Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

These experiments were done to determine the effectiveness of oncotic and oncotic/diuretic ( oncodiuretic ) therapy in dogs with experimental cerebral edema induced by a cold lesion. Dogs were divided into 3 groups and were treated for 6 h with either crystalloid (control group), a 12% hetastarch solution, or a 24% hetastarch solution plus furosemide. The cerebral effects of treatment were evaluated by intracranial pressure (ICP) measurements and by autopsy measurements of brain density and brain water content. The systemic effects were evaluated by measuring fluid balance, wedge pressure, hematocrit, free-water clearance, and serum vasopressin level. Hetastarch and hetastarch /furosemide significantly reduced ICP, increased brain density, and decreased water content of the edematous brain. Hetastarch alone caused a positive fluid balance and marked hemodilution but did not normalize vasopressin levels, whereas hetastarch /furosemide caused a marked diuresis without changing the hematocrits, and normalized vasopressin levels. Oncodiuretic therapy, in contrast to traditional fluid restriction, seems to decrease ICP effectively by causing normovolemic dehydration.
 ...
PMID:Intracranial and systemic effects of hetastarch in experimental cerebral edema. 620 63

Allogeneic blood resuscitation is the treatment of choice for hemorrhagic shock. When blood is unavailable, plasma expanders, including crystalloids, colloids, and blood substitutes, may be used. Another treatment modality is vasopressin, a vasoconstrictor administered to redistribute blood flow, increase venous return, and maintain adequate cardiac output. While much information exists on systemic function and oxygenation characteristics following treatment with these resuscitants, data on their effects on the microcirculation and correlation of real-time microvascular changes with changes in systemic function and oxygenation in the same animal are lacking. In this study, real-time microvascular changes during hemorrhagic shock treatment were correlated with systemic function and oxygenation changes in a canine hemorrhagic shock model (50-55% total blood loss with a MAP of 45-50 mmHg as a clinical criterion). Following splenectomy and hemorrhage, the dogs were assigned to five resuscitation groups: autologous/shed blood, hemoglobin-based oxygen carrier/Oxyglobin, crystalloid/saline, colloid/Hespan (6% hetastarch), and vasopressin. Systemic function and oxygenation changes were continuously monitored and periodically measured (during various phases of the study) using standard operating room protocols. Computer-assisted intravital video-microscopy was used to objectively analyze and quantify real-time microvascular changes (diameter, red-cell velocity) in the conjunctival microcirculation. Measurements were made during pre-hemorrhagic (baseline), post-hemorrhagic (pre-resuscitation), and post-resuscitation phases of the study. Pre-hemorrhagic microvascular variables were similar in all dogs (venular diameter = 42+/-4 microm, red-cell velocity = 0.55+/-0.5 mm/sec). All dogs showed significant (P < 0.05) post-hemorrhagic microvascular changes: approximately 20% decrease in venular diameter and approximately 30% increase in red-cell velocity, indicative of sympathetic effects arising from substantial blood loss. Microvascular changes correlated with post-hemorrhagic systemic function and oxygenation changes. All resuscitation modalities except vasopressin restored microvascular and systemic function changes close to pre-hemorrhagic values. However, only autologous blood restored oxygenation changes to pre-hemorrhagic levels. Vasopressin treatment resulted in further decreases in venular diameter (approximately 50%) as well as red-cell velocity (approximately 70%) without improving cardiac output. Our results suggested that volume replenishment - not oxygen-carrying capability - played an important role in pre-hospital/en route treatment for hemorrhagic shock. Vasopressin treatment resulted in inadvertent detrimental outcome without the intended benefit.
 ...
PMID:Comparison of treatment modalities for hemorrhagic shock. 1745 3

Chronic kidney disease (CKD) often accompanies cardiovascular complications, causing postoperative morbidity and even mortality. Since fluid and electrolyte homeostasis is deregulated in CKD patients, fluid therapy itself may cause postoperative morbidity. Recent studies have shown that forced diuresis through fluid overload offers no renoprotective effect and instead has harmful consequences. Fluid overload should be avoided, and the volume load should be used as the rationale for controlling hemodynamics. The emerging concept of a "zero-fluid balance policy" may be beneficial even for CKD patients. Hydroxyethylstarch might not be preferentially used for CKD patients. Hydroxyethylstarch is not contraindicated for CKD patients except in cases with long-term accumulation caused by increased vascular permeability, such as cases with sepsis, as long as an efficient volume expansion is beneficial to the patient. The regulation of renal function through the endocrine system (i.e., renin-angiotensin-aldosterone and vasopressin) is a key target for protecting the kidney in CKD. The recent development of a receptor blocker targeting these endocrine systems may be beneficial for correcting the fluid balance caused by excess intraoperative fluid therapy. The main issue for fluid therapy in surgical CKD patients may not be the quantity of fluid, but rational intervention affecting the endocrine system.
 ...
PMID:[Perioperative fluid therapy for surgical patients with chronic kidney disease]. 2436 71