Model of depressed myocardium shows orthostatic intolerance with or without reduced blood volume.

摘要

INTRODUCTION: The development of orthostatic hypotension (OH) is complex and multi-factorial. Previous simulation work indicates that myocardial contractility depression (MCD) may increase OH when there is a total blood volume decrease. This paper hypothesized that MCD increased OH in both humans with and without decrease in blood volume. METHODS: A model, which was previously used to reproduce cardiovascular response to lower body negative pressure (LBNP), hypovolemia, and MCD, was modified by incorporating the physiologic mechanism of plasma filtration into the interstitium during LBNP. The model was evaluated by human experimental results. Using the model, HR and BP response to LBNP were simulated at conditions of 10%, 20%, and 30% MCD. Additionally, HR and BP response to LBNP were simulated at conditions of 10% and 20% MCD with a 12% decrease in blood volume. RESULTS: Simulation results indicate that the increments of HR and decrements of systolic BP (SBP) and mean arterial pressure (MAP) rise withthe increases of MCD. Specifically, simulation results indicate that about 30% MCD would cause OH (HR: 117 bpm; SBP: 92 mmHg; MAP: 78 mmHg). It also indicates that about 20% MCD would cause OH (HR: 134 bpm, SBP: 84 mmHg, MAP: 73 mmHg) with a 12% decrease in total blood volume. CONCLUSION: It is suggested that MCD increases OH whether or not there is a total blood decrease, and further suggested that MCD induced by both spaceflight and heart disease may increase OH.