Application of negative tissue interstitial pressure improves functional capillary density after hemorrhagic shock in the absence of volume resuscitation.

Vinay P Jani,Krianthan Govender,Vivek P Jani,Alexander T Williams,Carlos J Munoz,Pedro Cabrales

doi:10.14814/phy2.14783

Vinay P Jani, Krianthan Govender + Show 4 more

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https://doi.org/10.14814/phy2.14783

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Abstract

Microvascular fluid exchange is primarily dependent on Starling forces and both the active and passive myogenic response of arterioles and post‐capillary venules. Arterioles are classically considered resistance vessels, while venules are considered capacitance vessels with high distensibility and low tonic sympathetic stimulation at rest. However, few studies have investigated the effects of modulating interstitial hydrostatic pressure, particularly in the context of hemorrhagic shock. The objective of this study was to investigate the mechanics of arterioles and functional capillary density (FCD) during application of negative tissue interstitial pressure after 40% total blood volume hemorrhagic shock. In this study, we characterized systemic and microcirculatory hemodynamic parameters, including FCD, in hamsters instrumented with a dorsal window chamber and a custom‐designed negative pressure application device via intravital microscopy. In large arterioles, application of negative pressure after hemorrhagic shock resulted in a 13 ± 11% decrease in flow compared with only a 7 ± 9% decrease in flow after hemorrhagic shock alone after 90 minutes. In post‐capillary venules, however, application of negative pressure after hemorrhagic shock resulted in a 31 ± 4% decrease in flow compared with only an 8 ± 5% decrease in flow after hemorrhagic shock alone after 90 minutes. Normalized FCD was observed to significantly improve after application of negative pressure after hemorrhagic shock (0.66 ± 0.02) compared to hemorrhagic shock without application of negative pressure (0.50 ± 0.04). Our study demonstrates that application of negative pressure acutely improves FCD during hemorrhagic shock, though it does not normalize FCD. These results suggest that by increasing the hydrostatic pressure gradient between the microvasculature and interstitium, microvascular perfusion can be transiently restored in the absence of volume resuscitation. This study has significant clinical implications, particularly in negative pressure wound therapy, and offers an alternative mechanism to improve microvascular perfusion during hypovolemic shock.

Highlights

Severe hemorrhagic shock is a known cause of widespread organ failure even after correction of systemic hemodynamics with transfusion(Cabrales et al,2004, 2007)
Interstitial edema can form due to changes in hydrostatic pressure, as observed in pulmonary edema secondary to left ventricular failure(Murray, 2011), or an increase in vascular permeability and subsequent loss of the glycocalyx-e ndothelial oncotic pressure gradient, as observed in acute respiratory distress syndrome (ARDS)(Monnet et al, 2007; Murray, 2011)
This study evaluates the effects of applied negative tissue interstitial pressure on microvascular perfusion both during normovolemia and after hemorrhagic shock

Summary

Introduction

Severe hemorrhagic shock is a known cause of widespread organ failure even after correction of systemic hemodynamics with transfusion(Cabrales et al, ,2004, 2007). Microvascular fluid flux is a function of capillary and interstitial hydrostatic and oncotic pressures. Modifications to the glycocalyx in diabetes, shock, and atherosclerosis have unexpected effects on the microvascular fluid flux that were previously underappreciated. In these cases, interstitial edema can form due to changes in hydrostatic pressure, as observed in pulmonary edema secondary to left ventricular failure(Murray, 2011), or an increase in vascular permeability and subsequent loss of the glycocalyx-e ndothelial oncotic pressure gradient, as observed in acute respiratory distress syndrome (ARDS)(Monnet et al, 2007; Murray, 2011). Few studies have investigated the effects of modulating interstitial hydrostatic pressure, in the context of hemorrhagic shock

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