Hypoxic Pulmonary Vasoconstriction and Gas Exchange During Exercise: RESULTS part 2
Exercise Before Nifedipine (vs Rest Before Nifedipine)
Exercise Vo2 (872 ml/min) averaged 53 ±5 percent of maximal predicted. This represented a substantial level of exercise for these patients, as it is shown by the significant decrease in arterial pH and base excess (BE) (Table 2). During exercise, pulmonary hypertension became severe and both TPVR (Table 2) and RVSWI increased (8.2±0.5 to 23.0±1.7 g-m/m2, p<0.001). Even though Pa02 showed a trend to fall (76 to 68 mm Hg, p = 0.07), because PaC02 increased simultaneously (39 to 43 mm Hg, p<0.001), P(A-a)02 did not change (28 to 31 mm Hg). The Vd/Vt fell from 50 to 42 percent (p<0.001). Exercise reduced Va/Q mismatching as estimated either by the significant decreases in Log Q and Log V or DISP R-E* (Table 2 and Fig 1 and 3). The Q shifted toward higher values (p<0.005) but V did not change.
Arterial Po2 was computed from the recovered Va/ Q distributions to predict the Pa02 expected on the basis of Va/Q mismatch alone (“predicted Pa02“). In this manner, diffusion limitation of 02 transfer from alveoli to the end-capillary blood is evident as a systematically higher predicted than measured Pa02. At rest, no significant difference was noticed between predicted and measured Pa02. However, during exercise, predicted Po2 (74 ±5 mm Hg) was systematically higher than measured Pa02 (68 ±4 mm Hg, p<0.002). In absolute terms, this difference was small (6±1 mm Hg) and accounted for 20 percent of the actual P(A-a)02. This observation suggests that pulmonary 02 transfer was partially diffusion limited in these patients with COPD during exercise. viagra 10 mg
FIGURE 1. Recovered VA/Q distributions in a representative subject (patient 1). From left to right and from top to botton: rest and exercise before nifedipine, and rest and exercise after nifedipine. Closed circles correspond to the distribution of pulmonary blood flow; open circles, the distribution of ventilation.
Exercise After Nifedipine (vs Rest After Nifedipine)
The behavior of most of the hemodynamic and gas exchange variables during exercise after nifedipine was similar to that seen during exercise before giving the drug (Table 2). However, the Vd/Vt ratio showed a different response to exercise depending on the presence or absence of nifedipine: as expected, Vd/Vt fell significantly during exercise before nifedipine, but it did not change after giving the drug (Table 2 and Fig 3). Finally, it is of note that predicted and measured Pa02 values during exercise after nifedipine fell along the same direction as during exercise before nifedipine, but differences just failed to reach statistical significance (70 ± 4 vs 66 ± 4 mm Hg, respectively [p = 0.09]).
Exercise After Nifedipine (vs Exercise Before Nifedipine
Oxygen uptake during exercise was similar before and after nifedipine, but Qt increased following it (p<0.005) (Table 2). Moreover, during exercise, Ppa, TPVR (Table 2), and RVSWI (20.3 ± 1.6 g-m/m2, p<0.05) were all lower after nifedipine. The pulmonary pressure-flow relationship was displaced toward higher flows in each patient (Fig 2). Although Pao2 during exercise was similar irrespective of the drug, P(A-a)02 was higher after nifedipine because the higher SIe lowered PaC02 (Table 2). Oxygen delivery was increased during exercise after nifedipine (2,182 ±187 vs 1,931 ±159 ml/min, p<0.002). Interestingly, since Vd/Vt did not change during exercise with nifedipine, it was higher after than before giving the drug (Table 2). Accordingly, the percentage of ventilation distributed to high Va/Q areas (10 to 100) increased almost twofold during exercise after nifedipine (3.7 to 6.2 percent), but differences failed to reach statistical significance. Overall, there was more Va/Q mismatching during exercise after than before nifedipine (higher DISP R-E*, pCO.OOl). The perfusion distribution was shifted to the left (lower Q) and the ventilation distribution was shifted to the right (higher V) (Table 2). The higher LogsD Q during exercise after nifedipine probably reflects release of HPV and subsequent interference with the ability of the pulmonary circulation to distribute blood flow during exercise in a more efficient manner (Fig 3). The dispersion of the ventilation distribution (LogsD V) during exercise was not modified by nifedipine (Table 2).
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FIGURE 2. Mean values (x±SEM) of cardiac output (Qr) and mean pulmonary artery pressure (Ppa) at rest (bottom) and during exercise (top), before (continuous line) and after nifedipine (dashed line). The pressure-flow relationship shifted to the right after nifedipine (p<0.01), indicating an active vasodilatory effect of the drug.
A synergistic effect between exercise and nifedipine could be demonstrated only for Vd/Vt. The physiologic significance of this interaction has already been discussed above.
