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)

The renin-angiotensin-aldosterone system plays an important role in the development of congestive heart failure (CHF). In patients with chronic heart failure, angiotensin-converting enzyme (ACE) inhibitors, such as captopril, enalapril, and quinapril, have been shown to improve hemodynamics, reduce symptoms of fatigue and dyspnea, increase exercise capacity, correct hyponatremia, reduce diuretic requirements and ventricular arrhythmias, and conserve potassium and magnesium. ACE inhibitors reduce circulating levels of angiotensin II and aldosterone and may reduce plasma norepinephrine and vasopressin levels. They are equally effective in patients with mild to moderate heart failure and in patients with severe cardiac impairment. ACE inhibitors are at least as beneficial as digitalis in patients with mild heart failure, and they may even be considered as first-line therapy. Promising results have also been obtained in patients with myocardial infarction, in whom long-term therapy with ACE inhibitors has prevented an increase in heart size. ACE inhibitors improve prognosis in patients with severe heart failure and in patients with hyponatremia; the question of effect on survival in mild to moderate heart failure has yet to be answered.
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PMID:ACE inhibitors in congestive heart failure. 267 Feb 20

Several studies have shown symptomatic and haemodynamic improvement after the introduction of angiotensin converting enzyme inhibitors in patients with heart failure treated with diuretics. The concomitant long term effects of the new orally effective long acting angiotensin converting enzyme inhibitor, enalapril, on symptoms, exercise performance, cardiac function, arrhythmias, hormones, electrolytes, body composition, and renal function have been further assessed in a placebo controlled double blind cross over trial with treatment periods of eight weeks. Twenty patients with New York Heart Association functional class II to IV heart failure who were clinically stable on digoxin and diuretic therapy were studied. Apart from the introduction of enalapril, regular treatment was not changed over the study period; no order or period effects were noted. Enalapril treatment significantly improved functional class, symptom score for breathlessness, and exercise tolerance. Systolic blood pressure was significantly lower on enalapril treatment. Echocardiographic assessment indicated a reduction in left ventricular dimensions and an improvement in systolic time intervals. In response to enalapril, the plasma concentration of angiotensin II was reduced and that of active renin rose; plasma concentrations of aldosterone, vasopressin, and noradrenaline fell. There were significant increases in serum potassium and serum magnesium on enalapril. Glomerular filtration rate measured both by isotopic techniques and by creatinine clearance declined on enalapril while serum urea and creatinine rose and effective renal plasma flow increased. Body weight and total body sodium were unchanged indicating that there was no overall diuresis. There was a statistically insignificant rise in total body potassium, though the increase was related directly to pretreatment plasma renin (r = 0.5). On enalapril the improvement in symptoms, exercise performance, fall in plasma noradrenaline, and rise in serum potassium coincided with a decline in the frequency of ventricular extrasystoles recorded during ambulatory monitoring. Adverse effects were few. In patients with heart failure, enalapril had a beneficial effect on symptoms and functional capacity. The decline in glomerular filtration rate on enalapril may not be beneficial in early heart failure.
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PMID:Effects of enalapril in heart failure: a double blind study of effects on exercise performance, renal function, hormones, and metabolic state. 299 98

Independently of phenomena related to rejection, atherosclerosis of the grafted heart or high blood pressure, there exists a qualitative and quantitative degradation of response to exercise in heart transplant recipients. Maximal oxygen consumption is generally reduced to 40 to 60% of normal levels. There are several interactive mechanisms. Paradoxically, the transplanted heart is a clear demonstration of the fact that several other elements are involved in the organisms response to exercise. Indeed, ventilation, exercise load, peripheral circulation, muscle metabolism and neurohormonal response also play a role. Vasoactivity of the peripheral arteries limits distribution and extraction of oxygen during exercise. Noradrenaline, renin, atrial natriuretic factor, vasopressin and endothelin levels are normal at rest, but an overreaction occurs during exercise. The percentage of type I (oxidative) fibres is reduced in muscles. Cyclosporine has also been shown to have a toxic effect on mitochondria in muscles. The deinnervated transplanted heart is thus called upon to work in coordination with peripheral elements which have also undergone alterations. Consequently, response to exercise cannot be significantly increased above the level reached before transplantation. Usually patients are not greatly hindered in their daily activities and rarely complain of breathlessness. Nevertheless, an improvement would be appreciated. A coherent physical rehabilitation programme can increase maximal oxygen consumption by 25 to 30% in these patients, essentially via improvement in peripheral anomalies. It is more difficult to modify cardiac response.
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PMID:[Exercise capacity after heart transplantation]. 854 31

We report a syndrome of inappropriate secretion of antidiuretic hormone (SIADH), neurotoxicity and facial erythema induced by several anti-cancer drugs in a case of malignant lymphoma of thyroid gland. A 68-year-old male was admitted, complaining of neck tumor and dyspnea. On admission, he was treated with vincristine (VCR) for bronchostenosis due to malignant lymphoma. Neck tumor and mediastinal lymph node swelling reduced. On the ninth day after chemotherapy of VCR, a consciousness disturbance was found and he was diagnosed as having SIADH. Following chemotherapy of cyclophosphamide, SIADH was also induced so he was treated with irradiation for neck and mediastinal field, instead of chemotherapy. During irradiation, however, enlargement of systemic lymph nodes appeared, and the chemotherapy was resumed. He achieved partial remission, but somnolence after ifosfamide and facial erythema after ranimustine were observed. In spite of the difference in the chemical structure of these anti-cancer drugs, several side effects occurred. It is suggested that the direct effects of drugs on the nervous system were SIADH and neurotoxicity.
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PMID:[Syndrome of inappropriate secretion of antidiuretic hormone and neurotoxicity induced by vincristine and alkylating agents during chemotherapy for malignant lymphoma of thyroid gland]. 957 77

A 65-year-old man who had muscle weakness and dysarthria was admitted for investigation of motor neuron disease. He had lost 12 kg of weight in 6 months. Neurological findings disclosed upper and lower motor neuron disturbances with normal sensory nerve function, and needle electromyography showed a neurogenic pattern. Laboratory findings on admission demonstrated dilutional hyponatraemia due to an excessive secretion of antidiuretic hormone (ADH). Based on these findings, the patient was diagnosed as having the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) associated with amyotrophic lateral sclerosis (ALS). During the night of first hospital day, the patient complained of severe dyspnoea, and mechanical ventilation was commenced. Following the mechanical ventilation, plasma ADH levels and serum sodium concentration were normalized. We propose that respiratory failure secondary to the atrophy of respiratory muscle might be responsible for the development of SIADH.
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PMID:Syndrome of inappropriate secretion of antidiuretic hormone associated with amyotrophic lateral sclerosis in respiratory failure. 1038 39

We report a patient with pulmonary adenocarcinoma complicated by the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) following systemic chemotherapy with cisplatin (CDDP) and vindesine (VDS). A 66-year-old woman was diagnosed as having pulmonary adenocarcinoma with malignant pleural effusion following investigations for cough and dyspnea. After drainage of the effusion she received combination chemotherapy with CDDP and VDS. She developed SIADH 48 hours following chemotherapy. Interestingly, the use of carboplatin (CBDCA) and VDS in the subsequent treatment course was well tolerated indicating that the SIADH was most likely to have been induced by administration of CDDP.
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PMID:Syndrome of inappropriate secretion of ADH (SIADH) following cisplatin administration in a pulmonary adenocarcinoma patient with a malignant pleural effusion. 1168 26

Chester-Erdheim disease is a rare non-Langerhans histiocytosis, affecting within the CNS mainly the neurohypophyseal unit, the retrobulbar space and the parenchyma of cerebellum, cerebrum and brainstem. Here we present a case of a 55-year-old woman who developed an exophthalmus, edema and dyspnea, finally leading to death 4 months post admission to the hospital. A cMRI showed a retrobulbar fibrosis, a tumor in the sella turcica, and further tumor formation expanding from the pons to the spinal cord, but without involvement of the dural sheet. Autopsy revealed multiple tumors attached to the pituitary gland, the tentorium, and the brainstem as well as a diffuse thickening of the dura. Histologically, the tumor tissue consisted of densely packed lipid-laden foamy macrophages positive for CD68 and intervening fibrillary cords. Interestingly, tumor cells did not infiltrate/affect the parenchyma but showed a strictly extracerebral/ subdural location. In addition, sections of the pituitary tumor revealed a chromophobe giant adenoma of the pituitary gland. As to our knowledge this is the first detailed description of an exceptional case of intracranial CED presenting with strictly extracerebral/subdural tumor masses accompanied by a giant adenoma of the pituitary gland.
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PMID:Extracerebral subdural manifestation of Chester-Erdheim disease associated with a giant adenoma of the pituitary. 1453 50

The preclinical diagnosis of shock is still based on the patient's history, the physical examination, the injury pattern and a few hemodynamic parameters available in the emergency set-up. The clinical picture is characterised by hypotension and tachycardia, tachypnoe and dyspnoea as well as cerebral impairment. Results from recent clinical trials indicate, that a adapted and specific therapeutic approach for the various shock forms is necessary. In case of traumatic hypovolemic-hemorrhagic shock it is of particular relevance if penetrating trauma and/or uncontrolled bleeding exists. Under these conditions an immediate definite surgical treatment is required ("scoop and run") and a moderate hypotension should be tolerated. ("treat and run"). Fluid substitution and therapy with catecholamines should be used conservatively. In all other forms of shock the treatment approach can and should be more aggressive in order to improve microvascular perfusion as early as possible. Besides adequate fluid resuscitation in a combination of crystalloid and colloid solutions catecholamines and-under specific circumstances-also vasopressin should be used. Of utmost importance in the pre-clinical management of patients in shock is the optimal selection of the centre that the patient is referred to in order to establish the fastest and best possible definite treatment for the patient.
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PMID:[Pre-clinical management of shock patients]. 1499 5

We report a 47-year-old man with multiple sclerosis (MS) with previous history of recurrent sensorimotor disturbance and visual deficit. The patient developed bilateral motor weakness in the upper limbs, and systemic malaise. An administration of 20 mg/day of prednisolone was ineffective for his symptoms and he complained dyspnea a week later. On admission, his clinical findings included brainstem dysfunction with optic nerve atrophy, motor disturbance in the bilateral upper limbs, hyperreflexia, and superficial sensory disturbance. Biochemical examination revealed marked reduction in serum Na (117 mEq/l) and C1 (85 mEq/l) with increased urinary Na excretion. Although his plasma osmotic pressure decreased to 233 mOsm/kg, urinary osmotic pressure increased to 409 mOsm/kg. Serum antidiuretic hormone (ADH) concentration was 26.1 pg/ml and plasma renin activity was 0.1 ng/ml/ hour. Renal function and adrenal function were normal. Cerebrospinal fluid contained increased protein concentration, IgG, and myelin basic protein. Syndrome of inappropriate secretion of antidiuretic hormone (SIADH) associated with MS was diagnosed. Intravenous Na infusion with restricted supplemental fluid and serial administration of methylprednisolone (1,000 mg/day for three days) improved his neurological abnormalities and normalized his serum serum Na level and plasma osmotic pressure. This suggests that demyelinating lesions in the hypothalamus due to MS may cause the transient increased ADH secretion.
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PMID:[Syndrome of inappropriate secretion of antidiuretic hormone (SIADH) associated with relapsing multiple sclerosis]. 1578 1

This is a report on a case of severe skin necrosis in a vasodilatory septic shock patient after the infusion of low-dose vasopressin through a central venous catheter. An 84-year-old male was hospitalized for edema on both legs at Asan Medical Center, Seoul, Korea. On hospital day 8, the patient began to complain of dyspnea and he subsequently developed severe septic shock caused by E. coli. After being transferred to the medical intensive care unit, his hypotension, which was refractory to norepinephrine, was controlled by an infusion of low-dose vasopressin (0.02 unit/min) through a central venous catheter into the right subclavian vein. After the infusion of low-dose vasopressin, severe skin necrosis with bullous changes developed, necessitating discontinuation of the low-dose vasopressin infusion. The patient expired from refractory septic shock. Although low-dose vasopressin can control hypotension in septic shock patients, low-dose vasopressin must be used with caution because ischemic complications such as skin necrosis can develop even with administration through a central venous catheter.
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PMID:Skin necrosis after a low-dose vasopressin infusion through a central venous catheter for treating septic shock. 1724 16


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