Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Patients with cirrhosis and portal hypertension exhibit characteristic haemodynamic changes with a hyperkinetic systemic circulation, abnormal distribution of the blood volume, and neurohumoral dysregulation. Moreover, the circulating levels of several vasoactive substances may be elevated. Splanchnic vasodilatation is of pathogenic significance for the low systemic vascular resistance and abnormal volume distribution, which are important elements in the development of the concomitant cardiac dysfunction, recently termed cirrhotic cardiomyopathy. The systolic and diastolic functions are impaired with direct relation to the degree of liver dysfunction. Significant pathophysiological mechanisms seem to include a reduced beta-adrenergic receptor signal transduction, defective cardiac excitation-contraction coupling, and conductance abnormalities. Various vasodilators. such as nitric oxide and calcitonin gene-related peptide, are among candidates in the vasodilatation and the increased arterial compliance recently described in advanced cirrhosis. Reflex-induced enhanced sympatho-adrenal activity, activation of the renin-angiotensin-aldosterone system, and elevated circulating vasopressin and endothelin-1 are implicated in the haemodynamic counter-regulation in cirrhosis. Recent research has focused on the assertion that the haemodynamic and neurohumoral abnormalities in cirrhosis are part of a general cardiovascular dysfunction influencing the course of the disease, with reduction of organ function and sodium-water retention as the outcome. These aspects are relevant to therapy.
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PMID:Vasoactive substances in the circulatory dysfunction of cirrhosis. 1168 31

Splanchnic arterial relaxation is the most important pathology in systemic circulation of portal hypertensive patients. Progressive decline of splanchnic vascular resistance is responsible for development of circulatory dysfunction syndrome (CDS), associated with reduction of effective blood volume within central vascular compartment and compensatory stimulation of vasopressor and natrium retaining hormonal mechanisms. Advanced CDS is characterized by increased cardiac output, tachycardia and low arterial pressure. Complications of CDS have functional nature and comprise: renal failure (hepatorenal syndrome), respiratory failure in context of hepatopulmonary syndrome, cardiac insufficiency produced by portopulmonary hypertension or portal cardiomyopathy, hemorrhages from digestive tract caused by hypertensive portal gastropathy or derangements of brain perfusion. The management of CDS relies on adequate filling of vascular system (albumin), constriction of arterial splanchnic vessels (beta-blocker, analogs of vasopressin and somatostatin), reduction of cardiac output (beta-blocker) and giving support to local vasoprotective mechanisms (prostaglandins, nitric oxide, blockade of ET-A receptors).
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PMID:[Circulatory dysfunction syndrome associated with liver cirrhosis]. 1619 May 66

The failing heart produces a variety of biologically active humoral factors such as catecholamines, vasopressin, angiotensin II, aldosterone, atrial natriuretic polypeptide (ANP), brain natriuretic polypeptide (BNP), cytokines and so on, in order to recover the cardiac function through the mechano- and chemo-receptors in vivo. In particular, it has recently shown that the central nervous system plays a pivotal role in the progression of cardiac remodeling and the heart failure. Thereby, endogenous digitalis-like factor, angiotensisn II, aldostereone, and inflammatory cytokines in the brain are acting as the mediators. In fact, mineralocorticoid receptor blockers, such as spironolactone and eplerenone, are clinically useful to treat cardiac failure. However, these biomarkers are not available as laboratory tests because they are under investigation clinically. On the other hand, failing heart by itself produces natriuretic hormones such as ANP and BNP to rescue it. They dilate resistant vessels to reduce the afterload of the heart with the lowest concentrations. Then, natriuresis is caused with the increased concentrations to reduce the pre-load to the heart. The natriuresis is brought partially by reducing concentrations of plasma aldosterone. Therefore, concentrations of these natriuretic hormones are excellent biomarkers for the cardiac function. They increase in a variety of disease states like hypertension, acute/old myocardial infarction, angina pectoris, arrhythmias, cardiac failure, cardiomyopathy, renal failure and myocarditis. In particular, they are remarkably increased in patients with heart failure. Recently, a new biomarker, N-terminal pro-BNP (NT-proBNP) is registered as a clinically available laboratory test, which may be superior to BNP at the laboratory stand of view. It is because NT proBNP is not degraded in the circulation, stable even in serum and the higher concentration as compared to BNP.
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PMID:[Pathophysiology of heart failure and the biomarkers; brain natriuretic hormone as the class-1 recommendation by the new Japanese Guideline for Heart Failure]. 1828 62

A 90-year-old woman who had received more than 100 electroconvulsive treatments (ECT) over many years requested another course for depression. After the third ECT, an electrocardiogram showed new T-wave inversion (V2-V6) and ST elevation (V2). Catheterization revealed severe left ventricular dysfunction but no coronary obstruction, leading to a diagnosis of Takotsubo cardiomyopathy (stress-related). The patient's recovery was uneventful. Recent literature cites three other cases post-ECT. It appears that elderly women are at greatest risk, repeated stress is generally required, and recovery is achieved quickly. Elevated levels of catecholamines and of vasopressin may be implicated.
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PMID:Takotsubo cardiomyopathy and electroconvulsive treatments: a case study and review. 2056 47

The syndrome of inappropriate antidiuretic hormone secretion (SIADH) is frequently responsible for chronic hyponatremia in the elderly due to age-related disruption of the inhibitory component of brain osmoregulatory mechanisms. Recent research has indicated that chronic hyponatremia is associated with gait disturbances, increased falls, and bone fragility in humans, and we have found that chronic hyponatremia causes increased bone resorption and reduced bone mineral density in young rats. In this study, we used a model of SIADH to study multi-organ consequences of chronic hyponatremia in aged rats. Sustained hyponatremia for 18 weeks caused progressive reduction of bone mineral density by DXA and decreased bone ash calcium, phosphate and sodium contents at the tibia and lumbar vertebrae. Administration of 10-fold higher vitamin D during the last 8 weeks of the study compensated for the reduction in bone formation and halted bone loss. Hyponatremic rats developed hypogonadism, as indicated by slightly lower serum testosterone and higher serum FSH and LH concentrations, markedly decreased testicular weight, and abnormal testicular histology. Aged hyponatremic rats also manifested decreased body fat, skeletal muscle sarcopenia by densitometry, and cardiomyopathy manifested as increased heart weight and perivascular and interstitial fibrosis by histology. These findings are consistent with recent results in cultured osteoclastic cells, indicating that low extracellular sodium concentrations increased oxidative stress, thereby potentially exacerbating multiple manifestations of senescence. Future prospective studies in patients with SIADH may indicate whether these multi-organ age-related comorbidities may potentially contribute to the observed increased incidence of fractures and mortality in this population.
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PMID:Chronic hyponatremia exacerbates multiple manifestations of senescence in male rats. 2221 80

There has been considerable recent progress liver transplantation (LTX). The postreperfusion syndrome has clearly defined and typically responds to vasopressin and/or methylene blue when refractory to catecholamine therapy. Diastolic dysfunction and cirrhotic cardiomyopathy are prevalent and important in LTX recipients. The high cardiovascular risk and the increasing medical complexity of the current liver transplant recipient have stimulated the publication of guidelines for cardiovascular assessment before LTX. Cardiac surgery is increasingly more successful in patients with cirrhosis, including simultaneous heart-liver transplantation. Cardiopulmonary bypass in LTX is indicated for hemodynamic rescue and, at some centers, serves as the hemodynamic platform for liver implantation. Although acute renal injury is common after LTX, early diagnosis is now possible with novel biomarkers. Earlier detection of postoperative renal dysfunction may prompt intervention for renal rescue. The metabolic milieu in LTX remains critical. Regular insulin therapy may be more effective than infrequent large bolus therapy for potassium homeostasis. Careful titration of insulin therapy may improve freedom from severe hyperglycemia to decrease morbidity. Since the organization of dedicated anesthesia care teams for LTX improves perioperative outcome, this aspect of perioperative care is receiving systematic attention to optimize safety and quality. The specialty of LTX is likely to continue to flourish even more, given these pervasive advances.
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PMID:Clinical update in liver transplantation. 2384 28

Catecholamine-induced cardiomyopathy associated with pheochromocytoma is a relatively well-recognized but rare entity. We report a case of 15-year old man with a pheochromocytoma and severe heart failure caused by a catecholamine-induced cardiomyopathy. He had symptoms such as fatigue, cold sweating, and dyspnea for 7 months. The chest x-ray showed an enlarged cardiac shadow and pulmonary edema. Echocardiography showed severe decreased left ventricular contractility with multiple thrombi and right ventricular hypokinesia with mild pulmonary hypertension. This report describes our experience of the anesthetic management for the removal of pheochromocytoma with catecholamine-induced cardiomyopathy, which barely responded to high vasopressin and epinephrine.
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PMID:Anesthetic experience of pheochromocytoma resection with catecholamine-induced cardiomyopathy and congestive heart failure : A case report. 3062 97

Among the complications of cirrhosis, hepatorenal syndrome (HRS) is characterized by having the worst survival rate. HRS is a disorder that involves the deterioration of kidney function caused primarily by a systemic circulatory dysfunction, but in recent years, systemic inflammation and cirrhotic cardiomyopathy have been discovered to also play an important role. The diagnosis of HRS requires to meet the new International Club of Ascites-Acute Kidney Injury (ICA-AKI) and Hepatorenal Syndrome-Acute Kidney Injury (HRS-AKI) criteria after ruling out other causes of kidney injury. At the time of diagnosis, it is important to start the medical treatment as soon as possible where three types of vasoconstrictors have been recognized: vasopressin analogs (ornipressin and terlipressin), alpha-adrenergic agonists (norepinephrine and midodrine) and somatostatin analogues (octreotide); all should be combined with albumin infusion. Among them, terlipressin and albumin are the first lines of treatment in most cases, although terlipressin should be monitor closely due to its adverse events. The best treatment of choice is a liver transplant, because it is the only definitive treatment for this disease.
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PMID:An Integrated Review of the Hepatorenal Syndrome. 3284 2


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