increase in ICP of >20 mmHg. Patients with elevated ICP were divided into two groups: group A received continuous 3% HTS infusion (0.5 mL/kg/h), and group B received intermittent 3% HTS boluses (3 mL/kg). The primary endpoint was the ONSD at 48 h. The secondary outcomes included serum Na and serum K at 6, 12, 24, 48, and 72 h. Results The ONSDs in the continuous HTS infusion and intermittent bolus groups decreased significantly and steadily, with no significant variance between the two groups at 48 h (P = 0.449). However, 3% HTS intermittent boluses caused a faster growth in sodium concentration at 6 and 12 h with noteworthy differences compared with continuous infusion (P = 0.013 and 0.001, respectively). Conclusions There were no differences in ONSD ultrasonographic values 48 h after treatment. Moreover, 3% HTS intermittent boluses caused an increase in sodium concentration at 6 and 12 h.

International clinical research of critical care medicine in 2021

The progress of critical care medicine in 2021 is still encouraging. The new international guideline for management of sepsis and septic shock came out after 4 years. Besides, a couple of preferable clinical evidences were released including restrictive blood transfusion strategy for patients with acute myocardial infarction, prevention of peripheral venous catheter infection, heparin inhalation and driving pressure setting in patients with acute respiratory distress syndrome (ARDS), lower oxygenation target for acute hypoxemic respiratory failure, low level positive end-expiratory pressure in non-ARDS patients with respiratory failure, light sedation or non-sedation strategy, biological phenotypes, as well machine learning in sepsis and ARDS. However, we also encounter negative results such as balanced solution during fluid resuscitation, hypothermia therapy after out-of-hospital cardiac arrest or traumatic brain injury, adrenomedullin-specific antibody adrecizumab therapy and coupled plasma filtration-adsorption (CPFA) therapy for patients with septic shock, extracorporeal carbon dioxide removal (ECCO2R) implementation in acute hypoxic respiratory failure, continuous infusion of hypertonic saline in patients with traumatic brain injury. Collectively, in the future, individualized diagnosis and management based on the principle of "wise choice" will become the daily practice scene for all intensivists.

Effect of continuous infusion of hypertonic saline vs standard care on 6-month neurological outcomes in patients with traumatic brain injury — the COBI randomized trial

Effect of continuous infusion of hypertonic saline vs standard care on 6-month neurological outcomes in patients with traumatic brain injury — the COBI randomized trial

A Trial of Continuous Hypertonic Saline Infusion in Traumatic Brain Injury

Hypertonic saline infusion is often used to prevent intracranial hypertension in patients with traumatic brain injury (TBI), but relatively limited

Effect of Continuous Infusion of Hypertonic Saline vs Standard Care on 6-Month Neurological Outcomes in Patients With Traumatic Brain Injury

Fluid therapy is an important component of care for patients with traumatic brain injury, but whether it modulates clinical outcomes remains unclear. To determine whether continuous infusion of hypertonic saline solution improves neurological outcome at 6 months in patients with traumatic brain injury. Multicenter randomized clinical trial conducted in 9 intensive care units in France, including 370 patients with moderate to severe traumatic brain injury who were recruited from October 2017 to August 2019. Follow-up was completed in February 2020. Adult patients with moderate to severe traumatic brain injury were randomly assigned to receive continuous infusion of 20% hypertonic saline solution plus standard care (n = 185) or standard care alone (controls; n = 185). The 20% hypertonic saline solution was administered for 48 hours or longer if patients remained at risk of intracranial hypertension. The primary outcome was Extended Glasgow Outcome Scale (GOS-E) score (range, 1-8, with lower scores indicating worse functional outcome) at 6 months, obtained centrally by blinded assessors and analyzed with ordinal logistic regression adjusted for prespecified prognostic factors (with a common odds ratio [OR] >1.0 favoring intervention). There were 12 secondary outcomes measured at multiple time points, including development of intracranial hypertension and 6-month mortality. Among 370 patients who were randomized (median age, 44 [interquartile range, 27-59] years; 77 [20.2%] women), 359 (97%) completed the trial. The adjusted common OR for the GOS-E score at 6 months was 1.02 (95% CI, 0.71-1.47; P = .92). Of the 12 secondary outcomes, 10 were not significantly different. Intracranial hypertension developed in 62 (33.7%) patients in the intervention group and 66 (36.3%) patients in the control group (absolute difference, -2.6% [95% CI, -12.3% to 7.2%]; OR, 0.80 [95% CI, 0.51-1.26]). There was no significant difference in 6-month mortality (29 [15.9%] in the intervention group vs 37 [20.8%] in the control group; absolute difference, -4.9% [95% CI, -12.8% to 3.1%]; hazard ratio, 0.79 [95% CI, 0.48-1.28]). Among patients with moderate to severe traumatic brain injury, treatment with continuous infusion of 20% hypertonic saline compared with standard care did not result in a significantly better neurological status at 6 months. However, confidence intervals for the findings were wide, and the study may have had limited power to detect a clinically important difference. ClinicalTrials.gov Identifier: NCT03143751.

Severe hyponatremia with seizures and confirmed mild brain edema by hysteroscopic myomectomy: a case report

BackgroundHyponatremia can be developed during hysteroscopic surgery with electrolyte-free irrigation fluid. We experienced severe hyponatremia with postoperative seizures and confirmed mild brain edema.Case presentationA quadragenarian female patient underwent a 2-h hysteroscopic myomectomy with electrolyte-free fluid for uterine distension under general anesthesia. Plasma sodium level of 84.1 mmol/L 100 min after the start of surgery indicated excessive absorption of the irrigation fluid. Acute severe hyponatremia was diagnosed with significant edema in the conjunctiva, lip, and extremities. She was treated with a continuous infusion of hypertonic saline. However, seizures and cerebral edema developed 7 h later. The patient recovered without neurological deficits at postoperative day 2.ConclusionThe electrolyte-free irrigation fluid can be absorbed rapidly during hysteroscopic surgery. Its interruption with hyponatremia should be considered against prolonged surgery. Especially under general anesthesia, caution should be exercised because the typical symptoms of hyponatremia such as nausea and confusion are blinded.

Concentrated hypertonic saline in severe pediatric traumatic brain injury

ABSTRACT Objective Describe outcomes associated with bolus and continuous infusions of hypertonic saline (HTS) in children with severe traumatic brain injury (TBI). Methods IRB-approved, single-center, retrospective review of children admitted between January 1, 2012 to August 30, 2018 with a diagnosis of severe TBI who received HTS. Results Forty-five children (age 9.3 ± 5.8 yr; 60% male) met inclusion criteria. One-hundred eighty-nine equiosmolar bolus doses of HTS were administered to 43 patients (3% HTS, n = 84 doses; 6% HTS, n = 38 doses; 12% HTS, n = 67 doses) for episodes of acute intracranial hypertension (pressure above 20 mmHg). Significant reductions in ICP were observed at 30, 60, and 120 min following HTS boluses with the greatest decrease observed in patients receiving 12%. Thirty-four patients received a continuous infusion of HTS. Higher concentrations of HTS were associated with a more favorable fluid balance (p < .001), fewer episodes of pulmonary edema (p = .003), and higher intake of protein and energy (p < .001). Conclusions Equiosmolar bolus doses of concentrated HTS were associated with significant reductions in ICP. Benefits of higher concentrations of continuous HTS may include improved fluid balance, less pulmonary edema, and greater amounts of protein and energy intake.

Effectiveness of continuous hypertonic saline infusion with an automated infusion pump for decompressive neuroplasty: a randomized clinical trial.

BackgroundHypertonic saline (HS) injections for decompressive neuroplasty (DN) can cause pain. We assessed whether a continuous infusion of HS through an infusion pump would reduce injection-related pain compared with repeated bolus administrations.MethodsFifty patients scheduled for DN were randomized to either the bolus injection or the continuous infusion group. After appropriately placing the epidural catheter, 4 mL of 5% NaCl was injected as four boluses of 1 mL each at 15-minute intervals or infused over 1 hour using an infusion pump. The severity of pain induced by HS injection, as measured by the 11-point numerical rating scale (NRS), was the primary outcome. The severity of low back or lower extremity pain, as measured by the 11-point NRS and Oswestry Disability Index (ODI), 3 months following the procedure, was the secondary outcome.ResultsData from 21 patients in the bolus group and 23 in the continuous infusion group were analyzed. No statistically significant difference in injection-related pain was identified between the two groups during the initial HS administration (P = 0.846). However, there was a statistically significant reduction in injection-related pain in the continuous infusion group compared to the bolus injection group from the second assessment onwards (P = 0.001, < 0.001, and < 0.001, respectively). No significant between-group differences in the NRS and ODI scores 3 months post-procedure were noted (P = 0.614 and 0.949, respectively).ConclusionsOur study suggests that administering HS through a continuous infusion is a useful modality for reducing HS injection-related pain during DN.

The effect of continuous hypertonic saline infusion and hypernatremia on mortality in patients with severe traumatic brain injury: a retrospective cohort study.

Hypertonic saline (HTS) is used to control intracranial pressure (ICP) in patients with traumatic brain injury (TBI); however, in prior studies, the resultant hypernatremia has been associated with increased mortality. We aimed to study the effect of HTS on ICP and mortality in patients with severe TBI. We performed a retrospective cohort study of 231 patients with severe TBI (Glasgow Coma Scale [GCS] ≤ 8) admitted to two neurotrauma units from 2006-2012. We recorded daily HTS, ICP, and serum sodium (Na) concentration. We used Cox proportional regression modelling for hospital mortality and incorporated the following time-dependent variables: use of HTS, hypernatremia, and desmopressin administration. The mean [standard deviation (SD)] age of patients was 34 (17) and the median (interquartile range [IQR]) GCS was 6 [3-8]. Hypertonic saline was administered as a continuous infusion in 124 of 231 (54%) patients over 788 of 2,968 (27%) patient-days. Hypernatremia (Na > 145 mmol·L(-1)) developed in 151 of 231 (65%) patients over 717 of 2,968 (24%) patients-days. In patients who developed hypernatremia, the median [IQR] Na was 146 [142-147] mmol·L(-1). Overall hospital mortality was 26% (59 of 231 patients). After adjusting for baseline covariates, neither HTS (hazard ratio [HR], 1.07; 95% confidence interval [CI], 0.56 to 2.05; P = 0.84) nor hypernatremia (HR, 1.31; 95% CI, 0.68 to 2.55; P = 0.42) was associated with hospital mortality. There was no effect modification by either HTS or hypernatremia on each another. Patients who received HTS observed a significant decrease in ICP during their ICU stay compared with those who did not receive HTS (4 mmHg; 95% CI, 2 to 6; P < 0.001 vs 2 mmHg; 95% CI, -1 to 5; P = 0.14). Hypertonic saline and hypernatremia are not associated with hospital mortality in patients with severe TBI.

Worsening of proteinuria caused by combination therapy of hypertonic saline and low-dose furosemide for treatment of acute decompensated heart failure with overt diabetic nephropathy

A combination of hypertonic saline and furosemide has been proposed as a new therapeutic approach for treating acute decompensated heart failure (ADHF). The advantages of this combination have not only been demonstrated in ADHF but also in refractory ascites due to liver cirrhosis. However, the therapeutic effects of this regimen have never been evaluated in ADHF with overt diabetic nephropathy (ODN). Here, we present an interesting case of a 35-year-old patient admitted to our hospital for ADHF with shortness of breath and systemic edema, complicated with hypertension, type 2 diabetes, and ODN. Echocardiography showed left ventricular enlargement and diffuse hypokinesis, with ejection fraction of 33%. Urinary findings showed total proteinuria of 3597mg/day during the first day of hospitalization. We initiated decongestion therapy with continuous infusion of hypertonic saline and furosemide. In spite of increased diuresis, edema remained the same and serum albumin decreased from 2.7g/dl to 2.0g/dl, and proteinuria increased up to 7344mg/day. The amount of proteinuria and serum albumin level gradually recovered over time after cessation of the therapy. These data suggest that the combination therapy worsens glomerular hypertension and ODN. Therefore, hypertonic saline and furosemide combination therapy should not be recommended for patients with ODN.<Learning objective: Hypertonic saline and low-dose furosemide combination therapy has been proposed as a treatment option for ADHF, especially in refractory congestive heart failure cases. Nevertheless, the efficacy of this treatment in ADHF cases complicated with overt proteinuria is not fully elucidated. This therapy may induce increment of proteinuria in these patients due to aggravation of glomerular hypertension, and may be ineffective for decongestion or to treat edema.>

Treatment of Endocrine Disorders in the Neuroscience Intensive Care Unit

This review discusses concepts and treatments associated with the most clinically relevant areas of acute endocrine dysfunction amongst patients with common diseases in neuroscience intensive care units (Neuro ICUs). We highlight the following points:• While a thorough work-up for hyponatremia when it is present is always warranted, subarachnoid hemorrhage (SAH) patients who are in a time window concerning for cerebral vasospasm and who are hyponatremic with high urine output are generally thought to have cerebral salt wasting. These patients are typically treated with a combination of continuous hypertonic saline infusion and fludrocortisone.• Diabetes insipidus (DI) is often seen in patients fulfilling death by neurological criteria, as well as in patients with recent pituitary surgery and less often in SAH and traumatic brain injury patients who are not brain dead. Patients with DI in the Neuro ICU often cannot drink to thirst and may require a combination of desmopression/vasopressin administration, aggressive fluid repletion, and serum sodium monitoring.• Diagnosing adrenal insufficiency immediately following pituitary injury is complicated by the fact that the expected atrophy of the adrenal glands, due to lack of a stimulus from pituitary adrenocorticotropic hormone, may take up to 6weeks to develop. Cosyntropin testing can be falsely normal during this period.• Both hyperglycemia (glucose >200mg/dL) and hypoglycemia (glucose <50mg/dL) are strongly associated with neurological morbidity and mortality in ICUs and should be avoided. Glucose concentrations between 120-160mg/dL can serve as a reasonable target for insulin infusion protocols.• There is no data to suggest that treatment of abnormal thyroid function tests in nonthyroidal illness syndrome/sick euthyroid leads to benefits in either mortality or morbidity. True myxedema coma is a rare clinical diagnosis that is treated with intravenous levothyroxine accompanied by stress-dose steroids.

Complications Associated With Prolonged Hypertonic Saline Therapy in Children With Elevated Intracranial Pressure

Safe upper limits for therapeutic hypernatremia in the treatment of intracranial hypertension have not been well established. We investigated complications associated with hypernatremia in children who were treated with prolonged infusions of hypertonic saline. Retrospective chart analysis. PICU in university-affiliated children's hospital. All children from 2004 to 2009 requiring intracranial pressure monitoring (external ventricular drain or fiberoptic intraparenchymal monitor) for at least 4 days who were treated with hypertonic saline infusion for elevated intracranial pressure and did not meet exclusion criteria. Continuous hypertonic saline infusion on a sliding scale was used to achieve target sodium levels that would keep intracranial pressure less than 20 mm Hg once the conventional therapies failed. Eighty-eight children met inclusion criteria. Etiologies of elevated intracranial pressure included trauma (n = 48), ischemic or hemorrhagic stroke (n = 20), infection (n = 8), acute disseminated encephalomyelitis (n = 5), neoplasm (n = 2), and others (n = 5). The mean peak serum sodium was 171.3 mEq/L (range, 150-202). The mean Glasgow Outcome Score was 2.8 (± 1.1) at time of discharge from the hospital. Overall mortality was 15.9%. Children with sustained (> 72 hr) serum sodium levels above 170 mEq/L had a significantly higher occurrence of thrombocytopenia (p < 0.001), renal failure (p < 0.001), neutropenia (p = 0.006), and acute respiratory distress syndrome (p = 0.029) after controlling for variables of age, gender, Pediatric Risk of Mortality score, duration of barbiturate-induced coma, duration of intracranial pressure monitoring, vasopressor requirements, and underlying pathology. Children with sustained serum sodium levels greater than 165 mEq/L had a significantly higher prevalence of anemia (p < 0.001). Children treated by continuous hypertonic saline infusion for intracranial hypertension whose serum sodium levels exceeded certain thresholds experienced significantly more events of acute renal failure, thrombocytopenia, neutropenia, anemia, and acute respiratory distress syndrome than those whose sodium level was maintained below these thresholds.

Early Fluid Resuscitation With Hypertonic Solution in a Rat Crush Injury Model

The aim of the study was to evaluate the effects of bolus infusion of hypertonic hydroxyethyl starches (HHESs) and continuous infusion of hypertonic saline (HTS) in the early resuscitation in crush syndrome. A rat model of crush injury was established. Rats were randomly divided into five groups: (1) HHES group, (2) HTS group, (3) volume resuscitation group, (4) normal resuscitation (NR) group, and (5) sham group. Blood samples were collected 6 h after the crush period for biochemical evaluation. Blood pressure was monitored throughout this experiment. Muscles and kidneys were evaluated morphologically 24 h after reperfusion. Twenty rats in each group were taken for survival observation for 72 h. Compared with the NR and HTS groups, the HHES group had significantly increased the survival rate 72 h after release (P < 0.05). In the first 2 h after release, mean arterial blood pressure in the HHES group was significantly higher than in HTS, volume resuscitation, and NR groups (respectively, P < 0.05). Animals that received HHES infusion showed a better acid-base balance and renal function. However, there was no significant difference in survival rate between the HTS and NR groups. Furthermore, animals in the HTS group showed a bad acid-base balance and a higher serum sodium level. Bolus infusion of HHES combined with normal saline could be an effective therapy for crush syndrome in the early resuscitation period. However, continuous HTS injection was not seemed to be a suitable choice particularly in the absence of monitoring equipment for serum irons or blood gases (institutional protocol no. ZN5R20110016).

Chapter 8. Hyperosmolar therapy

Chapter 8. Hyperosmolar therapy

Early continuous hypertonic saline infusion in patients with severe cerebrovascular disease

Early continuous hypertonic saline infusion in patients with severe cerebrovascular disease

Early continuous hypertonic saline infusion in patients with severe cerebrovascular disease

To study the safety and the effects of early continuous hypertonic saline infusion in patients with cerebral edema and underlying cerebrovascular disease. Retrospective analysis. University medical center. Neurologic intensive care unit population with mixed cerebrovascular diseases. None. Between May 2008 and December 2009, 100 patients with severe intracerebral hemorrhage, cerebral ischemia, or aneurysmal subarachnoid hemorrhage and signs of intracranial hypertension received within ≤72 hrs after symptom onset a continuous infusion of hypertonic saline (3%, target sodium 145-155 mmol/L, target osmolality 310-320 mOsm/kg) over 13 (4-23) days. We analyzed the frequency of episodes with elevated intracranial pressure (new anisocoria or intracranial pressure >20 mm Hg for ≥20 mins), inhospital mortality, and the occurrence of adverse effects theoretically associated with hypertonic saline. The findings were compared with those of a historical control group (n = 115, 2007-2008) with equal underlying disease. In the treatment group, fewer episodes of critically elevated intracranial pressure (92 vs. 167, p = .027) in fewer patients (50 of 100 = 50.0% vs. 69 of 115 = 60.0% patients, p = .091) were observed, and inhospital mortality was significantly decreased (17.0% vs. 29.6%, p = .037). Adverse events, including cardiac arrhythmia, heart, liver or renal dysfunction, or pulmonary edema, occurred in both groups to a similar extent. Early and continuous infusion of hypertonic saline in patients with severe cerebrovascular disease and impending intracranial hypertension is safe and might reduce the frequency of intracranial pressure crises and mortality rate. A randomized controlled trial is warranted to confirm our findings and to evaluate the effects of hypertonic saline on functional outcomes.

Effects of Continuous Hypertonic Saline Infusion on Perihemorrhagic Edema Evolution

Mass effect of hematoma and the associated perihematomal edema are commonly responsible for neurological deterioration after intracerebral hemorrhage. Efficacy of surgical and medical therapy is limited. We studied the effect of early continuous hypertonic saline infusion on development of perihematomal edema after severe spontaneous supratentorial hemorrhage. Patients with spontaneous lobar and basal ganglia/thalamic bleeding >30 mL (n=26) were treated with early (<72 hours) continuous hypertonic saline infusion (3%) to achieve sodium of 145 to 155 mmol/L and osmolality of 310 to 320 mOsmol/kg. Evolution of absolute edema volume and relative edema volume (ratio absolute edema volume/initial hematoma volume) was assessed on repeated cranial CT and compared to historical patients (n=64) identified on database with hematoma >30 mL. In the treatment group, absolute edema volume was significant smaller between day 8 and day 14 (P(absolute edema volume)= 0.04) and relative edema volume was significant smaller between day 2 and day 14 (P(relative edema volume)=0.02). Intracranial pressure crisis (>20 mm Hg for >20 minutes or new anisocoria) occurred less frequently in the treatment group (12 versus 56; P=0.048). In-hospital mortality was 3 (11.5%) in the hypertonic saline group and 16 (25%) in the control group (P=0.078). Side effects theoretically associated with hypertonic saline including cardiac arrhythmia and acute heart and renal failure occurred in both groups to a similar extent. Early and continuous infusion of hypertonic saline in patients with severe spontaneous intracerebral hemorrhage was feasible and safe. The beneficial effect of this treatment regimen on edema evolution and outcome has to be demonstrated in a controlled trial.

ANG II-induced attenuation of salt gland function in Pekin ducks is not catecholamine-dependent

Pekin ducks (Anas platyrhynchos) were bilaterally adrenalectomized (biADX), injected with 1 mg of triamcinolone (TRIAM) kg bw(-1) im and given 0.9% saline drinking water during a 24 h recovery period followed by chemical sympathectomy with 6OH DOPA 3 h before the start of experimental observations. Baseline plasma dopamine (DA) concentrations decreased from 283 +/- 88.5 pmol ml(-1) to 42.4 +/- 11.1 pmol ml(-1); epinephrine (E) from 142 +/- 46 pmol ml(-1) to 18.4 +/- 9.2 pmol ml(-1) and norepinephrine (NE) from 742 +/- 84 pmol ml(-1) to 406 +/- 38 pmol ml(-1) 1 day after biADX + TRIAM but before chemical sympathectomy. Baseline MABP increased from 132 +/- 3.2 mmHg to 209 +/- 14.3 mmHg (P < 0.05) in response to TRIAM. After chemical sympathectomy with 6OH DOPA there was an additional 90% decrease in plasma NE to 42 +/- 9.4 pmol ml(-1) and a concurrent 60% decrease in MABP to 83.4 +/- 6.9 mmHg (P < 0.05). Nasal fluid secretion was maintained by the continuous infusion of hypertonic saline (1,000 mosmol kg H(2)O(-1) at a rate of 0.3 ml kg(-1) min(-1)). Rates of nasal fluid secretion and fluid electrolyte concentrations were unchanged following biADX + TRIAM + 6OH DOPA. Angiotensin II (ANG II; dose 1 microg kg bw(-1) i.v.), attenuated nasal fluid secretion showing that the response to ANG II was not NE- dependent. Plasma NE concentrations decreased following Tyramine i.v. (33 +/- 8.5 pmol ml(-1)) there being no vasopressor response. This is the first report of the ANG II induced attenuation of duck salt gland secretion in the absence of measurable E and NE.