Trauma is the leading cause of death in patients younger than 45 years, brain injury and uncontrollable hemorrhage being the first and second most important entities, respectively, leading to early, ie, less than 48 h, fatal outcome. BLate [mortality is mostly due to multiple organ failure resulting from a systemic inflammatory response, which is triggered by mechanical tissue damage per se (1), shock-related tissue hypoxia, and reperfusion injury associated with the restoration of the peripheral circulation. Blunt chest trauma and consecutive alveolar hypoxia further aggravate this hyperinflammation (2). Given the complex sequence of the trauma, the consecutive circulatory shock, and the pathophysiological mechanisms that subsequently lead to the response of the organism to the injury, it is not surprising that numerous models of traumatichemorrhagic shock and resuscitation have been described (for reviews, see References 1 and 3Y5). Murine models enable us to study pathophysiological mechanisms due to the availability of gene knockout and overexpression strains, but the small size makes surgery difficult and limits repetitive blood sampling. Rats are certainly easier to handle and have a 10 times higher blood volume than do mice; their response to injury may markedly differ from that of humans, in particular with respect to oxidative and nitrosative stress (6, 7). Consequently, despite the cost, pigs have been frequently used to model trauma, hemorrhage, and resuscitation, because hemodynamic as well as metabolic and immunological responses are close to those in humans. In addition, skin wound healing in swine and humans is particularly similar (1). A number of different porcine models are available, which use either hemorrhage (8Y10) or blunt trauma (11, 12) alone or a variable combination of these two (13Y15). In this issue of Shock Hildebrand et al.(16) report on a new porcine model of traumatic and hemorrhagic shock, which comprises a Btriple trauma [consisting of blunt chest trauma induced by bolt gunshot, penetrating abdominal trauma with liver laceration, and a subsequent pressure-controlled hemorrhagic shock (mean blood pressure 30 T 5 mmHg) resulting from removal of up to 45% of the calculated blood volume. This model is unique in combining both abdominal trauma and blunt chest traumaYinduced acute lung injury with a controlled hemorrhage. In addition, the authors have the merit of modeling the early phase of intensive care; ie, data were recorded for 12 h after the initial resuscitation. Drugs (epinephrine, amiodarone) and crystalloid fluids were administered according to current guidelines of Acute Trauma Life Support and the European Resuscitation Council, and normothermia was maintained to avoid hypothermia-related coagulopathy. Finally, the authors also regularly performed lung recruitment maneuvers to counteract the otherwise progressive impairment of lung mechanics and gas exchange. This measure is crucial in porcine models, because swine are particularly susceptible to atelectasis formation in dependent lung regions because of the lack of alveolar collateral ventilation (17). It should be noted in this context that not only lung mechanics but also the pulmonary vascular response are different in swine when compared with human beings: as a result of the thickness of the media layer of the small pulmonary arteries, which resembles that of species indigenous to high altitude (18), swine easily develop severe pulmonary hypertension and, eventually, right ventricular failure. Despite all the aspects that strengthen the clinical relevance of the model, a number of issues should be studied in future investigations …