Cardiovascular and pulmonary responses to increased acceleration forces during rest and exercise.

BACKGROUND: The reduced cardiac output (CO) secondary to increased acceleration forces (+Gz) has applicability to daily life and pathophysiology. Increased +Gz and reduced CO affect the lung, resulting in reduced oxygen transport. A variety of studies have examined tolerance to high +Gz. METHODS: The present study examines the effect of +1 to +3 Gz on steady-state cardiopulmonary variables at rest and while exercising at +2 Gz and +3 Gz. This study also looks at the deterioration of steady-state cardiopulmonary variables with sustained increased +Gz and after de-training in eight male centrifuge trained subjects. RESULTS: CO (-1.53 L x min(-1)/+Gz), stroke volume (-30 ml/+Gz, SV), and pulmonary diffusing capacity (-3.42 ml x mmHg(-1)/+Gz, DL(co)) decreased linearly with increased +Gz at rest while heart rate (23 bpm/+Gz, HR), total peripheral resistance (0.0095 TPRU/Gz TPR), mean arterial pressure (13.2 mmHg/+Gz, MAP), and ventilation (4.13 L x min(-1)/+Gz, V(E)) increased linearly. During graded exercise, CO and SV increased less at +2 Gz and +3 Gz while MAP and VE increased more. Failure to endure increased +Gz and the effects of de-training were primarily due to the inability to regulate MAP. DISCUSSION: The incremental increase in increased +Gz from 1 to 3 resulted in increased MAP, which was accomplished by increasing TPR sufficiently so as to offset the reduced CO. The effects of increased +Gz and reduced CO compromised lung function and oxygen transport (-18-30%), thus compromising exercise capacity. The failure to regulate MAP at lower increased +Gz levels resulted in intolerance to higher increased +Gz.

Hypoxia due to shunts in pig lung treated with O2 and fluorocarbon-derived intravascular microbubbles.

RATIONALE: Earlier work has shown that experimental conditions calling for improved tissue oxygenation could be assisted by i.v. infusion of a dodecafluoropentane emulsion (DDFPe) forming oxygen-transporting microbubbles. OBJECTIVES: The present work investigated the effect of DDFPe on hypoxia due to experimental shunts in the pig lung. METHODS: Nineteen O(2) breathing, anesthetized pigs had glass beads administered into the trachea so as to significantly depress arterial oxygen tension (PaO(2)). PaO(2) was recorded for up to 12 hrs while 0.1 ml/kg DDFPe was administered 1-3 times. MAIN RESULTS: The animals were divided into two groups based on arterial oxygen saturation (SaO(2)) after shunt induction, combined with oxygen breathing: the "SaO(2) >90% group" (n=6) and the "SaO(2) <90% group" (n=13). In the "SaO(2) <90% group," the PaO(2) increased stepwise with each infusion from 56.6+/-2.9 to 88.6+/-14.6 mmHG (P