Biology subjects

Jordan, J. E.

Publications and source records attributed to Jordan, J. E..

3 recordsLinked to original sources

bioRxiv2026

A translational porcine model to assess the graded impact of hemorrhage and aortic occlusion on cardiovascular hemodynamics and renal perfusion

Resuscitative Endovascular Balloon Occlusion of the Aorta (REBOA) is a lifesaving intervention used to manage non-compressible torso hemorrhage by temporarily occluding the aorta to minimize blood loss and preserve perfusion to vital organs. Partial REBOA (p-REBOA) has been proposed to mitigate ischemic injury associated with full-REBOA (f-REBOA). However, implementation of p-REBOA clinically has been challenging due to our limited understanding of the acute hemodynamics with p-REBOA particularly in relation to cardiac, carotid, and renal perfusion. In this study we developed and utilized a novel porcine model to continuously measure cardiac, carotid, renal and systemic hemodynamic responses to varying degrees of hemorrhagic shock and aortic occlusion. Yorkshire pigs (N=54) underwent instrumentation for continuous hemodynamic monitoring and hemorrhage was induced for 30 minutes to achieve 10%, 20%, or 30% blood volume loss (n=18/group), followed by randomized treatments of either no occlusion, p-REBOA, or f-REBOA occlusion strategies (n=6/group) for 30 minutes. After occlusion, shed blood was re-transfused over 15 minutes, and REBOA balloons were deflated and removed. This was followed by a 3-hour automated resuscitation and critical care period. Renal and carotid perfusion decreased progressively with hemorrhage severity. Interestingly, 30 minutes of f-REBOA resulted in significant ischemia-reperfusion injury where renal perfusion was profoundly suppressed to 40% of baseline renal flow. On the other hand, p-REBOA yielded superior renal perfusion, while maintaining cardiac function and carotid perfusion. p-REBOA also required less fluid and vasopressors. This translational pig model offers new opportunities to assess acute cardiovascular hemodynamics during interventions for the management of hemorrhagic shock.

physiology↗

bioRxiv2026

Calibration of a Closed-loop Model of Porcine Aortic Hemodynamics during Hemorrhage

Uncontrolled hemorrhage remains a leading cause of traumatic death, driven by rapid physiological deterioration that is often difficult to detect during the compensated phase. While large-animal models provide critical insights into these dynamics, they are resource-intensive, motivating the need for efficient computational frameworks that can mechanistically interpret cardiovascular responses. We developed and calibrated a closed-loop zero-dimensional (0D) lumped-parameter model (LPM) using hemodynamic data from 43 anesthetized swine subjected to controlled hemorrhage (10%, 20%, or 30% of total blood volume). The computational framework, incorporates a dynamic heart model with a custom time-varying elastance function, a multi-compartment aorta, and distal Windkessel models representing vascular beds. The model was calibrated at discrete time snapshots throughout the 30-minute hemorrhage protocol to reproduce group-averaged experimental waveforms for aortic flow, regional organ flows, and systemic pressures. The calibrated model successfully reproduced experimental hemodynamic targets and waveform morphology across all hemorrhage severities. Analysis of the calibrated parameters revealed distinct physiological mechanisms driving hemodynamic adaptation during hemorrhage: a preferential increase in renal resistance compared to carotid resistance, indicating flow redistribution to vital organs, and a progressive mobilization of venous unstressed volume to sustain cardiac filling. Furthermore, the model captured the distinct shift toward preload limitation state for 30% hemorrhage group. This study establishes a physiologically interpretable in-silico framework capable of predicting both global and regional hemodynamic responses to acute blood loss, providing a validated foundation for future applications in trauma care and resuscitation modeling.

physiology↗

bioRxiv2023

In Vitro Reduction of Device Thrombosis Using a Combined Nitrite and Red Light Treatment

Device thrombosis occurs in otherwise life-saving procedures involving blood-contacting medical devices. Despite the use of systemic blood thinners, anticoagulants, and antiplatelet agents, device thrombosis can lead to substantial neurological damage, limb loss, death, and prolonged illness. Systemic treatments can also lead to bleeding. New methods to locally reduce thrombosis are urgently needed. Earlier work has shown that nitrite is a unique nitric oxide (NO) donor that is well-suited to use in blood and that its ability to inhibit platelet activation is potentiated by far-red light. In this study, we have applied our combined nitrite/light treatment in a prototypical technique used to prevent device thrombosis in extracorporeal circulation. We show that circuit pressure and survival are improved by an average of 213 percent with our treatment compared to the control. In addition, the dual therapy preserved platelet numbers at the end of the circulation time (%17 difference in platelet loss), and it reduced circuit hemolysis 2.3 fold. Thus, the combination of nitrite and red-light illumination has potential to prevent device thrombosis and to lead new clinical applications and practices.

pathology↗