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Focal intra-colon cooling reduces organ injury and systemic inflammation after REBOA management of lethal hemorrhage in rats.

ABSTRACT: Resuscitative endovascular balloon occlusion of the aorta (REBOA) is a lifesaving maneuver for the management of lethal torso hemorrhage. However, its prolonged use leads to distal organ ischemia-reperfusion injury (IRI) and systemic inflammatory response syndrome (SIRS). The objective of this study is to investigate the blood-based biomarkers of IRI and SIRS and the efficacy of direct intestinal cooling in the prevention of IRI and SIRS. A rat lethal hemorrhage model was produced by bleeding 50% of the total blood volume. A balloon catheter was inserted into the aorta for the implementation of REBOA. A novel TransRectal Intra-Colon (TRIC) device was placed in the descending colon and activated from 10 min after the bleeding to maintain the intra-colon temperature at 37 °C (TRIC37°C group) or 12 °C (TRIC12°C group) for 270 min. The upper body temperature was maintained at as close to 37 °C as possible in both groups. Blood samples were collected before hemorrhage and after REBOA. The organ injury biomarkers and inflammatory cytokines were evaluated by ELISA method. Blood based organ injury biomarkers (endotoxin, creatinine, AST, FABP1/L-FABP, cardiac troponin I, and FABP2/I-FABP) were all drastically increased in TRIC37°C group after REBOA. TRIC12°C significantly downregulated these increased organ injury biomarkers. Plasma levels of pro-inflammatory cytokines TNF-α, IL-1b, and IL-17F were also drastically increased in TRIC37°C group after REBOA. TRIC12°C significantly downregulated the pro-inflammatory cytokines. In contrast, TRIC12°C significantly upregulated the levels of anti-inflammatory cytokines IL-4 and IL-10 after REBOA. Amazingly, the mortality rate was 100% in TRIC37°C group whereas 0% in TRIC12°C group after REBOA. Directly cooling the intestine offered exceptional protection of the abdominal organs from IRI and SIRS, switched from a harmful pro-inflammatory to a reparative anti-inflammatory response, and mitigated mortality in the rat model of REBOA management of lethal hemorrhage.

SUBMITTER: Arya AK

PROVIDER: S-EPMC8249469 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:Background:Thermal stimulation has been proposed as a modality to facilitate motor recovery in neurological populations, such as stroke. Recently (Ansari, Remaud & Tremblay, 2018), we showed that application of cold or warm stimuli distally to a single digit produced a variable and short lasting modulation in corticomotor excitability. Here, our goal was to extend these observations to determine whether an increase in stimulation area could elicit more consistent modulation. Methods:Participants (n = 22) consisted of a subset who participated in our initial study. Participants were asked to come for a second testing session where the thermal protocol was repeated but with extending the stimulation area from single-digit (SD) to multi-digits (MD, four fingers, no thumb). As in the first session, skin temperature and motor evoked potentials (MEPs) elicited with transcranial magnetic stimulation were measured at baseline (BL, neutral gel pack at 22 °C), at 1 min during the cooling application (pre-cooled 10 °C gel pack) and 5 and 10 min post-cooling (PC5 and PC10). The analysis combined the data obtained previously with single-SD cooling (Ansari, Remaud & Tremblay, 2018) with those obtained here for MD cooling. Results:At BL, participants exhibited comparable measures of resting corticomotor excitability between testing sessions. MD cooling induced similar reductions in skin temperature as those recorded with SD cooling with a peak decline at C1 of respectively, -11.0 and -10.3 °C. For MEPs, the primary analysis revealed no main effect attributable to the stimulation area. A secondary analysis of individual responses to MD cooling revealed that half of the participants exhibited delayed MEP facilitation (11/22), while the other half showed delayed inhibition (10/22); which was sustained in the post-cooling phase. More importantly, a correlation between variations in MEP amplitude recorded during the SD cooling session with those recorded in the second session with MD cooling, revealed a very good degree of correspondence between the two at the individual level. Conclusion:These results indicate that increasing the cooling area in the distal hand, while still eliciting variable responses, did produce more sustained modulation in MEP amplitude in the post-cooling phase. Our results also highlight that responses to cooling in terms of either depression or facilitation of corticomotor excitability tend to be fairly consistent in a given individual with repeated applications.

Project description:Introduction: Resuscitative Endovascular Balloon Occlusion of the Aorta (REBOA) is used for aortic control in hemorrhagic shock despite little quantification of its mechanism of resuscitation or cardiac injury. The goal of this study was to use pressure-volume (PV) loop analysis and direct coronary blood flow measurements to describe the physiologic changes associated with the clinical use of REBOA. Methods: Swine underwent surgical and vascular access to measure left ventricular PV loops and left coronary flow in hemorrhagic shock and subsequent placement of occlusive REBOA, partial REBOA, and no REBOA. PV loop characteristics and coronary flow are compared graphically with PV loops and coronary waveforms, and quantitatively with measures of the end systolic and end pressure volume relationship, and coronary flow parameters, with accounting for multiple comparisons. Results: Hemorrhagic shock was induced in five male swine (mean 53.6 ± 3.6 kg) as demonstrated by reduction of stroke work (baseline: 3.1 vs. shock: 1.2 L*mmHg, p < 0.01) and end systolic pressure (ESP; 109.8 vs. 59.6 mmHg, p < 0.01). ESP increased with full REBOA (178.4 mmHg; p < 0.01), but only moderately with partial REBOA (103.0 mmHg, p < 0.01 compared to shock). End systolic elastance was augmented from baseline to shock (1.01 vs. 0.39 ml/mmHg, p < 0.01) as well as shock compared to REBOA (4.50 ml/mmHg, p < 0.01) and partial REBOA (3.22 ml/mmHg, p = 0.01). Percent time in antegrade coronary flow decreased in shock (94%-71.8%, p < 0.01) but was rescued with REBOA. Peak flow increased with REBOA (271 vs. shock: 93 ml/min, p < 0.01) as did total flow (peak: 2136, baseline: 424 ml/min, p < 0.01). REBOA did not augment the end diastolic pressure volume relationship. Conclusion: REBOA increases afterload to facilitate resuscitation, but the penalty is supraphysiologic coronary flows and imposed increase in LV contractility to maintain cardiac output. Partial REBOA balances the increased afterload with improved aortic system compliance to prevent injury.

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Focal intra-colon cooling reduces organ injury and systemic inflammation after REBOA management of lethal hemorrhage in rats.

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