Pancreatic injury after thoracoabdominal aortic occlusion in a porcine model.

BACKGROUND: The aim of this study was to investigate pancreatic injury after 45 min of thoracoabdominal aortic occlusion in a porcine model. METHODS: Twenty-four pigs were used. Six pigs underwent sham operation and 18 intravascular balloon thoracoabdominal aortic occlusions for 45 min. The animals were randomly killed at 12, 48 and 120 h after reperfusion. After killing, all pancreata were examined macroscopically for any signs of acute pancreatitis, whereas gland specimens were harvested for histological study to evaluate pancreatic injury (haematoxylin and eosin staining) and acinar cell apoptosis (Terminal deoxynucleotidyl transferase mediated dUTP Nick-End Labelling staining). RESULTS: Pancreatic injury severity score was mildly increased in terms of oedematous features at 12 h after reperfusion, but normalized to sham levels by the second day and thereafter. Necrotic injury was not statistically significant at any time point. Acinar cell apoptotic index was mildly increased at 12 and 48 h, but showed a tendency to decrease towards sham levels by the fifth day. One animal developed acute pancreatitis. CONCLUSION: Acute pancreatitis is unlikely to occur after 45 min of thoracoabdominal aortic occlusion. However, an early, mild oedematous and apoptotic injury that occurs subclinically seems to be a constant event. This injury might have clinical significance when combined with pre-existent pancreatic pathologies.

Evolution of spinal cord injury in a porcine model of prolonged aortic occlusion.

BACKGROUND: Spinal cord injury and subsequent paraplegia remains an unpredictable and devastating complication of thoracoabdominal aortic surgery. The aim of this study was to investigate spinal cord injury due to prolonged thoracoabdominal aortic occlusion. MATERIALS AND METHODS: We used a highly reproducible porcine model of 45-min thoracoabdominal aortic occlusion, which was accomplished by two balloon occlusion catheters. Neurological evaluation after the end of experiment was performed by an independent observer according to the Tarlov scale. The lower thoracic and lumbar spinal cords were harvested at 10, 48, and 120 h (n = 6 animals per time point) and examined histologically with hematoxylin and eosin (H&E) stain and TUNEL method. Tarlov scores, number of neurons, and the grade of inflammation were analyzed. RESULTS: H&E staining revealed reduction in the number of motor neurons which occurred in two phases (between 0 and 10 h and between 48 and 120 h of reperfusion), as well as development of inflammation in spinal cord sections during the reperfusion period, reaching a peak at 48 h. TUNEL reaction was negative for apoptotic neurons at any time point. CONCLUSIONS: In this porcine model, we demonstrated that, after 45 min of thoracoabdominal aortic occlusion, motor neuron death seems to occur in two phases (immediate and delayed). Inflammation was a subsequent event of transient prolonged spinal cord ischemia and possibly a major contributor of delayed neuronal death. Using TUNEL straining we found no evidence of neuronal apoptosis at any time point of reperfusion.

Superiority of early relative to late ischemic preconditioning in spinal cord protection after descending thoracic aortic occlusion.

OBJECTIVE: We previously showed that ischemic preconditioning significantly reduced spinal cord injury caused by 35-minute aortic occlusion. In this study we investigated the effect of ischemic preconditioning on spinal cord injury after 45-minute aortic occlusion. METHODS: Thirty-two pigs were divided as follows: group 1 (n = 6) underwent sham operation, group 2 (n = 6) underwent 20 minutes of aortic occlusion, group 3 (n = 6) underwent 45 minutes of occlusion, group 4 (n = 6) underwent 20 minutes of occlusion and 48 hours later underwent an additional 45 minutes, and group 5 (n = 8) underwent 20 minutes of occlusion and 80 minutes later underwent an additional 45 minutes. Aortic occlusion was accomplished with two balloon occlusion catheters placed fluoroscopically after the origin of the left subclavian artery and at the aortic bifurcation. Neurologic evaluation was by Tarlov score. The lower thoracic and lumbar spinal cords were harvested at 120 hours and examined histologically with hematoxylin-eosin staining. The number of neurons was counted, and the inflammation was scored (0-4). Statistical analysis was by Kruskal-Wallis and 1-way analysis of variance tests. RESULTS: Group 5 (early ischemic preconditioning) had better Tarlov scores than group 3 ( P < .001) and group 4 (late ischemic preconditioning, P < .001). The histologic changes were proportional to the Tarlov scores, with the least histologic damage in the animals of group 5 relative to group 3 (number of neurons P < .001, inflammation P = .004) and group 4 (number of neurons P < .001, inflammation P = .006). CONCLUSION: Early ischemic preconditioning is superior to late ischemic preconditioning in reducing spinal cord injury caused by the extreme ischemia of 45 minutes of descending thoracic aortic occlusion.

Early ischemic preconditioning without hypotension prevents spinal cord injury caused by descending thoracic aortic occlusion.

OBJECTIVE: Postoperative neurologic deficits after thoracic aortic reconstruction vary widely. Our previous study showed that delayed ischemic preconditioning could prevent spinal cord injury caused by occlusion of the descending thoracic aorta in pigs. We investigated early ischemic preconditioning in the same model. METHODS: Twenty-eight pigs were divided into 4 groups: group 1 (n = 6) underwent a sham operation, group 2 (n = 6) underwent aortic occlusion for 20 minutes, group 3 (n = 8) underwent aortic occlusion for 35 minutes, and group 4 (n = 8) underwent aortic occlusion for 20 minutes and underwent aortic occlusion 80 minutes later without hypotension for 35 minutes. Aortic occlusion was accomplished by using 2 balloon occlusion catheters placed fluoroscopically at T6 to T8 above the diaphragm and at the aortic bifurcation. Neurologic evaluation was performed by an independent observer according to the Tarlov scale (0-4). The lower thoracic and lumbar spinal cords were harvested at 120 hours and examined histologically with hematoxylin-and-eosin stain. Histologic results (number of neurons and grade of inflammation) were scored (0-4) and were similarly analyzed. Statistical analysis was by means of the Kruskal-Wallis test. RESULTS: Group 4 had a better neurologic outcome at 24, 48, and 120 hours in comparison with group 3 (P <.001). The histologic changes were proportional to the neurologic test scores, with the more severe and extensive gray matter damage in animals of group 3 (number of neurons, P <.001; grade of inflammation, P <.001). CONCLUSION: Early ischemic preconditioning without hypotension protects against spinal cord injury after aortic occlusion, as confirmed by using the Tarlov score and histopathology.

Does ischemic preconditioning reduce spinal cord injury because of descending thoracic aortic occlusion?

OBJECTIVE: Ischemic preconditioning has been found to protect various organs from a subsequent longer ischemic insult. We investigated whether the late phase of ischemic preconditioning reduces spinal cord injury from occlusion of the descending thoracic aorta. METHODS: Twenty-four pigs (27 to 30 kg) were randomly divided in four groups: group I (n = 4) underwent a sham operation, group II (n = 4) underwent aortic occlusion for 20 minutes, group III (n = 8) underwent aortic occlusion for 35 minutes, and group IV (n = 8) underwent aortic occlusion for 20 minutes and, 48 hours later, aortic occlusion for 35 minutes. Aortic occlusion was accomplished with two balloon occlusion catheters placed fluoroscopically at T(6) to T(8) above the diaphragm and at the aortic bifurcation. Neurologic evaluation was performed by an independent observer according to Tarlov's scale (0 to 4, with 4 as normal). The lower thoracic and lumbar spinal cords were harvested at 120 hours and examined histologically with hematoxylin and eosin stain. Histologic results (number of neurons and grade of inflammation) were scored 0 to 4 (4, intact spinal cord; 0, no neurons and high inflammation) and were similarly analyzed. Results were expressed as the mean +/- the standard error of the mean, and statistical analysis used the Kruskal-Wallis test. RESULTS: Group IV had a better neurologic outcome at 24, 48, and 120 hours in comparison with group III (P <.001), although 120 hours after the end of the experiment, the neurologic outcome in group IV was worse than at 24 hours (P =.014). The histologic changes were proportional to the neurologic test scores, with the more severe and extensive gray matter damage in the animals of group III (number of neurons, P <.001; and grade of inflammation, P <.001). CONCLUSION: Ischemic preconditioning (late phase, 48 hours after the first occlusion) reduces spinal cord injury after aortic occlusion, as estimated with Tarlov's score and histopathology.