pituitrin and Hypertension--Pulmonary

Pulmonary hypertension (PH), an often unrelenting disease that carries with it significant morbidity and mortality, affects not only the pulmonary vasculature but, in turn, the right ventricle as well. The survival of patients with PH is closely related to the right ventricular function. Therefore, having an understanding of how to manage right ventricular failure (RVF) and acute pulmonary hypertensive crises is imperative for clinicians who encounter these patients. This review addresses the management of these patients in detail, addressing: (a) the pathophysiology of RVF, (b) intensive care monitoring of these patients in the intensive care unit, (c) imaging of the right ventricle, (d) intubation and mechanical ventilation, (e) inotrope and vasopressor selection, (f) pulmonary vasodilator use, (g) interventional and surgical procedures for the acutely failing right ventricle, and (h) mechanical support for RVF.

Topics: Biomarkers; Capnography; Central Venous Pressure; Critical Care; Echocardiography; Epinephrine; Epoprostenol; Extracorporeal Membrane Oxygenation; Heart Failure; Heart Ventricles; Humans; Hypertension, Pulmonary; Iloprost; Intensive Care Units; Milrinone; Nitric Oxide; Radiography, Thoracic; Respiration, Artificial; Spectroscopy, Near-Infrared; Vasodilator Agents; Vasopressins; Ventricular Dysfunction, Right; Ventricular Function, Right

Vasopressin is a peptide synthesized in the hypothalamus whose primary role is in fluid homeostasis. It has recently gained interest as a potential agent in the treatment of cardiorespiratory arrest. Initial human studies have shown benefits with vasopressin in patients with out of hospital ventricular fibrillation and asystolic cardiac arrest. One subgroup of patients not included in these trials is patients with pulmonary hypertension, who have a five-year mortality rate of 50%. Animal studies have shown vasopressin to be a vasodilator in the pulmonary vascular system of rats, under normoxic and hypoxic conditions, with conflicting results in canines. Human studies have shown conflicting results with increases, decreases and no changes seen in pulmonary artery pressures of patients with a variety of clinical conditions. Research needs to be done in patients with pulmonary hypertension regarding the potential role of vasopressin during cardiac arrest in this subgroup.

Topics: Animals; Dogs; Heart Arrest; Hemostatics; Humans; Hypertension, Pulmonary; Pulmonary Circulation; Rats; Respiratory Insufficiency; Swine; Treatment Outcome; Vasoconstrictor Agents; Vasopressins

Alveolar hypoxia and resulting tissue hypoxia initiates the pathophysiological sequence of high altitude pulmonary edema (HAPE). Very rapid ascent to high altitude without prior acclimatization results in HAPE, even in subjects with excellent tolerance to high altitude. Upon acute altitude exposure, HAPE-susceptible individuals react with increased secretion of norepinephrine, epinephrine, renin, angiotensin, aldosterone and atrial natriuretic peptide. In response to exercise at high altitude, subjects developing acute mountain sickness and HAPE secrete more aldosterone and antidiuretic hormone than subjects who remain well. This results in sodium and water retention, reduction of urine output, increase in body weight and development of peripheral edemas. The hypoxic pulmonary vascular response is enhanced in HAPE-susceptible subjects, thus favouring the development of severe pulmonary hypertension on exposure to high altitude. It has been postulated that uneven pulmonary vasoconstriction enhances filtration pressure in non-vasoconstricted lung areas, leading to interstitial and alveolar edema. The high protein content of the edema fluid in HAPE characterizes this edema as a permeability edema. The prophylactic administration of nifedipine prevents the exaggerated pulmonary hypertension of HAPE-susceptible subjects upon rapid ascent to 4559 m and thus prevents HAPE in most cases. This finding illustrates the crucial role of hypoxic pulmonary hypertension in the development of HAPE. The causal treatment of HAPE is descent, evacuation and administration of oxygen. Treatment of HAPE patients with nifedipine results in a reduction of pulmonary artery pressure, clinical improvement, increased oxygenation, decrease of the alveolar arterial oxygen gradient and progressive clearing of pulmonary edema on chest x-ray. Thus nifedipine offers a pharmacological tool for the treatment of HAPE.

Topics: Aldosterone; Altitude Sickness; Cell Membrane Permeability; Epinephrine; Humans; Hypertension, Pulmonary; Nifedipine; Norepinephrine; Pulmonary Edema; Radiography; Renin-Angiotensin System; Vasopressins

Much has been learned about the pathophysiological state that underlies the development of increased total body volume and edema in left ventricular failure. Very little, however, is known about the mechanism underlying systemic hypervolemia in patients with isolated right ventricular dysfunction. In this manuscript, we describe our randomized clinical trial to assess the relationship between severity of pulmonary arterial hypertension and neurohormonal activation, total plasma volume and renal function. We assess the role of aldosterone and vasopressin in volume retention in patients with pulmonary arterial hypertension with right ventricular failure. As understanding of the pathogenesis of left ventricular failure has been associated with improved therapies, the better understanding of the mechanisms of isolated right ventricular cardiac failure will also lead to improved patient care.

Topics: Aldosterone; Health Status Indicators; Humans; Hypertension, Pulmonary; Mineralocorticoid Receptor Antagonists; Pilot Projects; Pulmonary Artery; Research; Spironolactone; Vasoconstrictor Agents; Vasopressins; Ventricular Dysfunction, Right

Pulmonary hypertension in children is associated with high rates of adverse events under anesthesia. In children who have failed medical therapy, a posttricuspid shunt such as a Potts shunt can offload the right ventricle and possibly delay or replace the need for lung transplantation. Intraoperative management of this procedure, during which an anastomosis between the pulmonary artery and the descending aorta is created, is complex and requires a deep understanding of the pathophysiology of acute and chronic right ventricular failure. This retrospective case review describes the intraoperative management of children undergoing surgical creation of a Potts shunt at a single center.. A retrospective case review of all patients under the age of 18 who underwent Potts shunt between April 2013 and June 2022. Medical records were examined, and clinical data of demographics, intraoperative vital signs, anesthetic management, and postoperative outcomes were extracted.. Twenty-nine children with medically refractory pulmonary hypertension underwent surgical Potts shunts with a median age of 12 years (range 4 months to 17.4 years). Nineteen Potts shunts (65%) were placed via thoracotomy and 10 (35%) were placed via median sternotomy with use of cardiopulmonary bypass. Ketamine was the most frequently utilized induction agent (17 out of 29, 59%), and the majority of patients were initiated on vasopressin prior to intubation (20 out of 29, 69%). Additional inotropic support with epinephrine (45%), milrinone (28%), norepinephrine (17%), and dobutamine (14%) was used prior to shunt placement. Following opening of the Potts shunt, hemodynamic support was continued with vasopressin (66%), epinephrine (62%), milrinone (59%), dobutamine (14%), and norepinephrine (10%). Major intraoperative complications included severe hypoxemia (21 out of 29, 72%) and hypotension requiring boluses of epinephrine (10 out of 29, 34.5%) but no patient suffered intraoperative cardiac arrest. There were four in-hospital mortalities.. A Potts shunt offers another palliative option for children with medically refractory pulmonary hypertension. General anesthesia in these children carries high risk for pulmonary hypertensive crises. Anesthesiologists must understand underlying physiological mechanisms responsble for acute hemodynaic decompensation during acute pulmonary hypertneisve crises. Severe physiological perturbations imposed by thoracic surgery and use of cardiopulmonay bypass can be mitigated by aggresive heodynamic support of ventricle function and maintainence of systemic vascular resistance. Early use of vasopressin, before or immidiately after anesthesia induction, in combination with other inotropes is a useful agent during the perioperative care of thes. Early use of vasopressin during anesthesia induction, and aggressive inotropic support of right ventricular function can help mitigate effects of induction and intubation, single-lung ventilation, and cardiopulmonary bypass.. Our single center expereince shows that the Potts shunt surgery, despite high short-term mortaility, may offer another option for palliation in children with medically refractory pulmonary hypertension.

Topics: Anesthesia, General; Anesthetics; Child; Dobutamine; Epinephrine; Humans; Hypertension, Pulmonary; Infant; Milrinone; Norepinephrine; Retrospective Studies; Vasopressins

Vasopressin can constrict peripheral arteries without constricting the pulmonary artery. Theoretically, vasopressin is suitable for the perioperative treatment of pulmonary hypertension. Few studies have investigated the use of pituitrin (a substitute for vasopressin) after cardiac defect repair surgery. This study aimed to analyze the effect of pituitrin on hemodynamics and to determine whether pituitrin can be used after surgical repair in adult patients with pulmonary arterial hypertension-congenital heart disease (PAH-CHD).. A pulmonary artery catheter was used in all the patients for hemodynamic monitoring. Hemodynamic parameters were recorded before and at 0.5 h, 1 h, 6 h, 12 h and 24 h after pituitrin administration. The changes in the hemodynamic parameters before and after pituitrin use were analyzed through repeated measures analysis of variance.. A total of 110 patients with PAH-CHD underwent repair surgery; 23 patients were included in further analysis, including 11 with atrial septal defect, 9 with ventricular septal defect, and 3 with patent ductus arteriosus. Ten (43.5%) were men, with a mean age of 29.4 ± 6.8 years. Hemodynamic parameters before and after the oxygen test were as follows: radial artery oxygen saturation, 91.5% ± 4.4 vs. 97.9 ± 2.4%; pulmonary vascular resistance, 10.5 ± 1.8 Wood units (wu) vs. 5 ± 1.2 wu; systemic-pulmonary blood flow ratio (QP/QS), 1.1 ± 0.2 vs. 2.1 ± 0.9. With prolonged use, the systolic blood pressure of the radial artery increased significantly (P = 0.001), that of the pulmonary artery decreased significantly (P = 0.009), and RP/s decreased significantly (P < 0.001).. Pituitrin as an alternative to vasopressin can increase arterial pressure, decrease pulmonary artery pressure, and reduce the pulmonary artery pressure/arterial pressure ratio after repair surgery in adult patients with PAH-CHD.

Topics: Adult; Cardiac Catheterization; Cardiac Surgical Procedures; Female; Heart Defects, Congenital; Humans; Hypertension, Pulmonary; Male; Pituitary Hormones, Posterior; Vasopressins; Young Adult

To describe the clinical outcomes following treatment with vasopressin for a sub-cohort of critically ill preterm neonates who have refractory persistent pulmonary hypertension of the newborn (PPHN).. Case series.. Tertiary neonatal intensive care unit, Toronto, Canada.. Neonates born <37 weeks gestational age (GA) who received vasopressin for refractory PPHN (lack of response to inhaled nitric oxide) over a 4-year period.. Changes in physiological indices of cardio-pulmonary stability during vasopressin therapy were analyzed using one-way repeated measures ANOVA, compared to pretreatment values. Data regarding survival to discharge and neurodevelopmental outcomes at 18-24 months were described.. Thirteen neonates with a mean GA of 31.4 ± 3.3 weeks were included. Vasopressin was initiated at 28.5 ± 4.5 h of age. Overall, oxygenation and hemodynamic variables improved significantly following vasopressin therapy (. Vasopressin offers promise as a therapy for preterm neonates with refractory PPHN and hemodynamic instability, but prospective investigation is needed.

Topics: Administration, Inhalation; Humans; Hypertension, Pulmonary; Infant, Newborn; Nitric Oxide; Persistent Fetal Circulation Syndrome; Prospective Studies; Vasopressins

Despite its increasing use in neonates, the literature on the use of vasopressin (VP) in neonates is limited. The aim of this study is to evaluate the systemic and pulmonary effects of VP in neonates and to assess its safety among them.. This retrospective study enrolled all neonates in two level III neonatal intensive care units in Winnipeg, Manitoba, who had received VP therapy between 2011 and 2016. Infants with congenital malformations/chromosomal disorders were excluded. The changes in cardiovascular and pulmonary parameters were collected from patient charts. The primary outcome was the mean blood pressure (MBP) post-VP initiation. Secondary outcomes included systolic blood pressure (SBP) and diastolic blood pressure (DBP), vasoactive inotropic score (VIS), pH, urine output, lactate, base deficit (BD), mean airway pressure (MAP), and oxygen requirement.. A total of 33 episodes from 26 neonates were analyzed. The postnatal age at VP initiation was 14 days (interquartile range [IQR]: 4-25), and the median starting dose was 0.3 mU/kg/min (IQR: 0.2-0.5). MBP improved significantly after VP initiation from 28 to 39 mm Hg 24 hours after VP initiation (. VP appears to be a promising rescue therapy in catecholamine resistant shock or refractory pulmonary hypertension in neonates.

Topics: Blood Pressure; Female; Hemodynamics; Humans; Hypertension, Pulmonary; Hypotension; Infant, Newborn; Infant, Newborn, Diseases; Lung; Male; Retrospective Studies; Urine; Vasoconstrictor Agents; Vasopressins

An inborn term neonate weighing 2600 g developed meconium aspiration syndrome at birth. Baby had respiratory failure requiring high-frequency oscillatory ventilation support at 15 hours of life. He additionally developed hypotension with left ventricular dysfunction noted on point-of-care echocardiography (POCE), which required dopamine and epinephrine infusions. At 28 hours of life, he was started on inhaled nitric oxide (iNO), followed by milrinone due to hypoxaemic respiratory failure and the POCE revealed severe pulmonary artery hypertension (PAH). As PAH was refractory to iNO and milrinone, vasopressin was added which resulted in rapid improvement in oxygenation and normalisation of pulmonary artery pressures. Baby was weaned off from vasoactive support in the next 120 hours. Vasopressin proved to be the rescue agent in this case of iNO refractory PAH without any side effects during therapy. Baby was successfully extubated on day 18 and was discharged with a normal neurological examination finding.

Topics: Administration, Inhalation; Humans; Hypertension, Pulmonary; Infant, Newborn; Male; Meconium Aspiration Syndrome; Nitric Oxide; Pulmonary Artery; Vasopressins

A novel treatment with intravenous levosimendan and vasopressin for new-onset acute pulmonary hypertension after weaning from cardiopulmonary bypass is described.. Retrospective analysis of a case series.. Single-center study.. Nineteen patients undergoing cardiac surgery exhibited new-onset acute pulmonary hypertension with acute right ventricular dysfunction after cardiopulmonary bypass.. Pulmonary hypertension with acute right heart dysfunction was treated with levosimendan as inodilator therapy and vasopressin combined with norepinephrine for systemic vasopressor therapy.. Mean pulmonary artery pressure decreased from 32 ± 9 to 26 ± 6 mmHg (p = 0.039) in the first 24 hours along with an increase in cardiac output (3.2 ± 1 to 4.2 ± 1.1 L/min; p = 0.012) and resolution of lactic acidosis. The ratio between mean pulmonary artery pressure and mean arterial pressure decreased from 1:2 to 1:3, and Wood units decreased from 3 ± 1 to 1.5 ± 2 (p = 0.042). At 30 days after intervention, 3 patients died.. The combination of levosimendan for inotropic support of the right ventricle in conjunction with its vasodilatory effect on the pulmonary circulation, along with the combination of vasopressin and norepinephrine for systemic vasopressor therapy, may be an effective alternative for the treatment of acute new-onset pulmonary hypertension and acute right heart dysfunction after cardiopulmonary bypass. Although there are many confounding variables in this case series, these findings justify additional sufficiently powered trials.

Topics: Acute Disease; Aged; Aged, 80 and over; Arterial Pressure; Cardiopulmonary Bypass; Cardiotonic Agents; Dose-Response Relationship, Drug; Drug Therapy, Combination; Female; Follow-Up Studies; Humans; Hypertension, Pulmonary; Injections, Intravenous; Male; Retrospective Studies; Simendan; Treatment Outcome; Vascular Resistance; Vasoconstrictor Agents; Vasopressins

Persistent pulmonary hypertension of the newborn (PPHN) is due to a failure of pulmonary vascular relaxation. Vasopressin, a systemic vasoconstrictor acting on smooth muscle AVPR1a receptors, is used in treatment of PPHN. We sought to determine acute effects of vasopressin infusion on pulmonary hemodynamics in a large animal model of hypoxic PPHN.. PPHN was induced in 6 newborn piglets by 72 h normobaric hypoxia (FiO2 = 0.10); controls were 7 age-matched 3-day-old piglets. Animals were anesthetized and ventilated with central venous and arterial lines, and after stabilization, randomized using a crossover design to normoxic or hypoxic ventilation, then 30 min infusion of 0.0012 U/kg/min vasopressin, followed by 45 min vasopressin washout period. Echocardiographic parameters and oxygen consumption were measured before and after vasopressin. Relaxation to vasopressin was tested in isolated PPHN and control pulmonary arteries by isometric myography. Expression of AVPR1a receptor mRNA was quantified in arterial and myocardial tissues.. Vasopressin did not alleviate hypoxia-responsiveness of PPHN pulmonary circuit. There were no significant differences in pulmonary hypertension, cardiac function indices, or oxygenation indices after vasopressin infusion. Vasopressin did not dilate control or PPHN pulmonary arteries, and AVPR1 was minimally expressed.. Vasopressin does not have a direct pulmonary vasodilator effect in PPHN, within the timeframe studied.

Topics: Animals; Animals, Newborn; Disease Models, Animal; Female; Hemodynamics; Hypertension, Pulmonary; Male; Oxygen Consumption; Pulmonary Artery; Random Allocation; Respiration, Artificial; Swine; Vasoconstrictor Agents; Vasopressins

A pulmonary hypertensive crisis (PHC) can be a life-threatening condition. We established a PHC model by exposing rats with monocrotaline (MCT)-induced pulmonary hypertension to acute hypoxia, and investigated the effects of vasopressin, phenylephrine, and norepinephrine on the PHC.. Four weeks after MCT 60 mg kg. PHC was associated with increased RV dilatation and paradoxical septal motion. Vasopressin increased MBP [mean (standard error)] from 52.6 (3.8) to 125.0 (8.9) mm Hg and CI from 25.4 (2.3) to 40.6 (1.8) ml min. In this rat model of a PHC, vasopressin, but not phenylephrine or norepinephrine, resulted in better haemodynamic and vascular recovery.

Topics: Acute Disease; Animals; Drug Evaluation, Preclinical; Echocardiography; Hemodynamics; Hypertension, Pulmonary; Hypoxia; Male; Monocrotaline; Nordefrin; Oxygen; Partial Pressure; Phenylephrine; Rats, Sprague-Dawley; Vasoconstriction; Vasoconstrictor Agents; Vasopressins

Anesthesia for lung transplantation remains one of the highest risk surgeries in the domain of the cardiothoracic anesthesiologist. End-stage lung disease, pulmonary hypertension, and right heart dysfunction as well as other comorbid disease factors predispose the patient to cardiovascular, respiratory and metabolic dysfunction during general anesthesia. Perhaps the highest risk phase of surgery in the patient with severe pulmonary hypertension is during the induction of anesthesia when the removal of intrinsic sympathetic tone and onset of positive pressure ventilation can decompensate a severely compromised cardiovascular system. Severe hypotension, cardiac arrest, and death have been reported previously. Here we present 2 high-risk patients for lung transplantation, their anesthetic induction course, and outcomes. We offer suggestions for the safe management of anesthetic induction to mitigate against hemodynamic and respiratory complications.

Topics: Adrenergic alpha-Agonists; Anesthesia; Bronchodilator Agents; Calcium Chloride; Cardiopulmonary Resuscitation; Cardiotonic Agents; Epinephrine; Fatal Outcome; Female; Heart Arrest; Humans; Hypertension, Pulmonary; Lung Transplantation; Male; Middle Aged; Milrinone; Nitric Oxide; Norepinephrine; Sodium Bicarbonate; Vasoconstrictor Agents; Vasopressins

Acute pulmonary hypertension following cardiac surgery can have a significant effect on postoperative morbidity and mortality. However, limited data are available on the efficacy and potency of clinically used systemic vasopressors on the pulmonary vasculature. The aim of this study was to use human pulmonary artery to characterize the pharmacological effects of clinically used vasopressors on the human pulmonary vasculature.. Fifty-seven pulmonary artery rings of internal diameter 2-4 mm and 2 mm long, mounted in a multiwire myograph system, were used to measure changes in isometric tension. We constructed concentration response curves by cumulative addition to the myograph chambers of KCl, noradrenaline (NA), adrenaline (AD), vasopressin, endothelin-1 (ET-1) and prostaglandin F2a (PGF2a).. AD, NA, ET-1, PGF2a and KCl caused dose-dependent vasoconstriction in the pulmonary artery samples (EC50 246 nM [95% confidence interval, CI, 153-394 nM], 150 nM [95% CI 51-447 nM], 1.46 nM [95% CI 0.69-3.1 nM], 6.35 µM [95% CI 3.58-11.2 µM] and 17.24 mM [95% CI 12.43-24.07 mM], respectively), whereas vasopressin had no significant effect. The order of efficacy was KCl = PGF2a > AD > NA > ET-1 and the order of potency was ET-1 T-AD = NA > PGF2a > KCl.. This study demonstrated the efficacy and potency of clinically used vasopressors and endogenous vasopressors on human pulmonary vascular tone. PGF2a and KCl equally caused maximal amounts of constriction, whereas ET-1 had less effect and vasopressin had no effect. These effects may need to be taken into account in the clinical setting because they might result in the development of pulmonary hypertension.

Topics: Adult; Humans; Hypertension, Pulmonary; Models, Cardiovascular; Potassium Chloride; Pulmonary Artery; Vasoconstrictor Agents; Vasopressins

To determine the effect of vasopressin therapy on the efficacy of oxygenation and arterial pressure in infants with severe persistent pulmonary hypertension of the newborn.. Retrospective case study.. Neonatal ICU, Hospital for Sick Children, Toronto, Canada.. Neonates with severe persistent pulmonary hypertension.. Intravenous infusion of vasopressin.. Ten infants satisfied the inclusion criteria. Inhaled nitric oxide was used for median (interquartile range) duration of 15 hours (11-28 hr) prior to vasopressin commencement. Vasopressin was initiated at a mean dose of 0.0002 ± 0.0002 U/kg/min for a median (interquartile range) duration of 49 hours (13-95 hr). Administration of vasopressin was associated with an improvement in oxygenation index, peak effect 6 hours after drug initiation (p = 0.01), and a reduction in inhaled nitric oxide dose (p < 0.05). There was a concomitant improvement in blood pressure (p < 0.05) and urine output (p < 0.05), without drop in the serum sodium level or worsening in serum lactate level.. Although there is limited experience of vasopressin use in persistent pulmonary hypertension of the newborn infants, our case series suggests it to be a potential adjunctive therapy for improving the efficacy of oxygenation and systemic hypotension. A prospective randomized trial is needed to confirm its efficacy and safety in the management of severe persistent pulmonary hypertension of the newborn.

Topics: Administration, Inhalation; Blood Pressure; Canada; Female; Humans; Hypertension, Pulmonary; Infant, Newborn; Infusions, Intravenous; Intensive Care Units, Neonatal; Male; Nitric Oxide; Oxygen; Retrospective Studies; Treatment Outcome; Vasoconstrictor Agents; Vasopressins

Vasopressin is a systemic vasoconstrictor. Its pulmonary vasodilatory effect is controversial, and limited data are available on its use in neonates with pulmonary hypertension. Hypothesizing that the vasopressin-induced pulmonary vasodilation is developmentally regulated, we evaluated its pulmonary and systemic arterial response in newborn and adult rats.. Vessels were mounted on a wire myograph, and the vasopressin-induced changes in vasomotor tone measured. The vessel- and age-dependent differences in vasopressin V1a and V2 receptors' expression were evaluated by western blotting.. Vasopressin induced a dose-dependent increase in mesenteric arterial tone at both ages, but of greater magnitude in adult vessels (P < 0.01). At lower concentrations, vasopressin induced pulmonary vasodilation in adult vessels and vasoconstriction in newborn arteries. The adult vasopressin-induced pulmonary vasodilation was inhibited by ibuprofen, suggesting that the response is prostaglandin mediated. Pulmonary tissue V1a receptor protein expression was higher in adult, when compared with newborn arteries (P < 0.01). The adult vessels V1a expression predominated in the pulmonary arteries, and V2 was only detected in mesenteric arteries.. The vasopressin-induced pulmonary vasodilation is absent in newborn rats likely due to the lower tissue V1a expression early in life. These animal data challenge the therapeutic use of vasopressin in neonatal pulmonary hypertension.

Topics: Age Factors; Animals; Animals, Newborn; Arteries; Disease Models, Animal; Dose-Response Relationship, Drug; Hypertension, Pulmonary; Rats; Rats, Sprague-Dawley; Vasodilator Agents; Vasopressins

Vasopressin is emerging as a therapeutic adjunct option towards treatment of shock states in the pediatric population. Its effects on pulmonary vasculature are less well understood. This report describes a 5-month-old infant with nitric oxide-unresponsive pulmonary hypertension, oxygenation failure, and systemic hypotension. Vasopressin therapy improved oxygenation and blood pressure and biventricular function, allowing weaning of nitric oxide and inotropic support. No decrease in coronary flow was noted.. Vasopressin could be considered as an adjunct option in infants with pulmonary hypertension and systemic hypotension. Echocardiographic monitoring during treatment is recommended.

Topics: Administration, Inhalation; Blood Pressure; Cardiotonic Agents; Dose-Response Relationship, Drug; Drug Therapy, Combination; Endothelium-Dependent Relaxing Factors; Follow-Up Studies; Humans; Hypertension, Pulmonary; Infant; Infusions, Intravenous; Male; Nitric Oxide; Vasoconstrictor Agents; Vasopressins

Patients with left-sided heart dysfunction and volume overload often have associated elevations in vasopressin from neuroendocrine activation. The authors investigated perioperative levels of vasopressin in patients with isolated right-sided heart dysfunction from chronic thromboembolic pulmonary hypertension.. Prospective, observational study.. Single center, tertiary hospital.. Patients with chronic thromboembolic pulmonary hypertension undergoing pulmonary thromboendarterectomy.. Vasopressin levels were measured in 22 patients during the perioperative period.. Vasopressin was undetectable in 8/22 patients at baseline. As a group, vasopressin levels at baseline and after induction of anesthesia were 0.8 pg/mL (median; 0.5-1.5, interquartile range of 25% and 75%) and 0.7 pg/mL (median; 0.5-1.4, interquartile range of 25% and 75%), respectively. During cardiopulmonary bypass (CPB), vasopressin increased to 13.9 pg/mL (median; 6.7-19.9, interquartile range of 25% and 75%). Vasopressin remained elevated after deep hypothermic circulatory arrest (DHCA) at 10.5 pg/mL (median; 6.5-19.9 interquartile range of 25% and 75%) and after CPB at 19.9 pg/mL (median; 11.1-19.9 interquartile range of 25% and 75%).. Vasopressin levels in PTE patients are in the low-to-normal range at baseline and may be a clinically relevant issue in the hemodynamic management of PTE.

Topics: Adult; Aged; Cardiopulmonary Bypass; Dextrocardia; Female; Heart Arrest, Induced; Hemodynamics; Humans; Hypertension, Pulmonary; Male; Middle Aged; Prospective Studies; Pulmonary Embolism; Ultrasonography; Vasopressins; Young Adult

We report the successful use of vasopressin in the management of hypotension in association with severe right ventricular (RV) failure in two patients with advanced idiopathic pulmonary arterial hypertension. Both patients were pregnant and developed systemic hypotension after delivery by Caesarean section. Placental autotransfusion and possibly oxytocin use were thought to be the major contributing factors in worsening RV function. After the use of vasopressin in both patients, cardiovascular variables improved without untoward effect on RV function, and provided rescue therapy for systemic hypotension in this setting. Vasopressin, a direct vasopressor acting via V1 receptors on the vascular endothelium, has been shown to cause pulmonary vasodilatation experimentally and in animal models of pulmonary hypertension. Its synthetic analogue, terlipressin, has been shown to reduce pulmonary vascular resistance in humans with cirrhosis. Vasopressin may therefore have differential effects on the pulmonary and systemic circulations, allowing systemic pressure to be supported without detrimental effects on the pulmonary circulation.

Topics: Adult; Anesthesia, Obstetrical; Cesarean Section; Female; Humans; Hypertension, Pulmonary; Hypotension; Postoperative Complications; Pregnancy; Pregnancy Complications, Cardiovascular; Vasoconstrictor Agents; Vasopressins; Ventricular Dysfunction, Right

Topics: Blood Pressure; Female; Humans; Hypertension, Pulmonary; Infant, Newborn; Male; Postoperative Complications; Pulmonary Veno-Occlusive Disease; Vascular Patency; Vascular Resistance; Vasoconstrictor Agents; Vasopressins

Primary pulmonary hypertension (PPH) is a progressive disease with frequent morbidity and mortality, including the risk of cardiac decompensation and death, during general anesthesia. Administration of IV epoprostenol (Flolan) improves symptoms and survival of patients with PPH and thus is an increasingly used long-term treatment for this condition. This therapy is associated with impaired platelet aggregation, which may complicate the perioperative management of patients with PPH. We present a case report of a patient with severe PPH receiving a continuous epoprostenol infusion undergoing skin grafting for a leg ulcer under spinal anesthesia. An IV infusion of vasopressin was given to prevent systemic hypotension resulting from sympathetic blockade while avoiding increases in pulmonary vascular resistance that may have resulted from catecholamine usage.

Topics: Anesthesia, Spinal; Epoprostenol; Female; Hemodynamics; Hemostatics; Humans; Hypertension, Pulmonary; Infusions, Intravenous; Leg Ulcer; Middle Aged; Platelet Aggregation Inhibitors; Skin Transplantation; Vasopressins

Septic shock is still the major cause of death in surgical intensive care unit. Fluid support, inotropic agents, and broad spectrum antibiotics are still the mainstay of traditional therapy. Here, we present a case of septic shock arising from gangrenous ischemic bowel, complicated by chronic pulmonary hypertension, which was refractory to catecholamine vasoprerssors. We successfully stabilized the hemodynamics and reduce the pulmonary hypertension with low-dose vasopressin infusion.

Topics: Aged; Chronic Disease; Female; Humans; Hypertension, Pulmonary; Infusions, Intravenous; Shock, Septic; Vasoconstrictor Agents; Vasopressins

Our previous studies indicated that in the human paraventricular (PVN) and supraoptic (SON) nuclei, tyrosine hydroxylase (TH)--the first and rate-limiting enzyme in catecholamine synthesis--is localized mainly in magnocellular neurons and that antemortem factors regulate its expression. The purpose of the present study was to investigate the distribution of TH-immunoreactive (TH-IR) perikarya of the hypothalami of a large sample of well-documented adult subjects without neurological, psychiatric or endocrinological disease in order to identify factors that could regulate the expression of TH in the human neurosecretory neurons. Our material consisted of the hypothalami of 38 subjects studied immunohistochemically for TH using the peroxidase-antiperoxidase method. Striking individual differences were observed among the subjects studied concerning the number and distribution of TH-IR perikarya within the PVN and SON. These differences were evident throughout the entire rostrocaudal length of the hypothalamus and appeared to be related neither to the age or sex of the subjects nor to the postmortem interval or staining procedures. In the sample studied, a large number of TH-IR perikarya were observed specifically in all subjects that had suffered from right-sided heart failure due to pulmonary hypertension, liver cirrhosis or dehydration. In all the above illnesses, increased production and secretion of vasopressin (VP) are reported to occur due to a decrease in 'effective' blood volume or to osmotic stimulation. We conclude that somatic illnesses leading to prolonged osmotic or nonosmotic stimulation of VP release may induce increased expression of TH immunoreactivity in the human neurosecretory neurons related to neuronal activation.

Topics: Adult; Aged; Aged, 80 and over; Cardiac Output, Low; Dehydration; Disease; Female; Humans; Hypertension, Pulmonary; Immunohistochemistry; Liver Cirrhosis; Male; Middle Aged; Neurons; Osmosis; Paraventricular Hypothalamic Nucleus; Supraoptic Nucleus; Time Factors; Tyrosine 3-Monooxygenase; Vasopressins

Assessment of RAAS and vasopressin in patients with primary pulmonary hypertension (PPH).. Activity of plasma renin (APR), angiotensin-converting enzyme (ACE), plasma levels of angiotensin II (AII) and vasopressin (VP), serum concentration of aldosteron (AS) were measured by radioimmunoassay and enzyme immunoassay in 21 PPH patients with circulatory failure (age 34.7 +/- 2.1 years), 11 patients with NYHA functional class II-III, 10 with class IV, and 10 control subjects (age 29.8 +/- 1.5 years).. Compared to controls, 21 PPH patients had elevated RAAS parameters: APR up to 3.52 ng/ml/h (p < 0.05), activity of ACE up to 43.13 units, AII level up to 33.93 ng/ml (p < 0.01), AS up to 468.86 ng/ml (p < 0.01), VP up to 5.26 ng/ml (p < 0.001). Circulatory failure progression resulted in activation of all the RAAS components. This and VP activation was the greatest in PPH patients with ACE > 5 ng/ml/h. PPH patients with mean pressure in the pulmonary artery higher than 60 mm Hg demonstrated higher ARP, AS, VP, AII, ACE than those who had this pressure under 60 mm Hg.. PPH patients display a noticeable activation of RAAS and VP. This activation seems to be secondary as the changes increase with elevation of the pressure in the pulmonary artery and aggravation of circulatory insufficiency. Plasma renin activity determines the degree of RAAS activation as a whole. The discovered activation of RAAS in PPH gives grounds for doubts in the validity of using ACE inhibitors in the treatment of PPH.

Topics: Adolescent; Adult; Aldosterone; Angiotensin II; Biomarkers; Female; Humans; Hypertension, Pulmonary; Immunoenzyme Techniques; Male; Middle Aged; Peptidyl-Dipeptidase A; Pulmonary Wedge Pressure; Radioimmunoassay; Renin; Renin-Angiotensin System; Vasopressins

The degree to which pulmonary angiography may contribute to serious complications in patients with pulmonary hypertension has not been clarified and remains a matter of debate. Accordingly, this study was designed (1) to detect the potential release of vasoactive peptides and (2) to investigate the hemodynamic response after administration of a nonionic contrast medium in patients with pulmonary hypertension undergoing pulmonary angiography. Allergy-mediating substances also were measured to monitor for possible anaphylactoid reactions.. Pulmonary digital subtraction angiography was performed in 20 patients with pulmonary hypertension (mean pulmonary arterial pressure more than 20 mm Hg). Iopromide was administered as a total of 100 mL via a 7F catheter inserted from the right femoral vein. The injected volume and duration of injection (15 to 20 mL/sec) were kept constant. Hemodynamic parameters were continuously monitored, including electrocardiogram, heart rate, phasic and mean pulmonary arterial and peripheral arterial pressures. Blood samples were obtained before and after administration of contrast media to assay for the concentration of the following vasoactive peptides using radioimmunoassay techniques: renin, angiotensin-I-converting enzyme, angiotensin II, aldosterone, atrial natriuretic peptide, antidiuretic hormone, cyclic-guanosine monophosphate, and myoglobin, as well as allergy-mediating substances such as tryptase, eosinophil protein X, and eosinophil cationic protein.. Administration of iopromide caused significant increases in atrial natriuretic peptide (from 61.3 +/- 11.8 to 94.0 +/- 16.7) and antidiuretic hormone (from 6.6 +/- 1.9 to 12.3 +/- 3.1), whereas renin significantly decreased (from 3.0 +/- 0.6 to 1.3 +/- 0.5). After administration of contrast media, there were no significant changes in the other measured vasoactive peptides, allergy-mediating substances, and monitored cardiovascular parameters.. Administration of iopromide for pulmonary angiography in patients with pulmonary hypertension resulted in no appreciable hemodynamic alterations associated with the observed changes in atrial natriuretic peptide, antidiuretic hormone, and renin. No allergy-mediated reactions were observed in these patients.

Topics: Adult; Aged; Aldosterone; Anaphylaxis; Angiography, Digital Subtraction; Angiotensin II; Atrial Natriuretic Factor; Blood Pressure; Blood Proteins; Chymases; Contrast Media; Cyclic GMP; Electrocardiography; Eosinophil Granule Proteins; Eosinophil-Derived Neurotoxin; Female; Heart Rate; Humans; Hypertension, Pulmonary; Inflammation Mediators; Iohexol; Lung; Male; Middle Aged; Myoglobin; Peptides; Peptidyl-Dipeptidase A; Renin; Ribonucleases; Serine Endopeptidases; Tryptases; Vasopressins

Topics: Angiotensin II; Animals; Bradykinin; Epinephrine; Hemorrhage; Hexamethonium Compounds; Histamine; Hypertension, Pulmonary; Intracranial Pressure; Male; Norepinephrine; Organ Size; Pentolinium Tartrate; Phenoxybenzamine; Pulmonary Edema; Rats; Serotonin; Stereotaxic Techniques; Vagotomy; Vagus Nerve; Vasoconstrictor Agents; Vasopressins

Topics: Anesthesia, Intravenous; Animals; Aorta; Blood Cell Count; Blood Platelets; Blood Pressure; Carbon Dioxide; Cardiac Output; Cell Aggregation; Dextrans; Dogs; Endotoxins; Escherichia coli; Heart Atria; Hydrogen-Ion Concentration; Hypertension, Pulmonary; Leukocytes; Oxygen; Phenobarbital; Pulmonary Circulation; Shock, Septic; Time Factors; Urethane; Vasopressins; Venous Pressure

Topics: Adult; Arteriosclerosis; Ductus Arteriosus; Ductus Arteriosus, Patent; Familial Primary Pulmonary Hypertension; Humans; Hypertension; Hypertension, Pulmonary; Lung Diseases; Pathology; Pharmacology; Pulmonary Circulation; Rabbits; Research; Vasopressins