ascorbic-acid and Blood-Coagulation-Disorders

The human organism is incapable of producing vitamin C by biosynthesis. We are therefore totally dependent on the presence of this vitamin in our diet. Vitamin C is capable of essentially influencing the course of many metabolic processes, and it is therefore used in the treatment and prophylaxis of many diseases, including those that are a consequence of the activity of the so-called reactive forms of oxygen. The presence of vitamin C in the anti-oxidant protective system is believed to be very important, since it can react with the free radicals of oxygen and other oxidants, and "sweep" them away. Therefore, attention is more and more frequently focused on the possibility of using vitamin C in the treatment of those circulatory diseases that are believed to be associated with the action of free radicals. Routine administration of vitamin C should be therefore recommended in the treatment of patients with coronary arterial disease, treatment of patients after cardiac infarction or cerebral stroke, or in the treatment of arterial hypertension.

Topics: Antioxidants; Ascorbic Acid; Blood Coagulation Disorders; Cardiovascular Diseases; Dietary Supplements; Fruit; Humans; Magnoliopsida; Vegetables

Topics: Anemia; Ascorbic Acid; Blood Coagulation Disorders; Chronic Disease; Folic Acid; Hematologic Diseases; Hemolysis; Humans; Leukocytosis; Mononuclear Phagocyte System; Serum Albumin; Stress, Physiological; Syndrome; Thrombocytosis; Zinc

Topics: Animals; Ascorbic Acid; Aspirin; Blood Coagulation Disorders; Buffers; Dogs; Dosage Forms; Drug Synergism; Ethanol; Gastric Juice; Gastric Mucosa; Guinea Pigs; Humans; Hydrogen-Ion Concentration; Intestinal Absorption; Leukocytes; Occult Blood; Peptic Ulcer Hemorrhage; Permeability; Rabbits; Rats; Stomach Ulcer

Coagulopathy and inflammation induced by hemorrhagic shock and traumatic injury are associated with increased mortality and morbidity. Vitamin C (VitC) is an antioxidant with potential protective effects on the proinflammatory and procoagulant pathways. We hypothesized that high-dose VitC administered as a supplement to fluid resuscitation would attenuate inflammation, coagulation dysfunction, and end-organ tissue damage in a swine model of multiple injuries and hemorrhage.. Male Sinclair swine (n = 24; mean body weight, 27 kg) were anesthetized, intubated, mechanically ventilated, and instrumented for physiologic monitoring. Following stabilization, swine were subjected to shock/traumatic injury (hypothermia, liver ischemia and reperfusion, comminuted femur fracture, hemorrhagic hypotension), resuscitated with 500 mL of hydroxyethyl starch, and randomized to receive either intravenous normal saline (NS), low-dose VitC (50 mg/kg; LO), or high-dose VitC (200 mg/kg; HI). Hemodynamics, blood chemistry, hematology, and coagulation function (ROTEM) were monitored to 4 hours postresuscitation. Histological and molecular analyses were obtained for liver, kidney, and lung.. Compared with VitC animals, NS swine showed significant histological end-organ damage, elevated acute lung injury scores, and increased mRNA expression of tissue proinflammatory mediators (IL-1β, IL-8, TNFα), plasminogen activation inhibitor-1 and tissue factor. There were no statistically significant differences between treatment groups on mean arterial pressure or univariate measures of coagulation function; however, NS showed impaired multivariate clotting function at 4 hours.. Although correction of coagulation dysfunction was modest, intravenous high-dose VitC may mitigate the proinflammatory/procoagulant response that contributes to multiple organ failure following acute severe multiple injuries.. Prospective randomized controlled blinded trial study, Preclinical (animal-based).

Topics: Animals; Anti-Inflammatory Agents; Anticoagulants; Ascorbic Acid; Blood Coagulation Disorders; Disease Models, Animal; Inflammation; Male; Multiple Trauma; Random Allocation; Resuscitation; Shock, Hemorrhagic; Swine

Traumatic brain injury (TBI) and hemorrhagic shock (HS) can be associated with coagulopathy and inflammation, but the mechanisms are poorly understood. We hypothesized that a combination of TBI and HS would disturb coagulation, damage the endothelium, and activate inflammatory and complement systems.. A total of 33 swine were allocated to either TBI + HS (n = 27, TBI and volume-controlled 40% blood loss) or controls (n = 6, anesthesia and instrumentation). TBI + HS animals were left hypotensive (mean arterial pressure, 30-35 mm Hg) for 2 hours. Blood samples were drawn at baseline, 3 minutes and 15 minutes after injury, as well as following 2 hours of hypotension. Markers of coagulation, anticoagulation, endothelial activation/glycocalyx shedding, inflammation, complement, and sympathoadrenal function were measured.. The TBI + HS group demonstrated an immediate (3 minutes after injury) activation of coagulation (prothrombin fragment 1 + 2, 289 ng/mL vs. 232 ng/mL, p = 0.03) and complement (C5a, 2.83 ng/mL vs. 2.05 ng/mL, p = 0.05). Shedding of the endothelial glycocalyx (syndecan 1) was evident 15 minutes after injury (851.0 ng/ml vs. 715.5 ng/ml, p = 0.03) while inflammation (tumor necrosis factor α [TNF-α], 81.1 pg/mL vs. 50.8 pg/mL, p = 0.03) and activation of the protein C system (activated protein C, 56.7 ng/mL vs. 26.1 ng/mL, p = 0.01) were evident following the 2-hour hypotension phase.. The combination of TBI and shock results in an immediate activation of coagulation and complement systems with subsequent endothelial shedding, protein C activation, and inflammation.

Topics: Animals; Ascorbic Acid; Blood Coagulation Disorders; Brain Injuries; Complement Activation; Disease Models, Animal; Endothelium; Female; Fibrinolysis; Hemorrhage; Inflammation; Shock, Hemorrhagic; Swine

Topics: Adult; Aged; Aged, 80 and over; Anticoagulants; Ascorbic Acid; Blood Coagulation; Blood Coagulation Disorders; Chromatography, High Pressure Liquid; Dietary Supplements; Female; Humans; Male; Middle Aged; Stereoisomerism; Warfarin

The results of a complex investigation of the system of hemostasis in 14 women with Poland's syndrome have shown combined thrombocytic-coagulational disorders, symptoms of hypocoagulation. The functional properties were impaired against the background of the normal or moderately reduced number of thrombocytes. The data of examination, case history and results of investigation of the hemostasis system show the Poland syndrome to be a variant of mesenchymal dysplasias. Changes in a number of the indices of the thrombocytic link of hemostasis depend on the degree of the deformity. The scheme of preoperative medicamental correction has been mastered. The results of a control hemostasiological investigation have shown an improvement of hemostatic properties of the clot, normalization of the adhesive and aggregational properties of thrombocytes. Minimal hemorrhage from soft tissues was noted in operative procedures after medicamental pretreatment.

Topics: Adolescent; Adult; Aminocaproates; Ascorbic Acid; Blood Coagulation Disorders; Blood Coagulation Tests; Data Interpretation, Statistical; Ethamsylate; Female; Flavonoids; Hemostasis; Hemostatics; Humans; Poland Syndrome; Preoperative Care; Vitamin A

The authors analyze the results of examinations and treatment of 125 patients, suffering from juvenile uterine bleedings, divided into three age groups and subgroups with different status of the hemostasis. They consider the suggested complex of drug therapy as an additional diagnostic test for the detection of the underlying pathogenetic component of such bleedings and recommend a pathogenetically-based hemostasis and adequate therapy to regulate menstrual function.

Topics: Adolescent; Ascorbic Acid; Blood Coagulation Disorders; Calcium Gluconate; Child; Female; Genital Diseases, Female; Glucocorticoids; Hemostasis; Humans; Menstruation Disturbances; Puberty

Topics: Antifibrinolytic Agents; Ascorbic Acid; Blood Coagulation Disorders; Hemostatics; Humans; Liver Cirrhosis; Vitamin K

Topics: Adenosine Triphosphate; Arteriosclerosis; Ascorbic Acid; Blood Coagulation Disorders; Fibrinolytic Agents; Heparin; Humans; Inositol; Nicotinic Acids; Thrombosis

Topics: Adrenocorticotropic Hormone; Ascorbic Acid; Blood Coagulation Disorders; Diagnosis; Drug Therapy; Fibrinolysis; Humans; Ischemia; Necrosis; Pathology; Prednisone; Promethazine; Purpura; Purpura Fulminans; Tetracycline

Topics: Adrenocorticotropic Hormone; Ascorbic Acid; Blood Coagulation Disorders; Diagnosis; Drug Therapy; Fibrinolysis; Humans; Ischemia; Necrosis; Pathology; Prednisone; Promethazine; Purpura; Purpura Fulminans; Tetracycline

Topics: Ascorbic Acid; Blood Coagulation Disorders; Blood Protein Disorders; Cold Temperature; Cryoglobulinemia; Cysteamine; Dicumarol; Fibrinogen; Humans; Penicillin G; Penicillins; Pyridoxine; Sulfhydryl Compounds; Telangiectasis