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)

A spontaneous intrapericardial haemorrhage caused cardiac tamponade in a 29 year old paraplegic man who was being treated with warfarin. The associated persistent hyponatraemia, which was believed to be caused by an inappropriately high release of antidiuretic hormone, rapidly resolved after pericardiocentesis.
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PMID:Hyponatraemia secondary to an inappropriately high release of antidiuretic hormone in cardiac tamponade. 220 14

Cardiac tamponade was induced in dogs by the infusion of saline into the pericardial cavity. The mean arterial pressure dropped to approximately one-third and the cardiac output to one-fourth of the control level. This was accompanied by the release of vasoactive humoral mediators. Among the vasoconstrictor mediators measured in the plasma, the greatest rise during early tamponade occurred in vasopressin concentrations. Considerable elevations of epinephrine and nonrepinephrine concentrations and plasma renin activity were also demonstrated, these mediators reaching their maximum levels in late tamponade. This study for the first time demonstrates significant rises in plasma thromboxane B2 and histamine levels in cardiac tamponade. The histamine level elevation was greater in the portal venous blood than in the arterial blood. It is suggested that histamine may play a counterregulatory role in cardiac tamponade by attenuating excessive vasoconstriction caused by the activation of various vasoconstrictor systems.
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PMID:Humoral changes in shock induced by cardiac tamponade. 268 45

Atrial distension, rather than change in intra-atrial pressure, has been suggested as a principal mediator of release of atrial natriuretic factor (ANF). During cardiac tamponade, atrial pressures rise whereas transmural pressures and atrial stretch may not be affected. The roles of atrial pressure and atrial distension were investigated in six open-chest dogs subjected to cardiac tamponade and rapid volume expansion as disparate means of affecting intra-atrial pressures and atrial stretch. Hemodynamic measurements, immunoreactive ANF (ir-ANF), plasma renin activity, antidiuretic hormone, epinephrine, and norepinephrine were monitored before, during, and after three interventions: (1) tamponade, (2) rapid volume loading followed by tamponade, and (3) volume loading during tamponade. Volume expansion increased right atrial pressure and caused a significant rise in ir-ANF. Elevations of right atrial pressure caused by tamponade were comparable to those induced by volume infusion, but an increase in ir-ANF was not elicited during tamponade, and the ir-ANF response to volume loading was abolished when performed during tamponade. The relation between the change in ANF concentration and change in right atrial pressure were highly significant in the absence of tamponade, when atrial stretch was freely responsive to volume expansion (r = .73, p less than .0001), but not when stretch was inhibited (r = -.16, p = NS). These observations underscore the importance of considering the modulating effects of atrial compliance, transmural pressure, and atrial stretch on the relation between atrial pressures and ANF release.
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PMID:Hormonal responses to cardiac tamponade: inhibition of release of atrial natriuretic factor despite elevation of atrial pressures. 295 74

Many cancers and complications of cancer treatment may cause major critical care problems. Cardiopulmonary complications include pericardial effusion, cardiac tamponade, superior vena cava syndrome, pleural effusion, pulmonary embolism, radiation pneumonitis, and toxicities related to chemotherapy. Syndrome of inappropriate antidiuretic hormone (SIADH), Cushing's disease, and hypercalcemia are common endocrine complications associated with solid tumors. Astute nursing assessment plays an important role in preventing or reducing morbidity related to these complications.
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PMID:Heart, lung, and endocrine complications of solid tumors. 780 Sep 72

We describe two patients who developed acute renal failure secondary to severe pericardial effusion. In one patient, the pericardial effusion was due to coxsackievirus infection, and in the other patient, it was due to lung cancer. One patient was in cardiac tamponade, and the other was not yet in tamponade, as per echocardiographic criteria. Kidney function was relatively normal in both patients before the pericarditis episodes. In both patients, pericardiocentesis caused immediate massive diuresis with quick recovery of renal function back to baseline. In the first patient, blood urea nitrogen and serum creatinine decreased from 82 mg/dL and 7.6 mg/dL to 71 mg/dL and 4.6 mg/dL in the next 48 hours, then to 23 mg/dL and 1.3 mg/dL 5 days after the pericardiocentesis. In the second patient, blood urea nitrogen and serum creatinine decreased from 109 mg/dL and 2.9 mg/dL to 40 mg/dL and 0.9 mg/dL in the next 48 hours and 17 mg/dL and 0.7 mg/dL 3 days after release of tamponade. Pericardial effusion can affect renal hemodynamics in many different ways, including increased atrial natriuretic peptide secretion, increased renal efferent nerve activity, and increased secretion of renin and vasopressin. Although pericardial effusion is a complication of uremia, acute renal failure per se can occur in nonuremic cases of pericardial effusion. Two cases of acute renal failure resulting from pericardial effusion were reported in the literature in the past. Pericardial effusion should be included in the broad list of prerenal causes of acute renal failure.
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PMID:Pericardial effusion leading to acute renal failure: two case reports and discussion of pathophysiology. 1232 21

While fluid management is established in controlled hemorrhagic shock, its use in uncontrolled hemorrhagic shock is being controversially discussed, because it may worsen bleeding. In the irreversible phase of hemorrhagic shock that was unresponsive to volume replacement, airway management and catecholamines, vasopressin was beneficial due to an increase in arterial blood pressure, shift of blood away from a subdiaphragmatic bleeding site towards the heart and brain and decrease of fluid resuscitation requirements. The purpose of this multicenter, randomized, controlled, international trial is to assess the effects of vasopressin (10 IU IV) vs. saline placebo IV (up to 3 injections at least 5 min apart) in patients with prehospital traumatic hemorrhagic shock that persists despite standard shock treatment. The study will be carried out by helicopter emergency medical service teams in Austria, Germany, Czech Republic, Portugal, the Netherlands and Switzerland. Inclusion criteria are adult trauma patients with presumed traumatic hemorrhagic shock (systolic arterial blood pressure <90 mmHg) that does not respond to the first 10 min of standard shock treatment (endotracheal intubation, fluid resuscitation and use of vasopressors) after arrival of the first emergency physician at the scene. The time window for randomization will close after 30 min of shock treatment. Exclusion criteria are terminal illness, no intravenous access, age <18 years, injury >60 min before randomization, cardiac arrest before randomization, presence of a do-not-resuscitate order, untreated tension pneumothorax, untreated cardiac tamponade, or known pregnancy. Primary study end-point is the hospital admission rate, secondary end-points are hemodynamic variables, fluid resuscitation requirements and hospital discharge rate.
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PMID:[Vasopressin for therapy of persistent traumatic hemorrhagic shock: The VITRIS.at study]. 1726 38

We documented a hyponatremic patient who developed imminent cardiac tamponade upon oral salt supplement. A 72-year-old diabetic woman had hemorrhagic stroke; pericardial effusion; and chronic kidney disease, stage IV. She developed hyponatremia (serum sodium level, 125 mmol/L), compatible with the syndrome of inappropriate antidiuretic hormone, and received oral salt supplement 9 g/d for 4 days. Shortness of breathing and increasing heart rate ensued, and the echocardiography found accumulation of pericardial effusion with signs of impending cardiac tamponade. Pig-tail drainage through pericardiocentesis was done, and the vital signs were stabilized. We found the production of pericardial effusion increased from 100 to 220 mL/d after oral salt supplement at 3 g/d was reassumed. We discuss the relationship between serum sodium levels, the dose of salt supplement and the accumulation of pericardial effusion.
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PMID:Impending cardiac tamponade caused by salt supplement in a hyponatremic patient with chronic kidney disease. 2203 Jan 76

We describe a complex case of hyponatraemia with two aetiologies. A 49-year-old man who drank 6 litres of dilute alcohol per day presented confused and oedematous with a serum sodium of 95 mmol/litre. Urine sodium was <10 mmol/litre and urine osmolality 440 mOsmol/kg. Chest x-ray demonstrated a globular heart. ECG showed saddle-shaped ST elevation. ECHO demonstrated a large pericardial effusion causing marked tamponade. Following pericardiocentesis there was a marked diuresis; serum sodium returned to normal after 2 weeks. A full recovery ensued. Cardiac tamponade is associated with antidiuresis via release of antidiuretic hormone (ADH). Tamponade is also associated with antinatriuresis. Antidiuresis and antinatriuresis usually balance in cardiac tamponade; excessive fluid intake may have caused an imbalance in this case.
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PMID:Hyponatraemia associated with cardiac tamponade and chronic fluid excess. 2275 60