pituitrin and Thrombosis

Orthostatic hypertension-a condition characterized by a hyperactive pressor response to orthostatic stress-is an emerging risk factor for cardiovascular disease and is associated with hypertensive target-organ damage (resulting in silent cerebrovascular disease, left ventricular hypertrophy, carotid atherosclerosis and/or chronic kidney disease) and cardiovascular events (such as coronary artery disease and lacunar stroke). The condition is also considered to be a form of prehypertension as it precedes hypertension in young, normotensive adults. Orthostatic blood pressure changes can be assessed using orthostatic stress tests, including clinic active standing tests, home blood pressure monitoring and the head-up tilting test. Devices for home and for ambulatory blood pressure monitoring that are equipped with position sensors and do not induce a white-coat effect have increased the sensitivity and specificity of diagnosis of out-of-clinic orthostatic hypertension. Potential major mechanisms of orthostatic hypertension are sympathetic hyperactivity (as a result of hypersensitivity of the cardiopulmonary and arterial baroreceptor reflex) and α-adrenergic hyperactivation. Orthostatic hypertension is also associated with morning blood pressure surge and extreme nocturnal blood pressure dipping, both of which increase the pulsatile haemodynamic stress of central arterial pressure and blood flow in patients with systemic haemodynamic atherothrombotic syndrome.

Topics: Age Factors; Arteriosclerosis; Blood Pressure Monitoring, Ambulatory; Blood Volume; Brain Infarction; Cardiovascular Diseases; Diabetes Mellitus; Hemodynamics; Humans; Hypertriglyceridemia; Hypotension, Orthostatic; Posture; Prehypertension; Receptors, Adrenergic, alpha; Renal Insufficiency, Chronic; Risk Factors; Sympathetic Nervous System; Thrombosis; Tilt-Table Test; Vasopressins; Ventricular Remodeling

Vasopressin analogues are increasingly used for haemodynamic support of catecholamine-refractory, hyperdynamic septic shock. Arginine vasopressin (AVP) and terlipressin (TP) effectively increase mean arterial pressure and reduce catecholamine requirements in this condition. However, the use of either of the drugs may be linked to relevant haemodynamic side effects, including reductions in cardiac output, oxygen delivery and mixed-venous oxygen saturation. These alterations may result in impaired tissue perfusion and foster the genesis of ischemic tissue injury. In addition, decreases in platelet count and increases in aminotransferases activity and bilirubin concentration have been reported with the use of V1 agonists. However, it remains unclear whether these changes are of clinical relevance. This review article summarizes the previous data on adverse effects related to the therapy with vasopressin analogues and discusses potential options to prevent such adverse events. In summary, continuous TP infusion appears to be superior to bolus infusion. Maximum doses of 0.03 (-0.067) U min(-1) of AVP or 2 microg kg(-1) h(-1) of TP, respectively, should not be exceeded. Aggressive fluid therapy may prevent adverse haemodynamic effects linked to infusion of either AVP or TP. Finally, platelet count, surrogate variables of hepatic dysfunction, electrolytes and osmolality should be strictly monitored in patients treated with vasopressin analogues.

Topics: Animals; Chemical and Drug Induced Liver Injury; Humans; Ischemia; Kidney Diseases; Lypressin; Shock; Skin; Terlipressin; Thrombosis; Vasoconstrictor Agents; Vasopressins; Water-Electrolyte Imbalance

Topics: Administration, Oral; Adrenocorticotropic Hormone; Clofibrate; Epinephrine; Fibrinolysis; Fibrinolytic Agents; Humans; Hypoglycemic Agents; Testosterone; Thrombosis; Vasopressins

Topics: Accidents, Traffic; Acidosis; Acute Kidney Injury; Adult; Aged; Alkalosis; Aortic Diseases; Aortic Rupture; Body Composition; Calorimetry; Cholecystectomy; Convalescence; Craniocerebral Trauma; Dehydration; Duodenal Ulcer; Endocrine Glands; Female; Homeostasis; Humans; Iliac Artery; Infusions, Parenteral; Kidney; Lung Neoplasms; Male; Metabolism; Middle Aged; Natriuresis; Pancreatitis; Peptic Ulcer Perforation; Postoperative Care; Postoperative Complications; Thoracic Injuries; Thrombosis; Vasopressins; Water-Electrolyte Balance

Our previous data showed that the pancreatitis induced in rats by cerulein develops into hemorrhagic pancreatitis following water-immersion stress. The present study examined the effects of water-immersion stress and high doses of cerulein (intraperitoneal injection) on pancreatic blood flow. Five hours of water-immersion stress reduced the local pancreatic blood flow to approximately 30% of the initial value (253.75 +/- 12.58 ml/min/100 g) without causing any histological alterations. Blood flow was decreased as early as 1 h after the immersion and reached the lowest value (30% of initial value) 3 h after the immersion. The administration of 40 micrograms/kg body wt cerulein as two intraperitoneal injections reduced the pancreatic blood flow by 40% 5 h after the first cerulein injection. The injections of cerulein combined with water-immersion stress did not reduce the pancreatic blood flow more than did water-immersion stress alone. The systemic blood pressure was unaffected during 5 h of water immersion after the cerulein injections. These findings suggest that in rats the stress-induced decrease of local pancreatic blood flow may not produce pancreatitis, but may aggravate an existing acute pancreatitis.

Topics: Amylases; Animals; Capillaries; Dopamine; Endothelium, Vascular; Hemorrhage; Male; Organ Size; Pancreas; Pancreatitis; Rats; Rats, Sprague-Dawley; Regional Blood Flow; Stress, Physiological; Thrombosis; Vasopressins

Topics: Blood Loss, Surgical; Coronary Artery Bypass; Humans; Myocardial Infarction; Thrombosis; Vasopressins

In a series of 602 consecutive sclerotherapies, two cirrhotic patients who had received successful sclerotherapy for control of variceal bleeding while on vasopressin infusions developed mesenteric thrombosis. We found no other cases (in our institution or in literature review) where sclerotherapy or vasopressin infusion alone precipitated mesenteric thrombosis. During vasopressin infusion, there is portal stasis and an increased caudad flow of sclerosant. We suggest that mesenteric thrombosis is a consequence of the combination of these two effects. Direct injection of gastric varices is difficult because of increased postsclerotherapy bleeding, but sclerosis of esophageal varices often leads to their obliteration by the caudad flow of sclerosant. We propose, therefore, that vasopressin infusion during esophageal sclerotherapy may be beneficial in the obliteration of gastric varices. We conclude that (a) in patients without gastric varices, vasopressin infusion increases the incidence of mesenteric thrombosis, and (b) vasopressin infusion during sclerotherapy may enhance the sclerosis of gastric varices.

Topics: Adult; Aged; Esophageal and Gastric Varices; Female; Gastrointestinal Hemorrhage; Humans; Liver Cirrhosis; Male; Mesenteric Vascular Occlusion; Mesenteric Veins; Portal System; Sclerosing Solutions; Thrombosis; Vasopressins

We report the occurrence of acute portal vein thrombosis in three patients undergoing endoscopic variceal sclerosis (EVS) for bleeding esophageal varices. All patients received intravenous vasopressin in close proximity to or at the time of EVS. By increasing flow of sclerosant caudally into gastric veins during EVS, vasopressin may predispose to retrograde propagation of thrombus into the portal venous system. Combined use of vasopressin and EVS for treatment of bleeding esophageal varices should be undertaken with caution.

Topics: Acute Disease; Esophageal and Gastric Varices; Gastrointestinal Hemorrhage; Humans; Male; Mesenteric Vascular Occlusion; Mesenteric Veins; Middle Aged; Portal Vein; Sclerosing Solutions; Thrombosis; Vasopressins

Topics: Acute Disease; Humans; Portal Vein; Sclerosing Solutions; Thrombosis; Transfusion Reaction; Vasopressins

Vasopressin infusions in normal volunteers that produce concentrations in plasma comparable to those seen during stress, cause an increase in plasma factor VIII and shortening of the euglobulin clot lysis time (ECLT). We have investigated the relationship between endogenous vasopressin (aVP) release and haemostatic function in 7 patients undergoing major abdominal surgery. Blood samples were taken at nine intervals during the operative procedure. Plasma aVP levels peaked at median values of 51 pg/ml during bowel manipulation and remained elevated on the first post-operative day. Following, and in close temporal relationship with the rise in aVP there were increases in factor VIII coagulant activity, the ristocetin co-factor, von Willebrand antigen, plasminogen activator activity (10(6)/ECLT2) and fibrinopeptide A concentrations with shortening of the activated partial thromboplastin time. The relationship was similar to that seen following infusion of aVP in human volunteers. The results are consistent with the hypothesis that aVP is an important mediator of changes in haemostatic function which accompany stress and might contribute to the thrombotic risk associated with surgical operations.

Topics: Blood Coagulation; Factor VIII; Fibrinogen; Hemostasis; Humans; Plasminogen Activators; Postoperative Complications; Thrombosis; Vasopressins

A patient bleeding from oesophageal varices in whom injection sclerotherapy failed to control bleeding required peripheral vein vasopressin infusion for a total of five days. Three days after stopping the infusion she collapsed and died. Post mortem examination showed the cause of death to be intestinal infarction resulting from superior mesenteric and portal vein thrombosis. This complication has not previously been described in association with vasopressin infusion into peripheral veins. The duration of each infusion should be minimised and blood volume should be carefully monitored throughout. The condition should be suspected in patients who develop unexplained abdominal pain or collapse following vasopressin treatment.

Topics: Aged; Esophageal and Gastric Varices; Female; Gastrointestinal Hemorrhage; Humans; Infarction; Infusions, Parenteral; Intestines; Mesenteric Vascular Occlusion; Mesenteric Veins; Portal Vein; Thrombosis; Vasopressins

Hypernatraemic states are associated with an increased risk of thrombosis. To examine the relative contributions of sodium and vasopressin, we infused hypertonic saline in 11 male volunteers and measured the effect on factor VIII (FVIII), euglobulin clot lysis time (ELT) and fibrinopeptide A (FPA) generation. Samples were taken pre-infusion, hourly during a 3h infusion of 450 ml 6M saline and one hour after the infusion had stopped. Mean plasma osmolality (SEM) rose from 287(0.7) to 302(10) mOsm after 3h (p less than 0.01). Plasma vasopressin concentrations rose from 1.0(0.3) to 4(0.94) pg/ml over 3 hr (p 0.01). Plasminogen activator activity (10(6)/ELT2) rose from 65(10) to 372(55) units (p less than 0.001). There was a highly significant correlation between plasma osmolality and plasminogen activator activity (r = 0.5 p less than 0.0001). FPA generation time shortened from 7.2(0.4) to 5.4(0.6) min after 2h and 5.3(0.6) after 4h (n = 6). Values for FPA after 4 min incubation steadily increased from 5.8(1.2) to 14.3(4.6) pmol/ml during the infusion but differences failed to achieve statistical significance. FVIIIC (1 stage) remained constant at 75(5.5%) during the infusion. There was a small and statistically insignificant increase in FVIII RiCof after 3h and FVIII RAg decreased slightly. The results suggest that hypernatraemia and increasing plasma aVP concentrations produce changes in haemostatic function consistent with a hypercoaguable state. The mechanisms for the effect are unclear. These changes in haemostatic function might contribute to the thrombo-embolic complications of conditions such as hyperosmolar coma in diabetes mellitus or severe heatstroke in which degrees of hypernatraemia occur.

Topics: Factor VIII; Fibrinolysis; Humans; Hypernatremia; Kinetics; Male; Osmolar Concentration; Risk; Saline Solution, Hypertonic; Serum Globulins; Sodium Chloride; Thrombosis; Vasopressins

Topics: Angiography; Catheterization; Gastrointestinal Hemorrhage; Humans; Infusions, Intra-Arterial; Intestine, Large; Ischemia; Ischemic Attack, Transient; Thrombosis; Vasodilator Agents; Vasopressins

We reviewed the courses of 40 patients with variceal bleeding treated with a standardized protocol, including intravenous (IV) vasopressin (Pitressin) and transhepatic embolization. Twelve of the 32 patients with acute episodes of massive variceal bleeding responded to the administration of IV vasopressin alone. Of the 20 patients who did not respond to vasopressin therapy, emergency transhepatic portography with embolization produced cessation of bleeding in ten (50%). The remaining ten patients who failed to respond to either IV vasopressin therapy or transhepatic embolization died, regardless of whether they were treated with aggressive medical therapy or emergency portosystemic shunt. Transhepatic embolization in both the emergent and elective situation demonstrated a thrombotic complication rate of 20%, which limited or precluded eventual therapy with elective portosystemic shunt. Because of this relatively high incidence of occult portal thromboses after transhepatic embolization, transhepatic portography should be obtained routinely prior to elective portosystemic shunts in those patients who have a history of transhepatic embolization.

Topics: Adult; Aged; Embolization, Therapeutic; Esophageal and Gastric Varices; Female; Gastrointestinal Hemorrhage; Hemoperitoneum; Humans; Infusions, Parenteral; Male; Middle Aged; Portal System; Radiography; Thrombosis; Vasopressins

Topics: Aged; Cavernous Sinus; Humans; Hyponatremia; Male; Phenytoin; Pituitary Diseases; Secretory Rate; Syndrome; Thrombosis; Vasopressins

Topics: Angiography; Gastrointestinal Hemorrhage; Humans; Injections, Intra-Arterial; Male; Middle Aged; Thrombosis; Vasopressins

Topics: Esophageal and Gastric Varices; Female; Gastrointestinal Hemorrhage; Humans; Ileum; Infusions, Parenteral; Intestinal Diseases; Ischemia; Jejunum; Mesenteric Arteries; Mesenteric Vascular Occlusion; Middle Aged; Thrombosis; Vasopressins

Topics: Catheterization; Esophageal and Gastric Varices; Gangrene; Gastrointestinal Hemorrhage; Hepatic Encephalopathy; Humans; Intestinal Diseases; Male; Mesenteric Arteries; Mesenteric Vascular Occlusion; Middle Aged; Portal Vein; Sepsis; Thrombophlebitis; Thrombosis; Vasopressins

Topics: Anesthesia, Intravenous; Aneurysm; Angiography; Angiotensin II; Animals; Arteriovenous Fistula; Blood Pressure Determination; Dye Dilution Technique; Hypertension; Ischemia; Kidney; Norepinephrine; Phentolamine; Punctures; Rabbits; Spectrophotometry; Thrombosis; Trimethaphan; Urinary Catheterization; Vasopressins

Topics: Alcoholism; Angiography; Autopsy; Esophageal and Gastric Varices; Fatty Liver; Gastrointestinal Hemorrhage; Humans; Hypertension, Portal; Infarction; Injections, Intra-Arterial; Intestine, Small; Liver Cirrhosis; Male; Mesenteric Arteries; Mesenteric Vascular Occlusion; Mesenteric Veins; Thrombosis; Vasopressins

Topics: Animals; Dextrans; Heparin; Histocytochemistry; Humans; Infusions, Parenteral; Kidney Function Tests; Mannitol; Molecular Weight; Sheep; Thrombosis; Vasopressins

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