pituitrin and Anemia

Concomitant anemia, heart failure, and renal disease can be seen in a large proportion of patients with heart failure. The purpose of this review is to discuss the current definitions and mechanisms involved in this pathophysiological relationship, as well as the potential management and treatment options available for these patients.. Dysfunctional heart can promote the dysfunction of the kidneys through a variety of pathophysiological mechanism, the reciprocal holds true as well. Heart failure has been considered as the most common type of cardiovascular complication seen in patients with renal failure. Central to this relationship lies anemia, which can be the result or the cause of either heart or kidney disease.. Cardiorenal syndrome is a complex condition, which requires the collaboration and resources from cardiology, cardiac surgery, nephrology, and critical care. Of great importance is recognizing the presence of cardiorenal syndrome and appreciating the impact it can play on treatment options and survival.

Topics: Adenosine; Anemia; Chronic Disease; Diuretics; Heart Failure; Hemofiltration; Humans; Kidney Failure, Chronic; Prognosis; Renin-Angiotensin System; Risk Factors; Vasodilator Agents; Vasopressins

This is a review of the management of septic shock that suggests an approach to treatment (ABCDEF: Airway, Breathing, Circulation, Drugs, Evaluate the source of sepsis, Fix the source of sepsis) for clinicians. The incidence of septic shock is increasing and mortality ranges from 30% to 70%. The commonest sources of infection are lung (25%), abdomen (25%), and other sources. Septic shock occurs because of highly complex interactions between the infecting microorganism(s) and the responses of the human host. The innate immune response is rapidly followed by the more specific adaptive immune response. Septic shock is characterized by alterations in the coagulant/anticoagulant balance such that there is a more pro-coagulant phenotype. Lung protective ventilation (which means the use of relatively low tidal volumes of 4 -6 mL/kg ideal body weight) is recommended for treatment of patients who have septic shock. Rivers early goal-directed therapy is recommended because it showed a significant increase in survival. Surviving Sepsis guidelines recommend resuscitation of septic shock with either crystalloid or colloid. Patients who have septic shock should be treated with intravenous broad-spectrum antibiotics as rapidly as possible and certainly within one hour. Activated protein C (APC) is a vitamin K dependent serine protease that is an anticoagulant and is also cytoprotective and anti-inflammatory. APC (24 mg/kg/hour infusion for 96 hours) decreased mortality (APC 25% vs placebo 31%, relative risk 0.81P=0.005) and improved organ dysfunction in patients at high risk of death (e.g. APACHE II >25 [APC 31% vs placebo 44%]). APC is not recommended to treat surgical patients who have one organ system dysfunction. In 2006, the European regulatory authority indicated that there must be another randomized placebo-controlled trial of APC to further establish efficacy as assessed by mortality reduction. Vasopressin is a key stress hormone in response to hypotension. The VASST study was a randomized trial of vasopressin versus norepinephrine in septic shock. There was no difference in mortality between vasopressin versus norepinephrine-treated patients (35% versus 39% respectively). In patients who had less severe septic shock, patients treated with vasopressin may have lowered mortality compared with norepinephrine (26% vs 36%). Annane et al. found that hydrocortisone plus fludrocortisone (compared to placebo) was associated with lower mortality in patients who had an in

Topics: Adrenal Cortex Hormones; Anemia; Anti-Bacterial Agents; Anticoagulants; Blood Coagulation; Fluid Therapy; Humans; Hyperglycemia; Hypoglycemic Agents; Insulin; Protein C; Renal Insufficiency; Shock, Septic; Vasopressins

Topics: Adrenal Cortex Hormones; Anemia; Anti-Bacterial Agents; Blood Coagulation Factors; Humans; Hyperglycemia; Hypoglycemic Agents; Immune Tolerance; Insulin; Protein C; Renal Replacement Therapy; Respiration, Artificial; Sepsis; Vasopressins

Topics: Adrenal Cortex Hormones; Androgens; Anemia; Angiotensin II; Chemical Phenomena; Chemistry; Cobalt; Cyclic AMP; Erythropoiesis; Erythropoietin; Humans; Juxtaglomerular Apparatus; Kidney; Nervous System Physiological Phenomena; Norepinephrine; Oxygen; Polycythemia; Prostaglandins; Serotonin; Thyroid Hormones; Vasopressins

Arginine vasopressin (AVP) made by hypothalamic neurons is released into the circulation to stimulate water resorption by the kidneys and restore water balance after blood loss. Patients who lack this antidiuretic hormone suffer from central diabetes insipidus. We observed that many of these patients were anemic and asked whether AVP might play a role in red blood cell (RBC) production. We found that all three AVP receptors are expressed in human and mouse hematopoietic stem and progenitor cells. The AVPR1B appears to play the most important role in regulating erythropoiesis in both human and mouse cells. AVP increases phosphorylation of signal transducer and activator of transcription 5, as erythropoietin (EPO) does. After sublethal irradiation, AVP-deficient Brattleboro rats showed delayed recovery of RBC numbers compared to control rats. In mouse models of anemia (induced by bleeding, irradiation, or increased destruction of circulating RBCs), AVP increased the number of circulating RBCs independently of EPO. In these models, AVP appears to jump-start peripheral blood cell replenishment until EPO can take over. We suggest that specific AVPR1B agonists might be used to induce fast RBC production after bleeding, drug toxicity, or chemotherapy.

Topics: Anemia; Animals; Cell Differentiation; Cell Proliferation; Erythrocytes; Humans; Mice; Rats; Receptors, Vasopressin; Vasopressins

Topics: Africa, Eastern; Albumins; Anemia; Child; Coma; Critical Illness; Developing Countries; Dose-Response Relationship, Drug; Drug Administration Schedule; Fever; Fluid Therapy; Humans; Meningitis, Bacterial; Pneumonia; Randomized Controlled Trials as Topic; Resuscitation; Shock; Sodium Chloride; Vasopressins

We compared changes in gastric mucosal blood flow (GMBF) and left gastric artery blood flow (LGABF) in response to pharmacological, physiological, and pathological stimuli. GMBF and LGABF were measured by the hydrogen gas clearance and perivascular ultrasonic transit time techniques, respectively, under baseline conditions and following intravenous infusion of vasopressin or pentagastrin, isovolemic hemodilution, or gastric perfusion with HCl-taurocholate. Blood flow changes following vasopressin or hemodilution were significantly larger in the left gastric artery than in the gastric mucosa. In contrast, the increment in blood flow associated with pentagastrin-stimulated acid secretion was significantly greater in the gastric mucosa than in the extramural artery. Barrier disruption with acid-taurocholate induced similar changes in both measurement sites. The gastric hyperemia induced by either mechanism was significantly attenuated by blockade of NO synthesis. These data demonstrate that although functional changes in GMBF are primarily supported by changes in blood flow at the extramural gastric arteries, the gastric mucosal microvasculature is also under the influence of independent local control mechanisms.

Topics: Anemia; Animals; Arteries; Female; Gastric Acid; Gastric Mucosa; Hemodilution; Hydrogen; Hyperemia; Male; NG-Nitroarginine Methyl Ester; Nitric Oxide; Pentagastrin; Rats; Rats, Sprague-Dawley; Regional Blood Flow; Stomach; Taurocholic Acid; Ultrasonography; Vasoconstrictor Agents; Vasopressins

The aim of the study was to assess whether changes in gastric mucosal blood flow induced by acute normovolaemic anaemia influence the susceptibility of the gastric mucosa to ethanol-induced damage, and the relationship of these changes with nitric oxide biosynthesis. Acute normovolaemic anaemia, promoted by exchanging 3 ml of blood by a plasma expander, induced a significant increase in gastric mucosal blood flow measured by hydrogen gas clearance, without changes in arterial blood pressure. After intragastric 60% ethanol administration, gastric blood flow was still significantly higher in anaemic than in control rats, and this was associated with a lower macroscopic and microscopic gastric damage. Following ethanol administration, anaemic rats pretreated with an inhibitor of nitric oxide biosynthesis (L-NMMA, 50 mg/kg, i.v.) had a lower gastric blood flow and a higher macroscopic gastric damage than anaemic rats without pretreatment. Anaemic rats pretreated with vasopressin also had after ethanol administration a lower gastric blood flow and a higher macroscopic gastric damage. It is concluded that acute normovolaemic anaemia protects the gastric mucosa against damage induced by intragastric ethanol. The inhibition of nitric oxide biosynthesis reverts in part this protective effect, and this seems to be related with the capability of nitric oxide to increase gastric mucosal blood flow, since vasoconstriction by a nitric oxide-independent mechanism causes a similar effect.

Topics: Anemia; Animals; Arginine; Blood Flow Velocity; Ethanol; Gastric Mucosa; Gastrointestinal Diseases; Male; Nitric Oxide; omega-N-Methylarginine; Rats; Rats, Sprague-Dawley; Vasopressins

This study investigated the accuracy of laser-Doppler flowmetry (LDV) and reflectance spectrophotometry (RS) measurements as an index of blood flow in the gastric mucosa of the rat, in experimental conditions such as pharmacologically induced vasoconstriction, hypoxia, hyperoxia, and acute normovolemic anemia. Hydrogen gas clearance was used as a reference method. After vasopressin infusion, LDV signal and indexes of hemoglobin (IHb) and oxygen (ISO2) content in the gastric mucosa estimated by RS significantly decreased in parallel with the reduction of gastric mucosal blood flow (GMBF). Neither hypoxia (5% O2 administration) nor hyperoxia (100% O2) affected GMBF or LDV signal. However, both IHb and ISO2 significantly decreased or increased after hypoxia or hyperoxia, respectively. Acute normovolemic anemia induced a significant increase in GMBF, while LDV signal and ISO2 remained unchanged. IHb significantly decreased in linear relationship with the decrements in the hematocrit. It is concluded that 1) in pharmacologically induced GMBF changes, LDV and RS correlate with GMBF; 2) when changes in hemoglobin saturation are induced, LDV but not RS reflects GMBF; and 3) in acute normovolemic anemia, neither LDV nor RS reflects changes in GMBF.

Topics: Anemia; Animals; Evaluation Studies as Topic; Gastric Mucosa; Hypoxia; Laser-Doppler Flowmetry; Male; Oxygen; Rats; Rats, Sprague-Dawley; Regional Blood Flow; Spectrophotometry; Vasopressins

Topics: Anemia; Angiography; Celiac Artery; Colonic Diseases; Contrast Media; Gastrointestinal Hemorrhage; Humans; Intestinal Neoplasms; Melena; Mesenteric Arteries; Time Factors; Vasopressins

Topics: Aldosterone; Anemia; Anuria; Child; Child, Preschool; Diuresis; Diuretics; Glomerulonephritis; Humans; Infant; Kidney; Kidney Concentrating Ability; Kidney Diseases; Osmolar Concentration; Osmotic Pressure; Polyuria; Pyelonephritis; Thalassemia; Vasopressins; Water; Water-Electrolyte Balance

Topics: Adolescent; Anemia; Anemia, Sickle Cell; Black People; Body Weight; Child; Dehydration; Humans; Urine; Vasopressins; Water-Electrolyte Balance

Topics: Adolescent; Anemia; Appendectomy; Appendicitis; Blood Chemical Analysis; Child; Colonic Diseases; Hernia, Inguinal; Humans; Hypersplenism; Infant; Intestinal Obstruction; Intussusception; Jaundice; Jaundice, Obstructive; Megacolon; Osteomyelitis; Sinusitis; Surgical Procedures, Operative; Thrombosis; Vasopressins; Wilms Tumor

Topics: Abdomen; Anemia; Angiotensins; Antihypertensive Agents; Blood Circulation; Bradykinin; Coronary Vessels; Ganglionic Blockers; Heart Diseases; Hypertension; Hyperthyroidism; Hypothyroidism; Liver Circulation; Niacin; Pharmacology; Polycythemia; Serotonin; Shock; Vasopressins; Xanthines

Topics: Adrenocorticotropic Hormone; Anemia; Anemia, Myelophthisic; Anti-Bacterial Agents; Ascorbic Acid; Benzene; Biopsy; Blood Transfusion; Cortisone; Female; Hematologic Diseases; Hematology; Leukemia; Liver Extracts; Mortality; Occupational Diseases; Pathology; Poisoning; Prednisolone; Prednisone; Pregnancy; Pregnancy Complications; Pregnancy Complications, Hematologic; Tetracycline; Toxicology; Vasopressins; Vitamin B 12

Topics: Anemia; Anemia, Sickle Cell; Child; Erythrocytes, Abnormal; Humans; Kidney; Potassium; Vasopressins