Venous gas embolization - Hemodynamic and inflammatory consequences
Venous gas embolization (VGE) during surgery may cause pulmonary hypertension, lung inflammation, ventilation difficulties, heart arrest and severe neurological damages. The switch to laparoscopic surgery increase the risk of carbon dioxide emboli from intraperitoneal gas insufflation.
Many animal studies on VGE are very old, some more than 50 years, and recent observations in patients on the passage of air through the lungs from right to left side of the heart and into the coronary arteries and into the brain have not been studied in animal models. We aim to describe the hemodynamic consequences of VGE and the systemic side effects in a porcine model with new monitoring equipment. This could lead to life-saving therapy
In vitro studies conducted on plasma showed that bubbles of air can activate innate immunity and complement activation can play a detrimental role in the lung damage seen in VGE. However, the exact pathophysiological mechanism is not fully understood.
Our theory is that complement is activated on the microbubbles caused by VGE. We aim to study how these bubbles are lodged in the capillary system of the lungs, and how complement in turn – through cross-talk, triggers an inflammatory response and coagulation activation.
Provided that we can document an inflammatory reaction caused by VGE, we aim to administer a complement inhibitor to reduce the primary innate immunity-induced inflammatory reaction. This could lead to a pharmaceutical treatment of patients with perioperative VGE, and hopefully reduce morbidity and mortality.
VGE will be studied in non-surviving anesthetized pigs experiencing minimal pre-operative stress.Replacement is obtained through numerous in-vitro whole blood experiments upfront and reduction through the simultaneous use of animals in education of medical and veterinary students during some of the experiments, and anatomy dissection of deceased animals. Refinement includes minimal stressful handling as the animal is anesthetized almost immediately after leaving the crib on the farm Number of animals: 99
Many animal studies on VGE are very old, some more than 50 years, and recent observations in patients on the passage of air through the lungs from right to left side of the heart and into the coronary arteries and into the brain have not been studied in animal models. We aim to describe the hemodynamic consequences of VGE and the systemic side effects in a porcine model with new monitoring equipment. This could lead to life-saving therapy
In vitro studies conducted on plasma showed that bubbles of air can activate innate immunity and complement activation can play a detrimental role in the lung damage seen in VGE. However, the exact pathophysiological mechanism is not fully understood.
Our theory is that complement is activated on the microbubbles caused by VGE. We aim to study how these bubbles are lodged in the capillary system of the lungs, and how complement in turn – through cross-talk, triggers an inflammatory response and coagulation activation.
Provided that we can document an inflammatory reaction caused by VGE, we aim to administer a complement inhibitor to reduce the primary innate immunity-induced inflammatory reaction. This could lead to a pharmaceutical treatment of patients with perioperative VGE, and hopefully reduce morbidity and mortality.
VGE will be studied in non-surviving anesthetized pigs experiencing minimal pre-operative stress.Replacement is obtained through numerous in-vitro whole blood experiments upfront and reduction through the simultaneous use of animals in education of medical and veterinary students during some of the experiments, and anatomy dissection of deceased animals. Refinement includes minimal stressful handling as the animal is anesthetized almost immediately after leaving the crib on the farm Number of animals: 99