pituitrin has been researched along with Necrosis* in 33 studies
4 review(s) available for pituitrin and Necrosis
| Article | Year |
|---|---|
[A case of rhabdomyolysis with administration of intravenous vasopressin].
A 73-year-old man with alcoholic liver cirrhosis was admitted to our hospital because of massive hematemesis. He was treated with continuous intravenous infusion of vasopressin of 0.2 U/min. 22 hours after the infusion, he complained of myalgia, muscle weakness and skin mottling in the extremities. The skin lesion extended to the back. The serum CK and myoglobin levels were elevated to 52,280 IU/L and 84,400 ng/ml respectively. The urinary myoglobin level was elevated to 732,000 ng/ml. On the fifth hospital, he died of bleeding from the esophageal varices. Autopsy examination demonstrated necrosis of the skeletal muscle cells and myoglobin casts in the renal tubules. Our patient was probably hypersensitive to vasopressin because of underlying liver dysfunction. The massive myonecrosis might be induced from the following conditions; overreactive vasopressin-induced vasoconstriction resulted in ischemic muscle damage, and hypersensitive sarcoplasmic reticulum released excessive Ca2+ followed by muscle hypercontraction as seen in malignant syndrome or malignant hyperthermia. Topics: Aged; Esophageal and Gastric Varices; Humans; Infusions, Intravenous; Liver Cirrhosis, Alcoholic; Male; Muscle, Skeletal; Necrosis; Rhabdomyolysis; Vasopressins | 1995 |
[Cutaneous necrosis and rhabdomyolysis following the intravenous infusion of vasopressin].
We describe the case of a patient with hepatic cirrhosis treated with an intravenous infusion of vasopressin to control an upper digestive hemorrhage, who developed distance cutaneous necrosis and rhabdomyolysis. We review the other cases published in the international scientific literature and we discuss the possible pathogeny of these complications. Topics: Gastrointestinal Hemorrhage; Humans; Infusions, Intravenous; Liver Cirrhosis, Alcoholic; Male; Middle Aged; Necrosis; Rhabdomyolysis; Skin; Vasopressins | 1993 |
Rhabdomyolysis and cutaneous necrosis following intravenous vasopressin infusion.
A continuous IV infusion of vasopressin was administrated to a patient with cirrhosis of the liver and acute gastrointestinal bleeding from esophageal varices. In the first 24 hours, the patient developed rhabdomyolysis and cutaneous necrosis. Stopping vasopressin infusion resulted in relief of these lesions. The rarity of these complications suggests an idiosyncratic reaction of susceptible individuals that may be related to previous vascular disease or a failure in baroreceptor regulation. Topics: Aged; Esophageal and Gastric Varices; Gastrointestinal Hemorrhage; Humans; Infusions, Intravenous; Liver Cirrhosis; Male; Necrosis; Rhabdomyolysis; Skin Diseases; Vasopressins | 1991 |
Drug-induced renal disease.
The clinical manifestations of drug-induced renal disease may include all the manifestations attributed to natural or spontaneous renal diseases such as acute renal failure, chronic renal failure, acute nephritic syndrome, renal colic, haematuria, selective tubular defects, obstructive nephropathy, etc. It is therefore vital in any patient with renal disease whatever the clinical manifestations might be, to obtain a meticulous drug and toxin inventory. Withdrawal of the offending drug may result in amelioration or cure of the renal disorder although in the case of severe renal failure it may be necessary to utilise haemodialysis or peritoneal dialysis to tide the patient over the period of acute renal failure. Analgesic nephropathy is an important cause of terminal chronic renal failure and it is therefore vital to make the diagnosis as early as possible. The pathogenesis of some drug-induced renal disorders appears to be immunologically mediated. There are many other pathogenetic mechanisms involved in drug-induced renal disorders and some drugs may under appropriate circumstances be responsible for a variety of different nephrotoxic effects. For example, the sulphonamides have been incriminated in examples of crystalluria, acute interstitial nephritis, acute tubular necrosis, generalised hypersensitivity reactions, polyarteritis nodosa and drug-induced lupus erythematosus. Topics: Acute Disease; Analgesics; Humans; Hypercalcemia; Immune System Diseases; Kidney Calculi; Kidney Concentrating Ability; Kidney Diseases; Kidney Tubular Necrosis, Acute; Necrosis; Nephrosis; Nephrotic Syndrome; Potassium Deficiency; Proteins; Tetracyclines; Ureteral Diseases; Ureteral Obstruction; Urologic Neoplasms; Vascular Diseases; Vasopressins | 1979 |
29 other study(ies) available for pituitrin and Necrosis
| Article | Year |
|---|---|
An electrocardiographic, molecular and biochemical approach to explore the cardioprotective effect of vasopressin and milrinone against phosphide toxicity in rats.
The present study was conducted to identify the protective effect of vasopressin (AVP) and milrinone on cardiovascular function, mitochondrial complex activities, cellular ATP reserve, oxidative stress, and apoptosis in rats poisoned by aluminum phosphide (AlP). Rats were divided into five groups (n = 12) including control, AlP (12.5 mg/kg), AlP + AVP (2.0 Units/kg), AlP + milrinone (0.25 mg/kg) and AlP + AVP + milrinone. After treatment, the animals were connected to an electronic cardiovascular monitoring device to monitor electrocardiographic (ECG) parameter. Finally, oxidative stress biomarkers, mitochondrial complex activities, ADP/ATP ratio and apoptosis were evaluated on the heart tissues. Results indicated that AlP administration induced ECG abnormalities along with a decline in blood pressure and heart rate. AVP and milrinone significantly ameliorated these changes in all treated groups. Considerable protective effects on oxidative stress biomarkers, complex IV activity, ADP/ATP ratio and caspase-3 and -9 activities in treated groups were also found. These findings were supported by flow cytometry assay of cardiomyocytes. In conclusion, administration of AVP and milrinone, not only improve cardiovascular functions in AlP poisoned rats in the short time, but after a long time can also restore mitochondrial function and ATP level and reduce the oxidative damage, which prevent cardiomyocytes from entering the apoptotic phase. Topics: Adenosine Diphosphate; Adenosine Triphosphate; Aluminum Compounds; Animals; Apoptosis; Biomarkers; Cardiotonic Agents; Caspase 3; Caspase 9; Electrocardiography; Heart Diseases; Lethal Dose 50; Milrinone; Mitochondria, Heart; Myocytes, Cardiac; Necrosis; Oxidative Stress; Oxygen Consumption; Phosphines; Rats; Vasoconstrictor Agents; Vasopressins | 2015 |
Peripheral administration of vasopressin for catecholamine-resistant hypotension complicated by skin necrosis.
Topics: Catheterization, Peripheral; Female; Humans; Infusions, Intravenous; Middle Aged; Necrosis; Shock, Septic; Skin Diseases; Vasoconstrictor Agents; Vasopressins | 2006 |
Colon ischaemia and necrosis as a complication of prolonged but successful CPR.
Survival after prolonged cardiopulmonary resuscitation (CPR) is often associated with neurological and other sequelae. We describe a patient who survived prolonged cardiac arrest due to ventricular fibrillation neurologically intact but suffered colon ischaemia and necrosis in the post-resuscitation period. Subtotal colectomy was performed. We wonder whether this complication was related to the use of vasopressin. Topics: Adrenergic Agonists; Adult; Amiodarone; Anti-Arrhythmia Agents; Cardiopulmonary Resuscitation; Colectomy; Colon; Electric Countershock; Epinephrine; Female; Heart Arrest; Humans; Ischemia; Necrosis; Time Factors; Vasoconstrictor Agents; Vasopressins; Ventricular Fibrillation | 2006 |
Skin necrosis after a low-dose vasopressin infusion through a central venous catheter for treating septic shock.
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. Topics: Aged, 80 and over; Catheterization, Central Venous; Dose-Response Relationship, Drug; Fatal Outcome; Humans; Infusions, Intravenous; Male; Necrosis; Shock, Septic; Skin; Vasoconstrictor Agents; Vasopressins | 2006 |
Cardiac necrosis markers associated with low nitric oxide levels in the plasma of rabbits after treatment with vasopressin: protective effects of nitroglycerin administration.
It has been reported that the administration of vasopressin induces myocardial ischaemia in rats, which causes electrocardiographic ST segment alterations according to many authors. But rat electrocardiogram (ECG) lacks ST segment. Consequently it appears important to study the effects of vasopressin in rabbits, which show ST segment present in the ECG. Since cardiac necrosis markers are released in the plasma of humans with myocardial infarction, as well as in a variety of experimental models of myocardial necrosis, it is possible that the same may occur in rabbits with myocardial ischaemia induced by vasopressin. The main aim of this study was to investigate whether the administration of vasopressin causes the appearance of specific myocardial necrosis markers, such as cardiac troponin I, myoglobin or creatine kinase MB (CK MB) in rabbits in the presence or absence of modified ECG profile, and to also verify whether these markers are associated with the alterations in some coagulation parameters, that are known to be induced by vasopressin. As the effects of vasopressin are counteracted by nitric oxide (NO), another aim was to verify whether vasopressin also affects plasma NO levels and whether the administration of a NO donor can reverse these effects. Vasopressin was administered to rabbits and caused ischaemic alterations such as electrocardiographic changes, and significantly increased the levels of plasma cardiac necrosis markers (c-troponin I, myoglobin and CK MB). It also elevated diastolic blood pressure (BP), lowered heart rate (HR), increased procoagulation activity, and lowered plasma NO levels. The appearance of heart necrosis, demonstrated by plasma cardiac necrosis markers in the animals receiving vasopressin, was attributed to a drug-induced increase in vasoconstriction and coagulation activity. The intense vasoconstriction and thrombosis may lead to endothelium necrosis and a consequent drop in NO production. The administration of the NO donor nitroglycerin (NG) in the vasopressin treated animals restored NO values, and was capable of preventing the appearance of the plasma cardiac necrosis markers and altered coagulation values. The protective activity of NG was attributed to NO release, which lowers BP values and counteracts coagulation activity in vasopressin-treated animals. The described procedure may also be proposed for the study of early ischaemic myocardial lesions and the screening of NO donors preventing myocardial damage. Topics: Animals; Biomarkers; Creatine Kinase; Creatine Kinase, MB Form; Electrocardiography; Fibrinogen; Isoenzymes; Male; Myocardial Ischemia; Myocardium; Myoglobin; Necrosis; Nitric Oxide; Nitric Oxide Donors; Nitroglycerin; Partial Thromboplastin Time; Prothrombin Time; Rabbits; Troponin I; Vasopressins | 2002 |
Skin necrosis after extravasation of low-dose vasopressin administered for septic shock.
To describe a case of severe skin necrosis resulting from peripheral intravenous administration of low-dose vasopressin in a patient with catecholamine-resistant septic shock.. Case report.. Medical intensive care unit at the University of Chicago, Chicago, IL.. A 46-yr-old female with ventilator-dependent, proliferative-phase acute respiratory distress syndrome complicated by Pseudomonas aeruginosa bacteremia and sepsis.. A patient recovering from acute respiratory distress syndrome developed septic shock from Pseudomonas aeruginosa bacteremia while in the medical intensive care unit. Vasopressin (0.04 units/min) was administered through a peripheral venous catheter for hypotension unresponsive to exogenous catecholamines. The patient subsequently developed severe ischemic necrosis of the skin and soft tissue surrounding the catheter site. The vasopressin was stopped, and the skin lesion progressed to bullae formation with extensive superficial erosion.. Peripheral administration of low-dose vasopressin for septic shock should be discouraged because of the risk of ischemic skin complications. Topics: Dose-Response Relationship, Drug; Extravasation of Diagnostic and Therapeutic Materials; Female; Humans; Illinois; Infusions, Intravenous; Middle Aged; Necrosis; Pseudomonas Infections; Shock, Septic; Skin; Treatment Failure; Vasoconstrictor Agents; Vasopressins | 2002 |
Vasopressin-induced amber-like skin necrosis.
Case reports about vasopressin-induced cutaneous necrosis are not frequent. Here we report a further case, of which skin manifestations included not only mottling, cyanosis, ecchymosis, bullae and gangrene, but also amber-like change in focal areas. Besides, intermittent paling of the skin with or without deep pain sensation of the limbs over non-injection sites was observed that might be a warning sign of impending skin necrosis. Based on the literature about vasopressin-induced skin necrosis we discuss the possible role of coagulation enhancement of this molecule. Topics: Esophageal and Gastric Varices; Gastrointestinal Hemorrhage; Hemostatics; Humans; Male; Middle Aged; Necrosis; Pigmentation Disorders; Skin Diseases; Vasopressins | 1997 |
Ornithine-vasopressin gangrene and reconstruction of the upper lip. Case report.
A bilateral cleft lip and palate case received ornithine-vasopressin intra-operatively in preparation for a vasoconstricted field of the various lip segments prior to the repair of the cleft lip. A cyanotic tinge appeared immediately. This eventually led to total necrosis of the upper lip. Various relevant blood tests were done and a mild thrombocytosis was found. Surgical reconstruction of the upper lip was performed by means of a forked cross-lip flap--the main blood supply coming from the columella--as well as by means of an inferiorly pedicled cheek flap from the para-nasal area. Topics: Cleft Lip; Cleft Palate; Gangrene; Humans; Infant; Lip; Lip Diseases; Male; Necrosis; Ornithine; Surgical Flaps; Thrombocytosis; Vasopressins | 1989 |
[Skin necrosis following administration of vasopressin].
Topics: Aged; Female; Hemoptysis; Humans; Multiple Organ Failure; Necrosis; Skin; Tranexamic Acid; Vasopressins | 1987 |
Vasopressin-induced bullous disease and cutaneous necrosis.
Intravenous vasopressin is a commonly used modality for control of bleeding esophageal varices. The development of ischemic cutaneous complications is a recently described entity. In previous reports, cutaneous necrosis has occurred at sites of extravasation, at or proximal to intravenous catheter sites, or at isolated pressure points. We review the literature on vasopressin-induced cutaneous reactions and report a case of cutaneous necrosis and bulla formation in which multiple bullae formed during vasopressin therapy at sites distant from direct intravenous flow. Topics: Aged; Catheterization; Esophageal and Gastric Varices; Female; Humans; Infusions, Parenteral; Necrosis; Skin; Skin Diseases, Vesiculobullous; Vasopressins | 1986 |
Cellular mechanisms of drug-induced papillary necrosis.
2-Bromoethylamine hydrobromide (BEA) causes complete papillary necrosis within 24-hr of i.v. administration. The mechanism of this effect is unknown. To characterize further the effect of BEA in transporting epithelia, the urinary bladders of toads and turtles were exposed to varying concentrations of BEA in vitro. In the toad bladder, both cyclic AMP- and vasopressin-stimulated water flow were significantly inhibited after 3 hr of exposure to BEA at a concentration as low as 2.5 X 10(-4) g/ml; after 1 and 2 hr no effect on water transport was observed. Serosal administration of BEA to both toad and turtle bladders significantly inhibited sodium transport to 54% of control at the end of 3 hr. The effect on sodium transport was seen as early as 10 min. The threshold for the effect on sodium transport occurred at a concentration less than that observed for water transport. By contrast, BEA had no effect on hydrogen ion secretion in the isolated turtle bladder over a wide range of concentrations. In fact, after 1 hr, BEA significantly stimulated hydrogen ion secretion. In homogenates of stripped turtle bladder mucosa, BEA significantly inhibited total Na-K adenosine triphosphatase and ouabain sensitive Na-K adenosine triphosphatase. Thus, in anuran membranes, BEA inhibits water and sodium transport but has no effect on acidification. These results suggest that its action in vivo may be related to alterations in cell volume regulation resulting from inhibition of sodium transport rather than a nonspecific toxic effect on the inner medullary epithelium. Topics: Animals; Body Water; Bufo marinus; Cyclic AMP; Ethylamines; Hydrogen; Kidney Medulla; Necrosis; Sodium; Sodium-Potassium-Exchanging ATPase; Urinary Bladder; Vasopressins | 1985 |
Scrotal and abdominal skin necrosis complicating intravenous vasopressin therapy for bleeding esophageal varices.
Two patients with severe liver disease developed scrotal necrosis after intravenous vasopressin infusion for bleeding esophageal varices. One of these patients also developed anterior abdominal wall skin necrosis. Although ischemic complications secondary to vasopressin are probably not totally avoidable, attention to hypovolemia, concomitantly administered pressor drugs, patient position, and points of local pressure may decrease the likelihood of these previously unreported complications. Topics: Abdominal Muscles; Esophageal and Gastric Varices; Gastrointestinal Hemorrhage; Humans; Infusions, Parenteral; Male; Middle Aged; Necrosis; Scrotum; Skin Diseases; Vasopressins | 1985 |
Tongue necrosis after intraarterial vasopressin therapy.
Topics: Female; Humans; Injections, Intra-Arterial; Middle Aged; Necrosis; Tongue; Vasopressins | 1985 |
[Cutaneous necrosis caused by vasopressin].
Topics: Aged; Humans; Infusions, Parenteral; Male; Necrosis; Skin Diseases; Vasopressins | 1985 |
Bilateral nipple necrosis after intravenous vasopressin therapy.
Bilateral nipple necrosis developed in two patients after intravenous vasopressin therapy for bleeding esophageal varices. When vasopressin therapy was promptly tapered and discontinued, recovery of skin changes occurred gradually. The role and some of the reported complications of vasopressin therapy in bleeding esophageal varices are discussed herein. Topics: Adult; Breast Diseases; Esophageal and Gastric Varices; Female; Gastrointestinal Hemorrhage; Humans; Injections, Intravenous; Male; Middle Aged; Necrosis; Nipples; Vasopressins | 1984 |
Cutaneous necrosis following peripheral intravenous vasopressin therapy.
Vasopressin infusion through peripheral veins is a commonly used modality for control of bleeding esophageal varices. A cirrhotic patient in whom multiple areas of cutaneous necrosis developed during a course of vasopressin therapy is presented. The involved areas included the infusion sites as well as sites unrelated to infusion but subject to pressure. Patients receiving this form of therapy must be carefully observed for the development of ischemic cutaneous complications. Topics: Humans; Infusions, Parenteral; Male; Middle Aged; Necrosis; Skin; Vasopressins | 1982 |
Cerebellar degeneration in the rat following rapid correction of hyponatremia.
Degenerative lesions in the superior vermis of the cerebellum were produced in 8 of 14 rats that were first made hyponatremic for three days with vasopressin and water and then given hypertonic saline. Within the superior vermis, lesions were predominantly localized to the crests of the folia. These lesions were characterized by demyelination of folial white matter and necrosis of granule cells at the junction with the white matter. In severe degeneration, the entire width of the granule cell layer was involved and Purkinje cell necrosis was found as well. Hyponatremia alone or administration of hypertonic saline to normonatremic rats did not result in lesions. Because of the topographical and histopathological similarity of these lesions to those of alcoholic cerebellar degeneration, our findings raise the possibility of a contribution of electrolyte-induced injury to the pathogenesis of alcoholic cerebellar degeneration. Topics: Animals; Arginine Vasopressin; Cerebellum; Hyponatremia; Male; Myelin Sheath; Necrosis; Nerve Degeneration; Rats; Rats, Inbred Strains; Saline Solution, Hypertonic; Sodium; Sodium Chloride; Vasopressins | 1981 |
Gastric infarction: a complication of selective vasopressin infusion.
This report describes a case of massive gastric hemorrhage, initially controlled by selective arterial vasopressin infusion. Infusion was followed by extensive necrosis of the gastric wall which necessitated subtotal gastrectomy. Gastric necrosis following arterial infusion is rare and in this case appears to be due to migration of the infusion catheter into a peripheral branch of the left gastric artery in a patient whose gastric circulation had been compromised by prior surgery. The complications related to the use of arterial infusion for the control of gastric hemorrhage are discussed and the literature is reviewed. Topics: Angiography; Catheters, Indwelling; Constriction, Pathologic; Female; Gastrectomy; Gastric Mucosa; Gastrointestinal Hemorrhage; Humans; Infarction; Infusions, Intra-Arterial; Middle Aged; Necrosis; Stomach; Vasopressins | 1979 |
High arterial pressure versus humoral factors in the pathogenesis of the vascular lesions of malignant hypertension.
Topics: Angiotensin II; Animals; Arteries; Blood Pressure; Capillary Permeability; Humans; Hypertension, Malignant; Necrosis; Renin; Vascular Diseases; Vasopressins | 1977 |
Spontaneous infarction in pituitary tumors: neurologic and therapeutic aspects.
In addition to progressive endocrine dysfunction and progressive visual loss, pituitary neoplasms may annouce their presence by the more catastrophic alternative of spontaneous tumor infarction. In two patients reported, illness due to the spontaneous infraction of pituitary tumors was heralded by sudden onset of focal headache associated with diplopia. Stupor, confusion, and evidence of increased intracranial pressure occurred without subarachnoid hemorrhage or massive extrasellar extension of tumor. One patient developed inappropriate antidiuretic hormone secretion with spontaneous infarction in a large but clinically silent chromophobe adenoma. In both patients, skull x-rays suggested a long-standing intrasella mass. Both underwent prompt treatment with endocrinologic replacement therapy and subsequent successful transsphenoidal removal of voluminous, infarcted, pituitary masses. Topics: Adenoma, Chromophobe; Adult; Eye Manifestations; Female; Humans; Hypophysectomy; Male; Middle Aged; Necrosis; Pituitary Neoplasms; Sphenoid Sinus; Vasopressins | 1975 |
Inhibition of vasopressin-induced morbid effects on the rat kidney by pindolol and propranolol.
Topics: Animals; Female; Kidney; Kidney Cortex; Kidney Medulla; Male; Necrosis; Pindolol; Propranolol; Rats; Vasopressins | 1974 |
Left gastric artery embolization for control of gastric bleeding: a complication.
Topics: Aged; Angiography; Blood Transfusion, Autologous; Humans; Intubation, Gastrointestinal; Ischemia; Male; Necrosis; Peptic Ulcer Hemorrhage; Stomach; Stomach Diseases; Stomach Ulcer; Vasopressins | 1973 |
Pitressin and gastric ultrastructure.
Topics: Animals; Cortisone; Drug Synergism; Edema; Gastric Juice; Gastric Mucins; Gastric Mucosa; Microscopy, Electron; Necrosis; Pepsin A; Peptic Ulcer; Peptic Ulcer Hemorrhage; Rabbits; Vasoconstrictor Agents; Vasopressins | 1970 |
Cross-resistance between agents which condition for acute necrosis.
Topics: Acetates; Adaptation, Physiological; Animals; Cross Reactions; Female; Histamine; Histamine Release; Injections, Intravenous; Kaolin; Mast Cells; Necrosis; p-Methoxy-N-methylphenethylamine; Polymyxins; Polysaccharides; Rats; Serotonin; Vasopressins | 1969 |
Diabetes insipidus syndrome in hypopituitarism of pregnancy. Case report and a critical review of the literature.
Topics: Adult; Age Factors; Animals; Behavior, Animal; Diabetes Insipidus; Female; Headache; Humans; Hypertonic Solutions; Hypopituitarism; Hypothalamo-Hypophyseal System; Kidney; Necrosis; Osmolar Concentration; Oxytocin; Parity; Postpartum Hemorrhage; Pregnancy; Puerperal Disorders; Vasopressins; Water-Electrolyte Balance | 1969 |
Acute cutaneous necrosis following sensitization by heterologous blood.
Topics: Acetates; Animals; Blood Group Incompatibility; Blood Transfusion; Cats; Cattle; Chlorpromazine; Cricetinae; Cyproheptadine; Dogs; Dopamine; Guinea Pigs; Histamine; Humans; Necrosis; Phenoxybenzamine; Poultry; Promethazine; Rabbits; Rats; Reserpine; Skin Diseases; Swine; Vasopressins | 1967 |
Systemic vs. topical conditioning for acute necrosis.
Topics: Acetates; Animals; Dextrans; Epinephrine; Histamine; Hypersensitivity, Immediate; Kaolin; Necrosis; Norepinephrine; Polymyxins; Polysaccharides; Rats; Serotonin; Sodium Chloride; Vasopressins | 1967 |
Vasoconstrictors and experimental flaps.
Topics: Animals; Epinephrine; Lidocaine; Necrosis; Rats; Skin; Sodium Chloride; Vasopressins | 1966 |
[Role of vasopressin and corticostimulin (ACTH) in production of experimental lesions on fetal extremities (hemorrhages, necroses, congenital amputations)].
Topics: Adrenocorticotropic Hormone; Amputation, Surgical; Arginine Vasopressin; Congenital Abnormalities; Extremities; Humans; Necrosis; Vasopressins | 1951 |