pituitrin and Cardiomyopathies

Acute kidney injury (AKI) is frequent in patients with cirrhosis. AKI and hyponatraemia are major determinants of the poor prognosis in advanced cirrhosis. The hepatorenal syndrome (HRS) denotes a functional and potential reversible impairment of renal function. Type 1 HRS, a special type of AKI, is a rapidly progressive AKI, whereas the renal function in type 2 HRS decreases more slowly. HRS is precipitated by factors such as sepsis that aggravate the effective hypovolaemia in decompensated cirrhosis, by lowering arterial pressure and cardiac output and enhanced sympathetic nervous activity. Therefore, attempts to prevent and treat HRS should seek to improve liver function and to ameliorate arterial hypotension, central hypovolaemia and cardiac output, and to reduce renal vasoconstriction. Ample treatment of HRS is important to prevent further progression and death, but as medical treatment only modestly improves long-term survival, these patients should always be considered for liver transplantation. Hyponatraemia, defined as serum sodium <130 mmol/L, is common in patients with decompensated cirrhosis. From a pathophysiological point of view, hyponatraemia is related to an impairment of renal solute-free water excretion most likely caused by an increased vasopressin secretion. Patients with cirrhosis mainly develop hypervolaemic hyponatraemia. Current evidence does not support routine use of vaptans in the management of hyponatraemia in cirrhosis.

Topics: Cardiomyopathies; Creatinine; Glomerular Filtration Rate; Hepatorenal Syndrome; Humans; Hyponatremia; Liver Cirrhosis; Vasopressins

Topics: Angiotensin II; Animals; Cardiac Output; Cardiomyopathies; Dogs; Hemodynamics; Homeostasis; Humans; Hypertension; Hypertension, Renal; Norepinephrine; Rabbits; Renal Artery Obstruction; Renin-Angiotensin System; Vascular Resistance; Vasopressins

El Síndrome de Takotsubo es una disfunción ventricular aguda reversible en ausencia de obstrucción coronaria. Una mujer de 85 años de edad con antecedentes de reemplazo valvular aórtico transcatéter, ingresó por dos semanas de dolor severo por una cadera desplazada por osteosíntesis fallida. Mientras se programaba para cirugía, se documentó hiponatremia severa secundaria a secreción inapropiada de hormona antidiurética. Súbitamente desarrolló edema agudo pulmonar. El ecocardiograma confirmó una válvula protésica funcional y aquinesia medial y apical de las paredes del ventrículo izquierdo. Recibió tratamiento con ventilación mecánica no invasiva, restricción de líquidos y diuréticos. La hiponatremia y la cardiomiopatía resolvieron.. Takotsubo syndrome is a form of acute reversible left ventricular dysfunction in the absence of coronary obstruction. An 85-year-old lady with a medical history of transcatheter aortic valve replacement was readmitted complaining of 2 weeks of severe pain by a displaced hip and failed osteosynthesis. While she was scheduled for hip surgery, severe hyponatremia secondary to inappropriate antidiuretic hormone secretion was documented, and sudden-onset pulmonary edema ensued. Echocardiography confirmed normally functioning aortic prosthetic valve and classical features of Takotsubo. She was treated with non-invasive mechanical ventilation, water restriction, and diuretics. Hyponatremia and the cardiomyopathy resolved and the patient recovered completely.

Topics: Aged, 80 and over; Cardiomyopathies; Female; Humans; Retrospective Studies; Takotsubo Cardiomyopathy; Vasopressins

Ethanol (EtOH)-evoked oxidative stress, which contributes to myocardial dysfunction in proestrus rats, is mediated by increases in NADPH oxidase (Nox) activity, malondialdehyde (MDA), and ERK1/2 phosphorylation. Whether these biochemical responses, which are triggered by alcohol-derived acetaldehyde in noncardiac tissues, occur in proestrus rats' hearts remains unknown. Therefore, we elucidated the roles of alcohol dehydrogenase (ADH), cytochrome P4502E1 (CYP2E1), and catalase, which catalyze alcohol oxidation to acetaldehyde, in these alcohol-evoked biochemical and hemodynamic responses in proestrus rats.. Conscious proestrus rats prepared for measurements of left ventricular (LV) function and blood pressure (BP) received EtOH (1.5 g/kg, intravenous [i.v.] infusion over 30 minutes) or saline 30 minutes after an ADH and CYP2E1 inhibitor, 4-methylpyrazole (4-MP) (82 mg/kg, intraperitoneal), a catalase inhibitor, 3-AT (0.5 g/kg, i.v.), their combination, or vehicle. LV function and BP were monitored for additional 60 minutes after EtOH or saline infusion before collecting the hearts for ex vivo measurements of LV reactive oxygen species (ROS), Nox activity, MDA, and ERK1/2 phosphorylation.. EtOH oxidative metabolism plays a pivotal role in the EtOH-evoked LV oxidative stress and dysfunction in proestrus rats. Notably, catalase inhibition (3-AT) caused cardiac oxidative stress and hypotension.

Topics: Amitrole; Animals; Blood Pressure; Cardiomyopathies; Catalase; Central Nervous System Depressants; Enzyme Inhibitors; Ethanol; Female; Fomepizole; Neurophysins; Oxidative Stress; Proestrus; Protein Precursors; Pyrazoles; Rats; Rats, Sprague-Dawley; Vasopressins; Ventricular Function, Left

Pediatric heart failure (HF) is an important cause of morbidity and mortality in childhood. This article presents guidelines for the recognition, diagnosis, and early medical management of HF in infancy, childhood, and adolescence. The guidelines are intended to assist practitioners in office-based or emergency room practice, who encounter children with undiagnosed heart disease and symptoms of possible HF, rather than those who have already received surgical palliation. The guidelines have been developed using the Grading of Recommendations Assessment, Development and Evaluation (GRADE) methodology, and are accompanied by practical Recommendations for their application in the clinical setting, supplemented by online material. This work does not include Recommendations for advanced management involving ventricular assist devices, or other device therapies.

Topics: Adolescent; Algorithms; Angiotensin II Type 1 Receptor Blockers; Angiotensin-Converting Enzyme Inhibitors; Arrhythmogenic Right Ventricular Dysplasia; Biomarkers; Canada; Cardiomyopathies; Cardiotonic Agents; Catecholamines; Child; Child, Preschool; Combined Modality Therapy; Death, Sudden, Cardiac; Diagnosis, Differential; Diuretics; Echocardiography; Electrocardiography, Ambulatory; Evidence-Based Medicine; Heart Defects, Congenital; Heart Failure; Humans; Infant; Magnetic Resonance Imaging; Myocarditis; Myocardium; Prognosis; Risk Factors; Societies, Medical; Vasodilator Agents; Vasopressins

Transthoracic intra-aortic balloon pump (IABP) insertion has been a relatively rare and uncommon procedure. However, it is an established beneficial option in patients with severe peripheral vascular disease (PVD) accompanied with bi-lateral femoral arterial occlusion. There are several viable alternatives to trans-aortic IABP insertion, including trans-axillary or in abdominal aorta (requiring a laparotomy). Cardiac surgery has the advantage of an open sternum, facilitating effortless direct intra-aortic balloon (IAB) insertion into the aorta. The IAB can be inserted either through a 9-mm graft or directly into the ascending aorta. During cardiac surgery, direct insertion into the ascending aorta with the balloon tip lying distally in the abdominal aorta is facilitated with an open sternum. The base of the balloon lies approximately 2 cm below the left subclavian and can be confirmed through a trans-esophageal echocardiogram (TEE). Elimination of a graft insertion saves the team from time-consuming maneuvers and additional hemorrhagic complications. In our experience, postoperative vasoplegic syndrome coupled with myocardial edema contributed to patent instability and was treated with vasopressin and transthoracic IAB insertion. The CS 100 (Datascope Corp., Mahwah, NJ) console allowed the ability to time the balloon accurately. This case report details our experience with one such patient and establishes trans-aortic counter-pulsation as a safe and viable option in patients with severe PVD, where percutaneous insertion is precluded or has failed.

Topics: Aged; Cardiomyopathies; Counterpulsation; Edema, Cardiac; Humans; Intra-Aortic Balloon Pumping; Male; Peripheral Vascular Diseases; Postoperative Complications; Vasopressins

To assess the sublingual microcirculation in a patient during vasopressin administration for a distributive shock after cardiopulmonary bypass.. Case-report in the Department of Intensive Care of a university hospital.. A 53 year-old man developed severe distributive shock after cardiac transplant, requiring massive doses of vasopressor agents.. Vasopressin administered twice at a dose of 0.02 U/min increased mean blood pressure and allowed partial weaning of other vasopressor drugs. Microcirculatory alterations were assessed by orthogonal polarization spectral technique: 50% and 60% of capillaries were perfused at baseline, and these proportions did not worsen when vasopressin was administered.. Despite its strong vasopressor effects vasopressin infusion did not worsen microcirculatory alterations in this patient with distributive shock following cardiac surgery.

Topics: Blood Pressure; Cardiomyopathies; Cardiopulmonary Bypass; Central Venous Pressure; Fluorescence Polarization; Heart Rate; Heart Transplantation; Hemodynamics; Humans; Infusions, Intravenous; Male; Microcirculation; Middle Aged; Mouth Floor; Oxygen Consumption; Pulmonary Wedge Pressure; Shock, Cardiogenic; Spectrometry, Fluorescence; Vasoconstrictor Agents; Vasopressins

The aim of this study was to develop a new model of vasopressin-induced chronic myocardial damage based on sustained ST-segment depression in electrocardiogram (ECG) with progression of myocardial fibrosis in rats. Furthermore, using this model, we examined the prophylactic potential of fasudil, a Rho-kinase inhibitor, against myocardial damage induced by vasopressin. In 10-week old male Donryu rats, intravenous administration of arginine vasopressin (0.5 iu/kg) induced significant ST-segment depression. Two days and one week after the administration of vasopressin, ST-segment depression was -0.19 +/- 0.02 and -0.14 +/- 0.02 mV, respectively. Fasudil (10 and 30 mg/kg, p.o.) significantly attenuated the ST-segment depression induced by vasopressin. One week after the administration of vasopressin, the percent area of myocardial fibrosis in control animals (0.42 +/- 0.11%, p < 0.01) was significantly greater than that in normal animals (0.05 +/- 0.01%). Fasudil (10 and 30 mg/kg) significantly prevented the development of the fibrosis. We present a new model of chronic myocardial damage based on sustained ST-segment depression with progression of myocardial fibrosis in rats, and suggest that this model may be useful to investigate the treatment of chronic angina. Inhibition of Rho-kinase is efficacious in preventing the ECG change and development of fibrosis induced by vasopressin in this model.

Topics: 1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine; Animals; Cardiomyopathies; Chronic Disease; Disease Models, Animal; Disease Progression; Electrocardiography; Enzyme Inhibitors; Fibrosis; Intracellular Signaling Peptides and Proteins; Kinetics; Male; Protein Serine-Threonine Kinases; Rats; rho-Associated Kinases; Vasopressins

Topics: Adult; Aldosterone; Angiotensin II; Cardiomyopathies; Cardiomyopathy, Dilated; Heart Transplantation; Hemodynamics; Humans; Middle Aged; Postoperative Period; Renin; Renin-Angiotensin System; Tissue Donors; Vasopressins; Ventricular Function, Right

Animal studies have shown that vasopressin secretion is modulated by arterial baroreceptors and cardiopulmonary volume receptors. Whether this is the case also in humans is controversial, however. To determine whether vasopressin is reflexly modulated by cardiac volume receptors, we studied the effect on plasma vasopressin (venous blood, radioimmunoassay) of reducing venous return and left ventricular end-diastolic diameter (echocardiography) by producing a 20-minute lower body negative pressure in 14 healthy subjects (aged 49.3 +/- 3.8 years, mean +/- SEM). The data were compared with those of 14 age-matched heart-transplant recipients, i.e., subjects with cardiac denervation. In healthy subjects, lower body negative pressure at -15 mm Hg caused a modest reduction in left ventricular end-diastolic diameter (-5 +/- 3.4%) and no change in vasopressin, whereas lower body negative pressure at -37.5 mm Hg caused a more marked reduction in left ventricular end-diastolic diameter (-12 +/- 2.5%) and a small, variable, but overall statistically significant (p < 0.05) increase in vasopressin (+145 +/- 46%, p < 0.01). The left ventricular end-diastolic diameter changes induced by the two lower body negative pressure stimuli were similar in heart-transplant recipients, but the vasopressin increase seen with the lower body negative pressure at -37.5 mm Hg was abolished. The marked increase in plasma renin activity and forearm vascular resistance induced by lower body negative pressure in healthy subjects was also abolished or drastically attenuated in heart-transplant recipients.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Adult; Blood Pressure; Cardiomyopathies; Female; Forearm; Heart Rate; Heart Transplantation; Hemodynamics; Humans; Male; Middle Aged; Muscles; Norepinephrine; Pressoreceptors; Reference Values; Regional Blood Flow; Renin; Vascular Resistance; Vasopressins

Hamsters of the BIO 14.6 strain characteristically develop cardiomyopathy as they age, and hamsters of this strain have overt signs of heart failure by 11 months of age. Plasma levels of the posterior pituitary hormone arginine-vasopressin (AVP) were found to be elevated (approximately 2-fold) in 11 month old BIO 14.6 hamsters, compared to age-matched hamsters of a control strain. AVP appeared inappropriately elevated in these animals, since they were neither hyperosmotic nor markedly hypotensive. The elevated levels of AVP observed in these animals appears to contribute to vasomotor tone, since intravenous administration of a specific antagonist of the vasoconstrictor action of AVP [d(CH2)5Ome(TYR)AVP] elicited a fall in arterial pressure (9 +/- 2 mm Hg, n = 6, p less than 0.05). The AVP antagonist had no effect on arterial pressure in hamsters of a control strain, and vehicle administration had no effect on arterial pressure in either strain. These data indicate that inappropriately elevated levels of AVP contribute to the cardiovascular state of myopathic hamsters. Since elevated plasma AVP has been noted in human congestive heart failure, these results suggest that AVP may contribute to the cardiovascular status during congestive heart failure.

Topics: Age Factors; Animals; Cardiomyopathies; Cricetinae; Disease Models, Animal; Heart Failure; Mesocricetus; Rodent Diseases; Vasoconstriction; Vasopressins

A simple, rapid and sensitive radioimmunoassay for plasma arginine-vasopressin (AVP) has been developed for routine use. AVP is first extracted from plasma with use of an octadecasilyl silica cartridge. The mean (+/- SEM) recovery is 73.1 +/- 2.1% (n = 24). The antibody and the 125I-AVP are both obtained from commercial sources. Following a 48 h incubation time, bound and free fractions of AVP are separated by dextran-charcoal. The reproducibility of the method is acceptable (between- and within-assay CV of 9.5 and 7.6%). This technique allows the detection of 0.39 pg/tube of AVP. This assay is applicable to determination of human plasma AVP levels; mean (+/- SEM) plasma AVP levels in normal human subjects in standing or sitting positions, or after an oral water load, were respectively 5.2 +/- 0.7, 3.6 +/- 0.4 and 2.7 +/- 0.4 pg/mL. This method has also been validated by determinations of plasma AVP levels in rabbits and hamsters in various conditions. The commercial availability of the antibody and radioactive AVP, and the simplicity of the method, make this technique suitable for clinical and research purposes.

Topics: Animals; Cardiomyopathies; Cricetinae; Drinking; Humans; Male; Posture; Rabbits; Radioimmunoassay; Radioimmunosorbent Test; Vasopressins

Topics: Animals; Aspartate Aminotransferases; Cardiac Complexes, Premature; Cardiomyopathies; Creatine Kinase; Dogs; Electrocardiography; Epinephrine; Ethanol; Heart Ventricles; Isoproterenol; Myocardium; Nicotine; Time Factors; Vasopressins