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Query: UNIPROT:P01185 (
vasopressin
)
23,126
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Vasopressin and its analogue terlipressin are potent vasoconstrictors which reduce mesenteric blood flow and have been used in the therapy of variceal hemorrhage. This vasoconstrictor effect applies on vascular beds throughout the body. Since in literature
vasopressin
is rarely described to determine
lactic acidosis
, we report of a patient in whom a severe metabolic (probably lactic) acidosis appeared, associated with terlipressin administration for bleeding esophageal varices. By exclusion, the temporal sequence with terlipressin therapy, the contemporary increase of arterial blood pressure and autoptic data in the case presented make likely a diagnosis of terlipressin-induced
lactic acidosis
. Because of the seriousness of metabolic acidosis observed in our patient we suggest a careful monitoring of acid-base parameters in patients under treatment with
vasopressin
analogues.
...
PMID:Terlipressin-induced metabolic acidosis. 185 46
The cardiorespiratory, sympathetic and biochemical effects of T-2 toxin were examined in conscious rats and guinea pigs. The pithed rat preparation was also used to evaluate possible direct effects of T-2 on the heart and vasculature. Injection of T-2 (0.5-2.0 mg/kg i.v.) into conscious rats produced prolonged (6-8 hr) hypertension and tachycardia, followed by hypotension. Total peripheral resistance was increased and cardiac output decreased. In guinea pigs, a steady decrease in pressure and rate occurred. Intravenous administration of T-2 to pithed rats did not alter blood pressure or heart rate at a time when, in conscious rats, both blood pressure and heart rate were increased. Significant elevations of arterial plasma norepinephrine, epinephrine and dopamine occurred after T-2, with metabolic acidosis, hypocarbia and hyperoxemia in both conscious rats and guinea pigs. In the rat, increase in plasma
vasopressin
and prostacyclin were elevated, but thromboxane and leukotriene C4-immunoreactivity were not changed. In pithed rats, T-2 did not increase basal or stimulated plasma catecholamines but produced the same changes in blood gases, pH and lactate. The LD50 values for i.v. T-2 in the rat and guinea pig were 0.74 and 1.30 mg/kg, respectively. The data are consistent with the hypothesis that T-2 toxin disrupts cellular aerobic metabolism, resulting in
lactic acidosis
, sympathoadrenomedullary activation, variable initial circulatory responses and eventual cardiovascular collapse.
...
PMID:Cardiorespiratory, sympathetic and biochemical responses to T-2 toxin in the guinea pig and rat. 397 27
The objectives of fluid therapy in the burned child can be simply stated and defined, and they should represent the basis for the resuscitation process. During the first 24 h after the burn, the ultimate goal is restoration of the patient's volume and electrolyte homeostasis. All efforts should be directed at monitoring or restoring organ function while simultaneously minimizing edema formation. Only the minimum amount of fluids and other nutrients needed to restore cell function should be provided. Electrolyte deficits and
lactic acidosis
must be promptly corrected and every attempt should be made to prevent further derangement in body homeostasis by replacing concurrent losses and anticipating maintenance fluid and electrolyte requirements. Restoration and maintenance of perfusion pressures should lead to maximal oxygenation of injured and noninjured tissues, which promotes spontaneous healing, minimizes wound conversion, decreases bacterial colonization and prepares the injured areas for early excision and grafting. It must be emphasized, however, that restoration of fluid and electrolyte balance and organ function does not necessarily imply a return to normal of all physiological variables. The cardiac output, for example, may not return to preburn levels for 24-48 h post injury, even when the intravascular volume has been completely replenished. Likewise, oliguria may persist for 48-72 h, or even longer, after the burn, as a result of excessive secretion of
antidiuretic hormone
stimulated by the stress of the injury rather than its effect on fluid balance. Thus, while the objectives can be easily enumerated and defined, they are difficult to meet.
...
PMID:Fluid resuscitation of pediatric burn victims: a critical appraisal. 791 69
Lactic acidosis
is a rare complication in lung cancer. We report a case of lung cancer accompanied by both syndrome of inappropriate secretion of
antidiuretic hormone
(SIADH) and
lactic acidosis
. A 70-year-old man was referred to our hospital for examination of a left hilar mass shadow on a chest X-ray film. Small cell lung cancer (SCLC) was demonstrated by brushing the bronchial mucosa of the left lower lobe bronchus. His laboratory data showed SIADH and
lactic acidosis
that were probably due to SCLC. Fluid restriction improved SIADH, and combination chemotherapy for SCLC improved the
lactic acidosis
although the tumor size did not change.
...
PMID:Small cell lung cancer accompanied by lactic acidosis and syndrome of inappropriate secretion of antidiuretic hormone. 1004 78
The acute tumor lysis syndrome (ATLS) is characterized by the rapid development of hyperuricemia, hyperkalemia, hyperphosphatemia, and acute renal failure (ARF). Hematologic malignancies are responsible for most cases of ATLS. Control of hyperuricemia and the achievement of a high urine flow are the mainstays of prevention. Urinary alkalinization should be performed only when hyperuricemia is present. Hypercalcemia occurs in 10% to 20% of patients with cancer at some time during the disease course. Parathyroid hormone-related protein (PTHrP) is the most common mediator of humoral hypercalcemia of malignancy (HHM), while local osteolysis is the principal mechanism in patients with bone metastasis. Hydration with saline and administration of pamidronate control hypercalcemia in most patients. Hyponatremia with an increase in total-body salt and water content, manifested as edema and/or ascites, is the most common electrolyte abnormality in cancer patients. Hyponatremia due to salt depletion may occur in patients who receive cisplatin. The syndrome of inappropriate
antidiuretic hormone
secretion (SIADH) may occur in association with cancer of the lung, after high-dose cyclophosphamide, and during vigorous fluid administration in patients with chemotherapy-associated emesis.
Lactic acidosis
without tissue hypoperfusion may be seen in patients with extensive liver metastasis or with certain hematologic malignancies. In the latter cases, lactate levels parallel disease activity and chemotherapy often leads to resolution of the
lactic acidosis
. Idiopathic hyperammonemia has been described after intensive chemotherapy for hematological malignancies and following bone marrow transplantation.
...
PMID:Metabolic emergencies in the cancer patient. 1086 20
In patients with advanced cirrhosis with ascites disorders of water and electrolyte metabolism are often present and they are associated with changes in acid-base balance. These changes can be very complicated, their diagnosis and treatment difficult. Dilutional hyponatremia is the most common disorder. Hyponatremia in these patients is associated with increased morbidity and mortality before and after liver transplantation. Other common disorders include hyperchloremic acidosis, hypokalemia, metabolic alkalosis,
lactic acidosis
, respiratory alkalosis. If renal impairment occurs (for example hepatorenal syndrome), metabolic acidosis and retention of acid metabolites may develop. The pathogenesis of these conditions applies primarily hemodynamic changes. Activation of renin-angiotensin-aldosterone system and non-osmotic stimulation of
antidiuretic hormone
trigger serious changes in water and natrium-chloride metabolism. This activation is clinically expressed like oedema, ascites, hydrothorax, low to zero natrium concentration in urine and increased urinary osmolality, which is higher than serum osmolality. In practice, the evaluation can be significantly modified by the ongoing diuretic therapy. Closer monitoring of water and electrolyte metabolism together with acid-base balance in patients with ascitic liver cirrhosis is important, not only in terms of diagnosis but especially in terms of therapy.
...
PMID:[Disorders of water and electrolyte metabolism and changes in acid-base balance in patients with ascitic liver cirrhosis]. 2872 61
Vasopressin is a potent vasopressor used for improving organ perfusion during cardiac arrest, septic and catecholamine-resistant shock; with reference to this, it is useful for the treatment of vasoplegic shock because, restoring organ perfusion pressure by contraction of vascular smooth muscle through a non-catecholamine receptor pathway, it can be employed when catecholamines are ineffective. A 49-yr-old woman was admitted to the Emergency Department after having intentionally taken 95.2g of metformin, 1.6g of pioglitazone and 40 UI of insulin glargine in a suicide attempt. Despite fluid resuscitation, CVVHDF (continuous veno-venous hemodiafiltration) treatment, norepinephrine and epinephrine infusion, she developed a severe
lactic acidosis
and a catecholamines-refractive vasodilatory shock. Only the
vasopressin
infusion, in association with catecholamines, gradually stabilized the patient's hemodynamic status.
...
PMID:Metformin intoxication: Vasopressin's key role in the management of severe lactic acidosis. 2908 89