Cold and warm infusion of Ringer's acetate in healthy volunteers: the effects on haemodynamic parameters, transcapillary fluid balance, diuresis and atrial peptides

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Abstract
The effects of Ringer's acetate (RAc) infusion with different temperatures, 18d̀C compared to 36d̀C, were studied in 20 healthy volunteers. An infusion volume of 20% of the estimated extracellular volume was given over 45 min. Before and after the RAc infusion, interstitial colloid osmotic pressure and interstitial fluid hydrostatic pressure were measured on the lateral part of the thorax and in the lower leg. Blood sampling and pressure measurements were performed through a cannula placed in the left radial artery, and arterial oxygen saturation was measured by pulse oximetry. Atrial peptides ANF (99–126) and ANF (1–98) in plasma were measured as indicators of volume loading. Cold RAc infusion increased mean arterial pressure from 82 (s.d. ± 7) to 96 (s.d. ± 9) mmHg (10.9–12.8 kPa) at the end of the infusion with a simultaneous fall in heart rate. Warm RAc infusion gave no changes in blood pressure or heart rate. The arterial oxygen saturation during the infusion of cold RAc was higher than during warm RAc infusion. Cold infusion produced the expected haemodilution with a fall in erythrocyte volume fraction (EVF) from 0.39 (± 0.03) to 0.33 (± 0.03) and a fall in plasma colloid osmotic pressure (COPp) from 21.7 (± 1.1) mmHg to 15.0 (± 1.3) mmHg (2.9–2.0 kPa). Warm infusion induced a nearly identical haemodilution. Interstitial colloid osmotic pressure fell from 11.6 (± 2.3) mmHg to 8.9 (± 2.7) mmHg (1.5–1.2 kPa) after warm infusion while cold infusion gave no changes. The changes in interstitial fluid hydrostatic pressure were not significant. Cold infusion induced a higher diuresis compared to warm RAc infusion. ANF increased during cold, but not during warm infusion. We conclude that infusions of RAc at 18d̀C vs. 36d̀C have different volume effects. Cold infusion increased blood pressure and diuresis, while warm infusion induced peripheral vasodilation with increased capillary leakage and subcutaneous oedema formation.