Pathways

Bivalirudin is a direct thrombin inhibitor that treats heparin-induced thrombocytopenia and prevents thrombosis. It binds reversibly to the active site of thrombin inhibiting its activation of fibrinogen and coagulation factor XIII. Without the conversion of fibrinogen into fibrin the formation of a thrombus is stopped. Inactivation of coagulation factor XIII further inhibits blood clot formation, as this factor is responsible for stabilizing cross-linking fibrin creating the meshwork for the clot. This drug is commonly administered intravenously and is metabolized by proteolytic cleavage. Bivalirudin is cleared from plasma by the renal system and proteolytic cleavage. This drug interacts with food, echinacea needs to be avoided in addition to herbs and supplements that have anticoagulant and antiplatelet activity. These herbs and supplements include ginger, garlic, bilberry, danshen, piracetam and ginkgo biloba.

Bivalirudin, marketed as Angiomax or Angiox, is a bivalent direct thrombin inhibitor that binds directly to the active site of thrombin, as well as its exosite. It is synthetically created, and is structurally similar to the drug hirudin, which is found in medicinal leeches. It is used in preventing coagulation and formation of blood clots due to the inactivation of the enzyme that catalyzes activation of coagulation factors V, XIII and fibrinogen. Bivalirudin is a reversible direct thrombin inhibitor, as over time, thrombin can cleave the bonds between it and bivalirudin, allowing it to become active again. After injection, bivalirudin enters the blood stream and directly binds to thrombin, preventing its use as an enzyme. This prevents catalyzation of factor V to factor Va, which would form the prothrombinase complex and create more thrombin. It also prevents the catalysis fibrinogen or factor I to fibrin, which then polymerizes to form the blood clot. The lack of useable thrombin also prevents the catalysis of factor XIII to factor XIIIa, which is necessary to crosslink the polymerized fibrin to form a water insoluble clot.

Bithionol is a drug that is not metabolized by the human body as determined by current research and biotransformer analysis. Bithionol passes through the liver and is then excreted from the body mainly through the kidney.

Metabolites of Bisphenol A diglycidyl ether are predicted with biotransformer.

Bisoprolol is a cardioselective beta 1 blocker. It can be administered orally, where it passes through hepatic portal circulation, and enters the bloodstream and travels to act on cardiomyocytes. In bronchial and vascular smooth muscle, bisoprolol can compete with epinephrine for beta adrenergic receptors. By competing with catecholamines for adrenergic receptors, it inhibits sympathetic stimulation of the heart. The reduction of neurotransmitters binding to beta receptor proteins in the heart inhibits adenylate cyclase type 1. Because adenylate cyclase type 1 typically activates cAMP synthesis, which in turn activates PKA production, which then activates SRC and nitric oxide synthase, its inhibition causes the inhibition of cAMP, PKA, SRC and nitric oxide synthase signaling. Following this chain of reactions, we see that the inhibition of nitric oxide synthase reduces nitric oxide production outside the cell which results in vasoconstriction. On a different end of this reaction chain, the inhibition of SRC in essence causes the activation of Caspase 3 and Caspase 9. This Caspase cascade leads to cell apoptosis. The net result of all these reactions is a decreased sympathetic effect on cardiac cells, causing the heart rate to slow and arterial blood pressure to lower; thus, bisoprolol administration and binding reduces resting heart rate, cardiac output, afterload, blood pressure and orthostatic hypotension. By prolonging diastolic time, it can prevent re-infarction. Clinically, it is used to increase atrioventricular block to treat supraventricular dysrhythmias. Bisoprolol also reduce sympathetic activity and is used to treat hypertension, angina, migraine headaches, and hypertrophic subaortic stenosis. Some side effects of using bisoprolol may include headaches, dizziness, weakness, and nausea.

Bisoprolol is a cardioselective beta 1 blocker. It can be administered orally, where it passes through hepatic portal circulation, and enters the bloodstream and travels to act on cardiomyocytes. In bronchial and vascular smooth muscle, bisoprolol can compete with epinephrine for beta-2 adrenergic receptors. By competing with catecholamines for adrenergic receptors, it inhibits sympathetic stimulation of the heart. The reduction of neurotransmitters binding to beta receptor proteins in the heart inhibits adenylate cyclase type 1. Because adenylate cyclase type 1 typically activates cAMP synthesis, which in turn activates PKA production, which then activates SRC and nitric oxide synthase, its inhibition causes the inhibition of cAMP, PKA, SRC and nitric oxide synthase signaling. Following this chain of reactions, we see that the inhibition of nitric oxide synthase reduces nitric oxide production outside the cell which results in vasoconstriction. On a different end of this reaction chain, the inhibition of SRC in essence causes the activation of Caspase 3 and Caspase 9. This Caspase cascade leads to cell apoptosis. The net result of all these reactions is a decreased sympathetic effect on cardiac cells, causing the heart rate to slow and arterial blood pressure to lower; thus, bisoprolol administration and binding reduces resting heart rate, cardiac output, afterload, blood pressure and orthostatic hypotension. By prolonging diastolic time, it can prevent re-infarction. Clinically, it is used to increase atrioventricular block to treat supraventricular dysrhythmias. Bisoprolol also reduce sympathetic activity and is used to treat hypertension, angina, migraine headaches, and hypertrophic subaortic stenosis.