The Effects of Primary Thoracic Blast Injury and Morphine on the Response to Haemorrhage in the Anaesthetised Rat

Abstract

Primary thoracic blast injury causes a triad of bradycardia, hypotension and apnoea mediated in part via a vagal reflex. Blast casualties may also suffer blood loss, and the response to progressive simple haemorrhage is biphasic: an initial tachycardia followed by a vagally mediated reflex bradycardia which can be attenuated by μ opioid agonists. The aims of this study were to determine the effects of thoracic blast injury on the response to subsequent haemorrhage, and the effects of morphine, administered after blast, on the response to blood loss. Male Wistar rats, terminally anaesthetised with alphadolone‐alphaxolone (19‐21 mg kg−1 h−1 I.V.), were allocated randomly to one of three groups: Group I, sham blast; Group II, thoracic blast; Group III, thoracic blast plus morphine (0.5 mg kg−1 I.V. given 5 min after blast). Blast (Groups II and III) resulted in significant (P < 0.05, ANOVA) bradycardia, hypotension and apnoea. Sham blast (Group I) had no effect. Ten minutes later, haemorrhage (40% of the estimated total blood volume (BV)) in Group I produced a biphasic response comprising a tachycardia followed by a peak bradycardia after the loss of 33% BV. Arterial blood pressure did not fall significantly until the loss of 13.3% BV. In Group II the haemorrhage‐induced tachycardia was absent and the bradycardia was augmented: peak bradycardia was seen after the loss of 23% BV. Mean arterial blood pressure (MBP) began to fall as soon as haemorrhage commenced and was significant after the loss of 10% BV. Morphine (Group III) prevented the haemorrhage‐induced bradycardia and delayed the significant fall in MBP until the loss of 30% BV. It is concluded that the response to thoracic blast injury augments the depressor response to haemorrhage while morphine attenuates this response.

CD43Lo classical monocytes participate in the cellular immune response to isolated primary blast lung injury

“…A transient bradycardia (as observed in Figure 1) is frequently reportedly in PBLI and is due to a vagal nerve mediated reflex, which in the absence of further insult resolves rapidly 7,8 . We saw a modest but sustained increase in respiratory rate after PBLI, which may have been compensatory as a result of pulmonary damage and reduced gasexchange, thereby maintaining peripheral oxygenation in subjects 33 throughout the study period.…”

“…Studies investigating the subsequent immune response have been reported most commonly in rats [5][6][7][8][9][10] , mice [11][12][13][14][15] and swine 16,17 . These studies have offered overwhelming evidence of the neutrophil response to PBLI in animal models, with increases in circulating and broncho-alveolar lavage fluid (BALF) neutrophils, increases in Myeloperoxidase (MPO) activity in the lung, and neutrophil staining by histology [9][10][11][12]14,18,19 .…”

Blast injury research models

“…Bias was likely to arise between blast and non-blast injured groups because haemorrhage after blast results in more rapid early falls in arterial blood pressure [53], resulting in greater uncontrolled blood loss from those subjected to haemorrhage without blast injury. The problem was solved by incorporating an initial phase of controlled haemorrhage (30% total estimated BV), at the conclusion of which arterial blood pressure had diminished to similar levels regardless of prior blast exposure.…”

Prolonged Permissive Hypotensive Resuscitation Is Associated With Poor Outcome in Primary Blast Injury With Controlled Hemorrhage

“…In civilian mass casualty situations, such as terrorist bombings in confined spaces, there is often disruption to infrastructure and security issues relating to secondary devices that can result in delayed evacuation. Furthermore, the response to hemorrhage can be modified significantly by concomitant injuries, 14,15 and consequently the effectiveness of resuscitation strategies may be influenced by the response to the injuries. Therefore, although permissive hypotension is a widely adopted strategy in trauma resuscitation, the success of this approach requires a full investigation and understanding of the mechanisms of injury and their physiological consequences.…”