Rapid intravenous infusion of 20 mL/kg saline alters the distribution of perfusion in healthy supine humans.
Rapid intravenous saline infusion, a model meant to replicate the initial changes leading to pulmonary interstitial edema, increases pulmonary arterial pressure in humans. We hypothesized that this would alter lung perfusion distribution. Six healthy subjects (29 ± 6 years) underwent magnetic resonance imaging to quantify perfusion using arterial spin labeling. Regional proton density was measured using a fast-gradient echo sequence, allowing blood delivered to the slice to be normalized for density and quantified in mL/min/g. Contributions from flow in large conduit vessels were minimized using a flow cutoff value (blood delivered > 35% maximum in mL/min/cm(3)) in order to obtain an estimate of blood delivered to the capillary bed (perfusion). Images were acquired supine at baseline, after infusion of 20 mL/kg saline, and after a short upright recovery period for a single sagittal slice in the right lung during breath-holds at functional residual capacity. Thoracic fluid content measured by impedance cardiography was elevated post-infusion by up to 13% (p<0.0001). Forced expiratory volume in 1s was reduced by 5.1% post-20 mL/kg (p=0.007). Infusion increased perfusion in nondependent lung by up to 16% (6.4 ± 1.6 mL/min/g baseline, 7.3 ± 1.8 post, 7.4 ± 1.7 recovery, p=0.03). Including conduit vessels, blood delivered in dependent lung was unchanged post-infusion; however, was increased at recovery (9.4 ± 2.7 mL/min/g baseline, 9.7 ± 2.0 post, 11.3 ± 2.2 recovery, p=0.01). After accounting for changes in conduit vessels, there were no significant changes in perfusion in dependent lung following infusion (7.8 ± 1.9 mL/min/g baseline, 7.9 ± 2.0 post, 8.5 ± 2.1 recovery, p=0.36). There were no significant changes in lung density. These data suggest that saline infusion increased perfusion to nondependent lung, consistent with an increase in intravascular pressures. Dependent lung may have been "protected" from increases in perfusion following infusion due to gravitational compression of the pulmonary vasculature.
Division of Physiology, Department of Medicine, University of California, San Diego, La Jolla, CA 92093-0623, United States. achenderson@ucsd.edu
A C
AC
Henderson
R C
RC
Sá
I A
IA
Barash
S
S
Holverda
R B
RB
Buxton
S R
SR
Hopkins
G K
GK
Prisk
D000328:Adult; D001826:Body Fluids / Q000502:physiology; D002307:Cardiography, Impedance; D003627:Data Interpretation, Statistical; D015633:Extravascular Lung Water / Q000502:physiology; D005260:Female; D006112:Gravitation; D006439:Hemodynamics / Q000502:physiology; D006801:Humans; D007091:Image Processing, Computer-Assisted; D007262:Infusions, Intravenous; D008168:Lung / Q000502:physiology; D008279:Magnetic Resonance Imaging; D008297:Male; D011522:Protons; D011652:Pulmonary Circulation / Q000187:drug effects* / Q000502:physiology; D012039:Regional Blood Flow / Q000502:physiology; D012965:Sodium Chloride / Q000008:administration & dosage / Q000494:pharmacology*; D013113:Spin Labels; D013147:Spirometry; D016683:Supine Position / Q000502:physiology*
D011522:Protons; D013113:Spin Labels; D012965:Sodium Chloride