Gene/Protein Disease Symptom Drug Enzyme Compound
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 28,634 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The case is reported of a 44-year-old European who was bitten on the foot in Djibouti, probably by an African viper. Unusually, there wasn't any pain, nor any cardiovascular collapse nor any local swelling. An oedema of the lower limb started the day afterwards. Two days after the bite, the patient presented a generalized haemorrhagic syndrome, which led to his admission. There was a consumption of fibrinogen and prothrombin, without any decrease in the platelet count. Heparin was started (100 IU.kg-1.day-1), as well as fluid replacement (albumin, fresh frozen plasma, packed red cells). This allowed him to be transferred to France, where he arrived in anuria, with hyperpyrexia, and severe lower limb oedema and a haemorrhagic syndrome. There was a major extensive retroperitoneal haematoma spreading to the perineum. The four limbs were ischaemic. The patient's condition continued to worsen, developing hypoxic pulmonary oedema. He died on the seventh day after the bite, during a session of haemodialysis, from cardiovascular failure resistant to all the usual drugs. The principles of anti-venom therapy are recalled. Indeed, this should be started early enough and relies on large amounts of serum (greater than 50 ml).
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PMID:[Fatal poisoning caused by African viper's bite (Echis carinatus)]. 144 1

It is sometimes necessary for the practitioner to transfuse the ruminant with whole blood or plasma. These techniques are often difficult to perform in practice and are time-consuming, expensive, and stressful to the animal. Acute loss of 20-25% of the blood volume will result in marked clinical signs of anemia, including tachycardia and maniacal behavior. The PCV is only a useful tool with which to monitor acute blood loss after intravascular equilibration with other fluid compartments has occurred. An acutely developing PCV of 15% or less may require transfusion. Chronic anemia with PCV of 7-12% can be tolerated without transfusion if the animal is not stressed and no further decline in erythrocyte mass occurs. Seventy-five per cent of transfused bovine erythrocytes are destroyed within 48 hours of transfusion. A transfusion rate of 10-20 ml/kg, recipient weight, is necessary to result in any appreciable increase in PCV. A nonpregnant donor can contribute 10-15 ml of blood/kg body weight at 2-4 week intervals. Sodium citrate is an effective anticoagulant, but acid citrate dextrose should be used if blood is to be stored for more than a few hours. Blood should not be stored more than 2 weeks prior to administration. Heparin is an unsuitable anticoagulant because the quantity of heparin required for clot-free blood collection will lead to coagulation defects in the recipient. Blood crossmatching is only rarely performed in the ruminant. In field situations, it is advisable to inject 200 ml of donor blood into the adult recipient and wait 10 minutes. If no reaction occurs, the rest of the blood can probably be safely administered as long as volume overload problems do not develop. Adverse reactions are most commonly seen in very young animals or pregnant cattle. Signs of blood or plasma transfusion reaction include hiccoughing, tachycardia, tachypnea, sweating, muscle tremors, pruritus, salivation, cough, dyspnea, fever, lacrimation, hematuria, hemoglobinuria, collapse, apnea, and opisthotonos. Intravenous epinephrine HCl 1:1000 can be administered (0.2 to 0.5 ml) intravenously or (4 to 5 ml) intramuscularly if clinical signs are severe. Pretreatment with antipyretics and slowing the administration rate may decrease the febrile response. Blood or plasma administered too rapidly will also result in signs of cardiovascular overload, acute heart failure, and pulmonary hypertension and edema. Furosemide and slower administration of blood or plasma should alleviate this problem.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Use of blood and blood products. 217 38

To assess myocardial lymphatics during the evolution of myocardial infarction we performed lymphangiographic studies thirty and three hundred sixty minutes after occlusion of the left anterior descending coronary artery in 92 dogs. A morphometric index was employed on a coded basis to assess the lymphangiograms. Well before myocardial necrosis was evident, at thirty minutes, a striking reduction was evident in lymphatic filling in the ischemic zone: similar changes were seen three hundred sixty minutes after occlusion. Heparin in doses that rendered blood incoagulable did not prevent the lymphatic occlusion or collapse, but they were prevented by two agents that act as cardiac lymphagogues, hyaluronidase and CLS 2210. Lymph flow from the heart was assessed in another 23 dogs. Lymph flow fell sharply after coronary artery occlusion in placebo-treated dogs but was well maintained in dogs treated with hyaluronidase and with CLS 2210. The reduction in cardiac lymphatic filling and lymph flow occurred too early to be a consequence of myocardial necrosis. To the extent that reduced lymphatic drainage allows the local accumulation of potentially toxic products, it could contribute to the local damage. Treatment with the lymphagogues not only maintained lymphatic patency but also reduced evidence of myocardial damage evident on examination by light and electron microscopy. These studies provide an alternative to commonly held concepts on how hyaluronidase reduces myocardial infarction after coronary artery occlusion and support the concept that lymphatic occlusion or collapse plays a role in myocardial infarction.
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PMID:Early disappearance of lymphatics draining ischemic myocardium in the dog. 381 24

To overcome the hemorrhagic complications that may occur during extracorporeal circulatory support for post cardiotomy shock patients, a heparinized circuit was introduced into the percutaneous cardiopulmonary support system and decreased systemically administered heparin during bypass. Heparin coated percutaneous cardiopulmonary support with low dose systemic heparinization was instituted in 13 patients (6 men and 7 women, mean age 62.2 +/- 8.5 years) who experienced circulatory collapse after cardiac surgery. Of the 13 patients, 9 could not be weaned from cardiopulmonary bypass and 4 had circulatory collapse in the operating room or in the intensive care unit. The duration of support ranged from 1 to 66 hr (mean 27.4 +/- 26.7), and the flow rate ranged from 1 to 3 L/min (2.2 +/- 0.5). An activated coagulation time of about 150 sec was maintained with or without minimal systematically administered heparin. Of the patients cannulated, 77% (10 of 13) were successfully weaned from percutaneous cardiopulmonary support and 39% (5 to 13) were long-term survivors. The causes of death were sepsis in three, progressive heart failure in three, lower leg ischemia in one, and vital infection in one. From the results of clinical or post mortem examinations, there was no massive bleeding or evidence of thromboembolism in the major organs. From observations made within 12 hr of initiation of percutaneous cardiopulmonary support, there was no significant decrease in the number of platelets, but platelet count had significantly decreased 24 hr after initiation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Heparin coated percutaneous cardiopulmonary support for the treatment of circulatory collapse after cardiac surgery. 785 34

Prevention of deep venous thrombosis is fundamental in the prevention of pulmonary embolism. Deep venous thrombosis is common after all surgical procedures, but the frequency differs, as does the effectiveness of various methods of prevention. Low-dose heparin, low molecular weight heparin, graduated compression elastic stockings, intermittent pneumatic compression, and oral anticoagulants have a role in the prevention of deep venous thrombosis, depending on the risks of deep venous thrombosis and their demonstrated effectiveness (or lack of effectiveness) in the particular circumstance. The optimal method of prophylaxis is specific to the predisposing condition. Heparin continues to be a mainstay of anticoagulant therapy. Major bleeding is rare in patients treated with low doses of heparin to prevent deep venous thrombosis. With therapeutic doses, however, major bleeding occurs in about 5% of patients. The optimal dose of warfarin and the method of evaluating the anticoagulant effect of warfarin have undergone modifications in recent years. It is now recognized that the prothrombin time ratio depends on the activity of the thromboplastin used for measuring the prothrombin time. An International Normalized Ratio, which relates to a standardized thromboplastin, has been developed, thus avoiding differences of the prothrombin time ratio that occur from batch to batch of thromboplastin reagent from the same manufacturer and that occur with different thromboplastin reagents from different animal sources and different manufacturers. The bedside diagnosis of pulmonary embolism is useful in helping a physician determine the extent to which diagnostic tests should be pursued. A sound bedside impression also contributes strongly to the formulation of a noninvasive diagnosis of pulmonary embolism. The clinical manifestations of pulmonary embolism form a recognizable constellation of findings that often lead to a correct diagnosis or exclusion of pulmonary embolism. Important clues to the diagnosis of pulmonary embolism relate to the initial syndrome. The presentation of pulmonary embolism is most often in the form of the pulmonary hemorrhage-pulmonary infarction syndrome. The next most common presentation is unexplained dyspnea, unaccompanied by pulmonary hemorrhage or infarction. Least common, but most severe, is the syndrome of circulatory collapse. Immobilization, usually caused by surgery, is the most frequent predisposing factor. Most patients with clinically recognizable pulmonary embolism have dyspnea or tachypnea. Dyspnea or tachypnea or pleuritic pain occurs in nearly all patients who have clinically apparent pulmonary embolism (97%). Ordinary tests such as the electrocardiogram and chest radiograph are helpful if the physician is attentive to nonspecific abnormalities.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Acute pulmonary embolism. 807

The authors report two cases of thrombosis occurring after partial interruption of the inferior vena cava. They presented as collapse and anuria with fatal outcome. Heparin induced thrombocytopenia was present in two cases and distal migration of filter in one case. Thrombo-embolic complications can follow heparin induced thrombocytopenia and justify first treatment with low molecular weight heparin and/or early treatment with oral anti-coagulant. Thrombosis, recurrent embolism or thrombosis of renal vena may occur after vena cava filter. Renal vena thrombosis especially follow filter movement and present as collapse and cardiac failure often with fatal outcome.
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PMID:[Heparin-induced thrombocytopenia and vena cava filter. Difficulties of treatment]. 812 Apr 65

Portable percutaneous cardiopulmonary support (PCPS) with heparin-coated circuits and a biopump was employed in a patient who had a massive pulmonary embolism with circulatory collapse after stripping of varicosities of the leg. Emergency pulmonary embolectomy was successfully performed. The main pulmonary incision was facilitated by cross-clamping of the main pulmonary arterial root. The bypass circuit was kept closed, and used with the normothermic beating heart without converting to conventional total cardiopulmonary bypass. Blood flow from the lung was removed by pump suction, stored in the reservoir, and intermittently returned to the venous circulation. Heparin was added to the circuits to keep the activated clotting time greater than 300 sec. In massive pulmonary embolism, PCPS is useful for preoperative, intraoperative, and postoperative support.
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PMID:Pulmonary embolectomy for acute massive pulmonary embolism under percutaneous cardiopulmonary support. 1022 7

It is sometimes necessary for the practitioner to transfuse the ruminant with whole blood or plasma. These techniques are often difficult to perform in practice, are time-consuming, expensive, and stressful to the animal. Acute loss of 20% to 25% of the blood volume will result in marked clinical signs of anemia, including tachycardia and maniacal behavior. The PCV is only a useful tool with which to monitor acute blood loss after intravascular equilibration with other fluid compartments has occurred. An acutely developing PCV of 15% or less may require transfusion. Chronic anemia with PCV of 7% to 12% can be tolerated without transfusion if the animal is not stressed and no further decline in erythrocyte mass occurs. Seventy-five percent of transfused bovine erythrocytes are destroyed within 48 hours of transfusion. A transfusion rate of 10 to 20 mL/kg recipient weight is necessary to result in any appreciable increase in PCV. A nonpregnant donor can contribute 10 to 15 mL of blood/kg body weight at 2- to 4-week intervals. Sodium citrate is an effective anticoagulant, but acid citrate dextrose should be used if blood is to be stored for more than a few hours. Blood should not be stored more than 2 weeks prior to administration. Heparin is an unsuitable anticoagulant because the quantity of heparin required for clot-free blood collection will lead to coagulation defects in the recipient. Blood cross-matching is only rarely performed in the ruminant. In field situations, it is advisable to inject 200 mL of donor blood into the adult recipient and wait 10 minutes. If no reaction occurs, the rest of the blood can probably be safely administered as long as volume overload problems do not develop. Adverse reactions are most commonly seen in very young animals or pregnant cattle. Signs of blood or plasma transfusion reaction include hiccoughing, tachycardia, tachypnea, sweating, muscle tremors, pruritus, salivation, cough, dyspnea, fever, lacrimation, hematuria, hemoglobinuria, collapse, apnea, and opisthotonos. Intravenous epinephrine HCl 1:1000 can be administered (0.2 to 0.5 mL) intravenously or (4 to 5 mL) intramuscularly (preferable) if clinical signs are severe. Pretreatment with antipyretics and slowing the administration rate may decrease the febrile response. Blood or plasma administered too rapidly will also result in signs of cardiovascular overload, acute heart failure, and pulmonary hypertension and edema. Furosemide and slower administration of blood or plasma should alleviate this problem. Administration rates have been suggested starting from 10 mL/kg/hr; faster rates may be necessary in peracute hemorrhage. Plasma should be administered when failure of absorption of passive maternal antibody has occurred or when protein-loosing enteropathy or nephropathy results in a total protein of less than 3 g/dL or less than 1.5 g albumin/dL. Plasma can be stored at household freezer temperatures (-15 to -20 degrees C) for a year; coagulation factors will be destroyed after 2 to 4 months when stored in this manner. To maintain viability of coagulation factors, plasma must be stored at -80 degrees C for less than 12 months. When administering plasma, a blood donor set with a built-in filter should always be used. When bovine plasma is thawed, precipitants form in the plasma and infusion of these microaggregates may result in fatal reactions in the recipient.
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PMID:Use of blood and blood products. 1057 16

Slit is a large secreted protein that provides important guidance cues in the developing nervous system and in other organs. Signaling by Slit requires two receptors, Robo transmembrane proteins and heparan sulfate (HS) proteoglycans. How HS controls Slit-Robo signaling is unclear. Here we show that the second leucine-rich repeat domain (D2) of Slit, which mediates binding to Robo receptors, also contains a functionally important binding site for heparin, a highly sulfated variant of HS. Heparin markedly enhances the affinity of the Slit-Robo interaction in a solid-phase binding assay. Analytical gel filtration chromatography demonstrates that Slit D2 associates with a soluble Robo fragment and a heparin-derived oligosaccharide to form a ternary complex. Retinal growth cone collapse triggered by Slit D2 requires cell surface HS or exogenously added heparin. Mutation of conserved basic residues in the C-terminal cap region of Slit D2 reduces heparin binding and abolishes biological activity. We conclude that heparin/HS is an integral component of the minimal Slit-Robo signaling complex and serves to stabilize the relatively weak Slit-Robo interaction.
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PMID:A molecular mechanism for the heparan sulfate dependence of slit-robo signaling. 1706 60

Heparin-induced thrombocytopaenia (HIT) is a life-threatening complication of exposure to heparin. It is mediated by autoantibodies to platelet factor-4 causing platelet activation, destruction and thrombosis. Given their rich arterial supply and a single central vein, the adrenal glands are particularly susceptible to congestive haemorrhage following venous thrombosis. We report a case of bilateral adrenal haemorrhage (BAH) associated with HIT following prophylactic use of unfractionated heparin for venous thromboembolism causing adrenal insufficiency. BAH is a life-threatening paradoxical complication associated with HIT, a prothrombotic state. The resulting adrenal insufficiency can lead to haemodynamic collapse if unrecognised. Early diagnosis, in the wake of vague symptoms, and prompt treatment primarily aimed at repletion of glucocorticoids and close monitoring of enlarging haemorrhage is of utmost importance. Likewise, early identification of HIT is important to prevent potential complications including adrenal haemorrhage.
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PMID:Bilateral adrenal haemorrhage: a cause of haemodynamic collapse in heparin-induced thrombocytopaenia. 2696 9


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