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Air embolism is a pathological condition rather than a molecular target; it occurs when gas bubbles enter the circulatory system, leading to mechanical obstruction of blood flow and a complex inflammatory response. It is traditionally divided into venous air embolism (VAE) and arterial air embolism (AAE), frequently arising as an iatrogenic complication of invasive medical procedures or as a result of barotrauma and decompression sickness in divers. The interaction between gas bubbles and the blood interface triggers thromboinflammation, characterized by the activation of the complement system (particularly C3), neutrophils, and platelets. Management centers on physical interventions such as hyperbaric oxygen therapy and patient positioning to alleviate vascular obstruction, while pharmacological research explores the use of surfactants and anti-inflammatory agents to mitigate end-organ damage. Because 'Air embolism' refers to a disease state and physical blockage rather than a protein or receptor, it is not considered a therapeutic target in the conventional molecular sense.
The primary management of air embolism involves hyperbaric oxygen therapy to physically compress gas bubbles and promote their dissolution into the blood, alongside 100% oxygen to create a diffusion gradient for the removal of nitrogen. Experimental pharmacological approaches focus on neuroprotection using lidocaine, bubble dissolution with perfluorocarbons, and the inhibition of bubble-induced thromboinflammation via complement inhibitors like eculizumab.
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