![]() However a significant mortality rate was noted, mostly from intracranial haemorrhage at 7 days, but later mortality was not significant amongst treated and non-treated patients. A meta-analysis of these trials concluded that rtPA given within 6 hours of a stroke significantly increased the odds of being alive and independent at final follow-up, particularly in patients treated within 3 hours. There have been 12 large scale, high-quality trials of rtPA in acute ischemic stroke. It can either be administered systemically, in the case of acute myocardial infarction, acute ischemic stroke, and most cases of acute massive pulmonary embolism, or administered through an arterial catheter directly to the site of occlusion in the case of peripheral arterial thrombi and thrombi in the proximal deep veins of the leg. The most common use is for ischemic stroke. TPA is used in some cases of diseases that feature blood clots, such as pulmonary embolism, myocardial infarction, and stroke, in a medical treatment called thrombolysis. The antidote for tPA in case of toxicity is aminocaproic acid. The use of this protein is contraindicated in hemorrhagic stroke and head trauma. They are used in clinical medicine to treat embolic or thrombotic stroke. Specific rtPAs include alteplase, reteplase, and tenecteplase. TPA can be manufactured using recombinant biotechnology techniques tPA produced by such means are referred to as recombinant tissue plasminogen activator ( rtPA). Human tPA has a molecular weight of ~70 kDa in the single-chain form. As an enzyme, it catalyzes the conversion of plasminogen to plasmin, the major enzyme responsible for clot breakdown. ![]() It is a serine protease ( EC 3.4.21.68) found on endothelial cells, the cells that line the blood vessels. Tissue plasminogen activator (abbreviated tPA or PLAT) is a protein involved in the breakdown of blood clots. trans-synaptic signaling by BDNF, modulating synaptic transmission.platelet-derived growth factor receptor signaling pathway. ![]()
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