Background We sought to determine the magnitude of the inherent inter-animal physiologic variability by automating a porcine Resuscitative Endovascular Balloon Occlusion of the Aorta (REBOA) protocol to minimize external influences that might alter physiology and confound experimental results. Methods Swine (n = 42) underwent a controlled 30% blood volume hemorrhage followed by 30 minutes of REBOA (ie, ischemic phase). The animals were weaned from REBOA autonomously over 15 minutes, beginning the reperfusion phase, while continuing to provide partial flow balloon support to maintain a target proximal mean arterial pressure (pMAP) of 65 mmHg. Simultaneously, shed blood was re-transfused as part of the resuscitation efforts. Physiologic data were continuously recorded, and serum samples were serially collected. Baseline characteristics, variance in vital signs, and 8-isoprostane levels were quantified during hemorrhage, REBOA, and reperfusion phases. Results There was no significant difference in baseline physiology across animals ( P > .05). Hemodynamic variability was highest for pMAP during the ischemic phase ( P = .001) and for distal mean arterial pressure (dMAP) during the weaning/reperfusion phase ( P = .001). The latter finding indicated the variable physiologic response to ischemia-reperfusion injury, as the automated balloon support required by each animal to maintain pMAP was highly variable. Circulating 8-isoprostane variance was significantly higher following the start of reperfusion compared to baseline levels ( P = .001). Discussion Despite subjecting animals to a highly consistent ischemia-reperfusion injury through automation, we noted significant variability in the hemodynamic and biochemical response. These findings illustrate the inherent physiologic variability and potential limitations of porcine large animal models for the study of shock.

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Background Resuscitative endovascular balloon occlusion of the aorta (REBOA) provides hemodynamic support to patients with non-compressible truncal hemorrhage. As cardiac output increases due to aortic occlusion (AO), aortic diameter will increase as a function of compliance, potentially causing unintended flow around the balloon. Materials and Methods Swine (N = 10) were instrumented to collect proximal mean arterial blood pressure (pMAP), distal MAP (dMAP), balloon pressure (bP), balloon volume (bV), and distal aortic flow (Qaorta). A 7-Fr automated REBOA catheter was positioned in Zone 1. At T0, animals underwent 30% total blood volume hemorrhage over 30 min followed by balloon inflation to complete AO. Automated balloon inflation occurred from T30-T60 when Qaorta was detected. Period of interest was T55-T60, while the balloon actively worked to maintain AO during transfusion of shed blood. Results Median weight of the cohort was 73.75 [IQR:71.58-74.45] kg. During T40-T55 and T55-T60, median pMAP was 88.95 [IQR:76.80-109.92] and 108.13 [IQR:99.13-119.51] mmHg, P = 0.07. Median Qaorta during T40-T55, and T55-T60 was 0.81 [IQR:0.41-0.96], and 1.53 [IQR:1.07-1.96] mL/kg/min, P = 0.06. Median number of balloon inflations during T40-T55 was 0.00 [IQR:0.00-0.75] and increased during active transfusion to 10.00 [IQR:5.25-14.00], P = 0.001. Discussion In clinical practice, following initial establishment of AO, progressive balloon inflations are required to maintain AO in response to intrinsic and transfusion-mediated increases in cardiac output, blood pressure, and aortic diameter.

Hepatitis C, caused by hepatitis C virus (HCV) was originally described as parenterally transmitted non-A non-B hepatitis. Since its discovery in 1989, the field of HCV research has become a shining example of successful translation of basic research wherein in a short of span of just 30 years the virus was discovered, highly sensitive and specific diagnostic assays were developed, epidemiology and clinical characteristics of the disease were well defined and now with the availability of highly efficacious antiviral therapies many countries are already on their way to achieving World Health Organization’s (WHO) elimination targets of hepatitis C by 2030.  However, much work needs to be done to eliminate hepatitis C especially in resource poor countries. Most recent data show an estimated 71 million people are currently infected with HCV worldwide and approximately 400,000 people die each year from causes related to HCV. Of these estimates, more than 13 million HCV infected persons are in India and Pakistan (Figure 1). Despite the availability of a cure for hepatitis C, only 20% of those infected patients have been diagnosed (1). In order to achieve the WHO targets of hepatitis C elimination, concerted efforts will have to made to make affordable and reliable diagnostics available worldwide.