Estimating the Starling equation parameters in living humans by using volume kinetic analysis.

IF 3.2 4区 医学 Q2 PHYSIOLOGY
Robert G Hahn
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引用次数: 0

Abstract

The transcapillary filtration of fluid is governed by the Starling forces. The purpose of the present study was to simultaneously estimate all Starling parameters in living humans by using likelihood mathematics. First, the capillary filtration was estimated by volume kinetic analysis at 3,015 time points during 193 intravenous infusion experiments using crystalloid and colloid fluid in adult volunteers and surgical patients placed in the supine position. Second, the obtained capillary filtration and the measured plasma colloid osmotic pressure were entered into a new kinetic analysis to estimate the five remaining parameters in the Starling equation. The result shows that the capillary hydrostatic pressure was 16 mmHg (Pc), the interstitial hydrostatic pressure - 2.2 mmHg (Pi), the interstitial colloid osmotic pressure 1.6 mmHg (πi), the reflection coefficient 0.79, and the capillary filtration coefficient (Kf) 306 mL/min/mmHg for the whole body when crystalloid volume loading was performed. Kf was significantly lower when colloid fluid (albumin 5% and 20%) was infused, and πi was lower in patients with subacute inflammation. Association plots showed that Pc was low in hypovolemia and inflammation but markedly higher when albumin was infused. Plots over time suggested that Kf was high early during an infusion, which was probably due to release of nitric oxide due to shear stress, but then decreased gradually. In conclusion, the parameters in the Starling equation could be estimated with acceptable confidence during fluid infusion experiments in humans. Changes of Kf appeared to be key parameter that modulated the capillary filtration rate during volume loading.

用体积动力学分析估算活人的Starling方程参数。
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来源期刊
CiteScore
8.80
自引率
2.20%
发文量
121
审稿时长
4-8 weeks
期刊介绍: Pflügers Archiv European Journal of Physiology publishes those results of original research that are seen as advancing the physiological sciences, especially those providing mechanistic insights into physiological functions at the molecular and cellular level, and clearly conveying a physiological message. Submissions are encouraged that deal with the evaluation of molecular and cellular mechanisms of disease, ideally resulting in translational research. Purely descriptive papers covering applied physiology or clinical papers will be excluded. Papers on methodological topics will be considered if they contribute to the development of novel tools for further investigation of (patho)physiological mechanisms.
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