deamino-arginine-vasopressin and Edema

To evaluate the effect of idiopathic orthostatic edema and the effect of thyrotoxicosis on weight fluctuation and fluid retention in the presence of surgically induced panhypopituitarism and diabetes insipidus controlled with hormone replacement.. Dextroamphetamine sulfate was used for weight gain when no other etiologic factor was found. Methimazole was used when weight loss occurred when serum T4 and free T4 indicated thyrotoxicosis.. Sympathomimetic amine therapy very effectively controlled the weight gain and methimazole controlled the weight loss.. Hypopituitarism and diabetes insipidus controlled with hormone replacement do not protect against fluid retention from idiopathic edema.

Topics: Antidiuretic Agents; Antithyroid Agents; Deamino Arginine Vasopressin; Dextroamphetamine; Diabetes Insipidus; Edema; Female; Humans; Hypopituitarism; Methimazole; Middle Aged; Posture; Sympathomimetics; Thyrotoxicosis; Weight Gain; Weight Loss

There is ongoing discussion regarding the mechanisms underlying edema formation in nephrotic syndrome (NS). Many studies published in the last decade reported that primary renal sodium retention was a major factor in edema formation. However, many of the factors influencing edema formation in NS remain unclear, including the role of arginine vasopressin (AVP).. We report a 12-year-old boy with steroid-dependent NS complicated by idiopathic central diabetes insipidus (CDI). He did not develop edema during his first relapse of NS after developing CDI, despite having hypoalbuminemia. He had polydipsia, polyuria, low urine osmolality, and a low serum arginine AVP level. His fractional excretion of sodium was only slightly low. Endocrinological testing and magnetic resonance imaging revealed idiopathic CDI. After starting desmopressin therapy, he developed edema when his NS relapsed.. This is the first known reported case of NS in a patient with CDI. The findings suggest that appropriate AVP secretion in response to an increase in serum osmolality caused by renal sodium retention is necessary for excess extracellular fluid accumulation in NS. Further investigation is needed to more fully understand the role of AVP in edema formation in NS.

Topics: Anti-Inflammatory Agents; Arginine Vasopressin; Child; Deamino Arginine Vasopressin; Diabetes Insipidus, Neurogenic; Edema; Humans; Male; Nephrotic Syndrome; Prednisolone; Water Deprivation

Although fragrances are often used in aromatherapy for the treatment of edema, few studies on their diuretic and/or antiedematous activities have been performed. In this study, the effects of four types of fragrant ingredients (d-limonene, piperitone, alpha-pinene, and cinnamaldehyde) were examined in a mouse model of fluid retention. The mice were loaded with water after treatment with desmopressin (an antidiuretic hormone). In addition, zingerone, a pungent component of ginger which is considered to be effective in the treatment of edema, was examined. Moreover, their effects were compared with those of furosemide, a representative diuretic. Among the five types of fragrant ingredients examined, all except for cinnamaldehyde increased the urine volume in the fluid retention mouse model when administered at a dose of 100 mg/kg. In particular, d-limonene and zingerone significantly increased the urine volume. Thus the effects of these two ingredients were further examined at lower doses of 10 and 30 mg/kg. d-Limonene significantly increased the urine volume in a dose-dependent manner. Zingerone resulted in a significant increase in the urine volume only at a dose of 30 mg/kg. In normal mice, d-limonene did not affect the urine volume at the same doses. In contrast, zingerone significantly increased the urine volume in normal mice at a dose of 30 mg/kg. Furosemide significantly increased the urine volume in both the fluid-retentive and normal mice. These results indicate that both d-limonene and zingerone exhibit diuretic actions; however, the former fragrance only exerted an action in the fluid-retentive state. This different action suggests that d-limonene might be promising for the treatment of edema.

Topics: Animals; Aromatherapy; Cyclohexenes; Deamino Arginine Vasopressin; Disease Models, Animal; Diuretics; Dose-Response Relationship, Drug; Edema; Furosemide; Guaiacol; Limonene; Male; Mice; Mice, Inbred Strains; Terpenes

Topics: Aminocaproic Acid; Blood Transfusion; Deamino Arginine Vasopressin; Edema; Factor VII Deficiency; Factor VIIa; Hemostatics; Humans; Liver Cirrhosis, Alcoholic; Male; Middle Aged; Postoperative Hemorrhage; Recombinant Proteins; Shock; Tooth Extraction; Vitamin K

Different morphologic and density classes of sickle cells (SS) may play distinct roles in the generation of vasoocclusion, explaining the complexity of this phenomena. The densest SS red blood cells (RBCs) (SS4) can induce vasoocculsion in ex vivo microcirculatory preparations as well as in an intact animal model. Previous studies of the interaction of SS deformable discocytes with endothelial monolayers or the rat ex vivo mesocecum preparation have shown adhesion that is desmopressin (dDAVP)-stimulated, von Willebrand factor (vWF)-mediated, and limited to the small venules. However, in vivo adhesion of SS RBCs to the endothelium has neither been demonstrated nor characterized; and, in particular, the relation of adhesion to vasoocclusion is unknown. Using an intact animal model that involves injecting saline-washed, density-defined SS RBCs into the femoral artery of a rat, we find that: (1) Quantitative studies of RBCs retained in the rat thigh using 99mTc-labeled RBCs and gamma camera imaging showed that dDAVP induces a threefold increase in retention of normal (AA) cells and deformable SS discocytes (SS2). (2) electron microscopy and Microfil injection show that the retention of SS2 cells is due to adhesion to the vascular endothelium with no evidence of obstruction. (3) H-1 magnetic resonance imaging showed that retention of SS4 cells induced a dose-dependent increase in tissue edema (presumable secondary to tissue hypoxia), while retention of AA or SS2 cells produced no change. We conclude that endothelial adhesion of deformable SS discocytes can be demonstrated in an in vivo animal model, that this adhesion is enhanced by dDAVP (presumably related to, but not necessarily limited to the release of vWF), and that this phenomenon per se does not lead to vasoocclusion. Nevertheless, adhesion of deformable SS discocytes may have consequences. We hypothesize that adhesion of SS discocytes could narrow the lumen of postcapillary venules and facilitate secondary trapping of SS4 cells and lead to subsequent vasoocclusion.

Topics: Anemia, Sickle Cell; Animals; Cell Adhesion; Deamino Arginine Vasopressin; Edema; Endothelium, Vascular; Erythrocytes; Female; Humans; Microcirculation; Microscopy, Electron, Scanning; Rats; Rats, Inbred Strains; Vascular Diseases