Bubbles are biologically active. They interact with the cellular elements in blood as well as plasma protein cascades - coagulation, complement, kinin and plasmin. In addition, bubbles denature lipoproteins, liberating blood lipids 54-57. Blood vessels, on the other hand, sustain damage through physical contact. This may range from minimal damage to bleeding 51'58.
Upon appearance of a bubble in blood, the catalyzing event appears to be the formation of a plasma-protein coat around the bubble. This bubble "skin" is made up of plasma glycoproteins, fibrinogen and gamma globulins 59'60. It is a biologically active interface that allows thrombocytes and white blood cells to become attached 61.
In time, activation of platelets leads to aggregation and coalescence around bubbles with entrapment of other blood constituents. Cellular blood elements - such as red blood cells - may become entangled in the growing fibrin web. This thickening of the bubble "skin" may reduce diffusion producing a mechanism for bubble stabilization and survival 62. General platelet adhesiveness also increases in response to bubbles. Some studies have reported platelet depletion following decompression, even in the absence of symptoms 63. However, thrombocytopenia or anti-platelet therapies do not appear to protect against DI. Also aggressive anticoagulation runs the risk of precipitating hemorrhage in DI affecting the spinal cord and inner ear 61>62>64>65. On the other hand, DI does induce a hypercoagulable state with a high risk of thromboembolism aggravated by paralysis. This should be actively prevented.
The activation of platelets and Hageman Factor also leads to activation of inflammatory cascades. Leukotrienes are released while the presence of gammaglobulin on the bubble skin, combined with the products of complement activation, attract white blood cells to the area 66. Leukocytes may interact directly with the bubble or with damaged endothelium. The relevance of inflammation in DI underlies the recommended use of antiinflammatory agents and, more recently, of lidocaine 67. Lidocaine also has leukocyte anti-adherent properties 68,69.
DI has also been shown to result in elevations of blood lipid levels with as yet undefined clinical implications 70.
While the role of various elements in blood in DI has become downplayed in recent literature, the significance has not disappeared: The search continues to find safe and effective drugs or interventions that may attenuate the various pathophysiological events following exposure to bubbles. Recently research on nitric oxide donors and exercise have suggested that they may have a modifying role in vivo 17.
The injection of 10-20^m bubbles into the carotid artery of a guinea pig has been shown to cause visible damage to the luminal surface surfactant layers of endothelial cells 71. This form of injury may result in alterations in vasomotor tone, precipitate platelet or leukocyte adhesion, and cause failure of the blood-brain barrier. In more extreme cases endothelial cells may actually be stripped, exposing the basement membrane to plasma proteins and platelets as well as adding bioactive cell remnants to the blood 61.
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