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Biomedical subjects

R Naeije

Publications and source records attributed to R Naeije.

At least 37 records · Page 2Linked to original sources
PubMed2001

Physiology in medicine: importance of hypoxic pulmonary vasoconstriction in maintaining arterial oxygenation during acute respiratory failure.

Hypoxic pulmonary vasoconstriction continues to attract interest more than half a century after its original report because of persistent mystery about its biochemical mechanism and its exact physiological function. Recent work suggests an important role for pulmonary arteriolar smooth muscle cell oxygen-sensitive voltage-dependent potassium channels. Inhibition of these channels by decreased PO2 inhibits outward potassium current, causing membrane depolarization, and calcium entry through voltage-dependent calcium channels. Endothelium-derived vasoconstricting and vasodilating mediators modulate this intrinsic smooth muscle cell reactivity to hypoxia. However, refined modeling of hypoxic pulmonary vasoconstriction operating as a feedback mechanism in inhomogeneous lungs, using more realistic stimulus-response curves and confronted with direct measurements of regional blood flow distribution, shows a more effective than previously assessed ability of this remarkable intrapulmonary reflex to improve gas exchange and arterial oxygenation. Further studies could show clinical benefit of pharmacological manipulation of hypoxic pulmonary vasoconstriction, in circumstances of life-threatening hypoxemia.

Acute Disease↗
PubMed2001

Medical therapy of pulmonary hypertension. Conventional therapies.

The 1-, 3-, and 5-year survival rates of the patients included in the National Institute of Health Registry on Primary Pulmonary Hypertension were 77%, 41%, and 27% respectively. It is unclear to what extent better applied conventional therapy contributes to improved survival rates that now are reported with calcium-channel blockers, prostacyclin, or even transplantation. To date, by far the most favorable results are reported with high-dose calcium-channel blockers combined with anticoagulant therapy, with survival rates at 3 years approximately 100%. It has to be emphasized, however, that such exceptionally favorable results are to be expected only in a small minority of patients who should not be considered to be cured because, sooner or later, their disease will continue to evolve. Further improvements obviously are needed for most patients with PAH. Interesting developments are likely in the coming years, with new multidrug approaches to control pulmonary vasoreactivity and remodeling and, hopefully, also with progress in lung transplantation. The past 2 decades have witnessed important progress in the treatment of PAH. Although significant improvements in quality of life and survival rate have been obtained with prostacyclin therapy, and better perspectives now are offered with atrial septostomy and lung transplantation, conventional therapy also has evolved. Patients now are counseled more adequately regarding how to remain physically active while avoiding exercise-induced anginal pain or syncope. Invasive and potentially risky medical procedures have been restricted in favor of noninvasive and functional evaluations whenever possible. Risk factors such as appetite suppressants, pregnancy, and hypobaric hypoxia are now better appreciated. The indications of supplemental oxygen, inotropic agents, and diuretics have been refined based on improved pathophysiologic understanding. Most patients now benefit from anticoagulant therapy with coumarin derivatives, although some uncertainty remains about the optimal international normalized ratio to be achieved. Safer acute reversibility testing now is performed with fewer and shorter-acting agents that are more specific to the pulmonary circulation to select the small proportion of patients who benefit from long-term high-dose calcium-channel blocker therapy.

Altitude↗
PubMed2001

Inhibition of hypoxic pulmonary vasoconstriction by carbon monoxide in dogs.

OBJECTIVE: We tested the hypothesis that carbon monoxide might participate in the modulation of hypoxic pulmonary vasoconstriction (HPV) by prostacyclin (PGI2) and nitric oxide. DESIGN: Prospective, interventional study. SETTING: University laboratory. SUBJECTS: Nineteen intact anesthetized mongrel dogs. INTERVENTIONS: Right heart catheterization for the measurements of mean pulmonary artery pressure (Ppa), left atrial pressure estimated from occluded Ppa (Ppao), pulmonary capillary pressure (Pcp) calculated from the Ppa decay curve after balloon occlusion, and cardiac output (Q); inferior vena cava balloon for the control of Q by manipulation of venous return; ventilation in hyperoxia (fraction of inspired O2, 0.4) or in hypoxia (Fio2, 0.1); inhibition of cyclooxygenase by indomethacin (Indo); inhibition of nitric oxide synthase by NG-nitro-l-arginine (L-NA); inhibition of heme oxygenase by mesoporphyrin IX (SnMP); inhalation of nitric oxide (20 ppm); and inhalation of carbon monoxide (100 ppm). MEASUREMENTS AND MAIN RESULTS: The first seven dogs were weak responders to hypoxia as assessed by a hypoxia-induced increase in the gradient between Ppa and Ppao, measured at one level of Q kept constant, by an average of only 2 mm Hg (p = NS). This HPV was markedly increased by the combined administration of Indo and L-NA. A further enhancement of HPV was observed after the addition of SnMP, leading to severe pulmonary hypertension with an average increase in Ppa to 39 mm Hg. Inhaled nitric oxide inhibited HPV only after the combined administration of Indo, L-NA, and SnMP. Inhaled carbon monoxide had no effect. The next 12 dogs were stronger responders to hypoxia, as assessed by a hypoxia-induced increase in the gradient between Ppa and Ppao, measured at several levels of Q, by an average of 3 mm Hg (p <.05). This HPV was of the same magnitude after administration of placebo (n = 6) or SnMP (n = 6). Addition of Indo enhanced HPV to the same extent in the placebo and in the SnMP groups. Addition of L-NA induced a further enhancement of HPV, which was, however, greater in the SnMP group. There was a slight increase in the capillary-venous segment relative to the arterial segment in hypoxic conditions, but the partitioning of pulmonary vascular resistance was otherwise unaffected by nitric oxide, carbon monoxide, or PGI2. CONCLUSIONS: Endogenous carbon monoxide modulates canine HPV only in the absence of nitric oxide. The vasodilation mediated by nitric oxide, PGI2, or carbon monoxide is essentially distributed between proximal and distal sites proportionally to the degree of constriction produced during hypoxia.

Administration, Inhalation↗
PubMed2001

Long term treatment of pulmonary arterial hypertension with beraprost, an oral prostacyclin analogue.

OBJECTIVE: To evaluate the effects of one year's treatment with beraprost, an orally active prostacyclin analogue, in patients with severe pulmonary hypertension. PATIENTS: 13 patients with severe pulmonary hypertension. This was primary in nine, thromboembolic in three, and caused by Eisenmenger syndrome in one. METHODS: All patients underwent right heart catheterisation. Mean (SD) right atrial pressure was 5 (3) mm Hg, mean pulmonary artery pressure was 48 (12) mm Hg, cardiac index was 2.6 (0.8) l/min/m(2), and mixed venous oxygen saturation was 68 (7)%. Beraprost was started at the dose of 20 microgram three to four times a day (1 microgram/kg/day), increasing after one month to 40 microgram three to four times a day (2 microgram/kg/day), with further increases of 20 microgram three to four times a day in case of clinical deterioration. MAIN OUTCOME MEASURES: New York Heart Association (NYHA) functional class, exercise capacity measured by distance walked in six minutes, and systolic pulmonary pressure (by echocardiography) were evaluated at baseline, after one month's treatment, and then every three months for a year. RESULTS: After the first month of treatment, NYHA class decreased from 3.4 (0.7) to 2.9 (0.7) (p < 0.05), the six minute walking distance increased from 213 (64) to 276 (101) m (p < 0.05), and systolic pulmonary artery pressure decreased from 93 (15) to 85 (18) mm Hg (NS). One patient died after 40 days from refractory right heart failure, and another was lost for follow up at six months. The 11 remaining patients had persistent improvements in functional class and exercise capacity and a significant decrease in systolic pulmonary artery pressure in the period from 1-12 months. Side effects were minor. CONCLUSIONS: Oral administration of beraprost may result in long lasting clinical and haemodynamic improvements in patients with severe pulmonary hypertension.

Administration, Oral↗
PubMed2001

Oleic acid-induced lung injury: thin-section CT evaluation in dogs.

PURPOSE: To validate lung attenuation measurements for quantifying extravascular lung water in oleic acid-induced pulmonary edema, compare subjective assessment with attenuation measurements, and compare this permeability-type pulmonary edema with hydrostatic-type pulmonary edema. MATERIALS AND METHODS: Thin-section computed tomography (CT) and pulmonary hemodynamic examinations were performed sequentially in six dogs before and after intravenous administration of 0.08 mg of oleic acid per kilogram of body weight. Extravascular lung water and pulmonary capillary pressure were measured. Results were compared with those reported in a canine model of hydrostatic edema. RESULTS: Oleic acid induced a progressive increase in extravascular lung water without a change in capillary pressure, which indicated pure permeability-type edema. Ground-glass opacification was detected as soon as extravascular lung water increased. Lung attenuation was highly correlated to extravascular lung water (r = 0.76, P<.001), as in hydrostatic edema, but was characterized by an almost absent gravitational gradient. CONCLUSION: Thin-section CT is sensitive for early detection and quantification of oleic acid-induced pulmonary edema in a canine model. Different from early canine hydrostatic edema, which is characterized by a gravitational gradient, early oleic acid-induced pulmonary edema in a supine dog is characterized by nearly homogeneous distribution, except for ventral sparing.

Animals↗
PubMed2001

[Pulmonary hemodynamics and right ventricular function].

Measurement of continuous blood flow by thermodilution catheter takes into account measures that are intermittent, though the estimation of mean pressures is satisfactory. Natural pulsatile pulmonary circulation would remain unknown. To evaluate pulsatile pulmonary hemodynamics and its importance in right ventricular function, the calculation of impedance based on spectral analysis of pressure and flow waves would allow their respective contributions to resistance, elastance and wave reflection upon after right ventricle loading. Computerization allows bedside monitoring of this sophisticated assessment of right ventricle after loading.

Cardiac Catheterization↗
PubMed2000

Echocardiographic and invasive measurements of pulmonary artery pressure correlate closely at high altitude.

Exaggerated hypoxia-induced pulmonary hypertension is a hallmark of high-altitude pulmonary edema (HAPE) and plays a major role in its pathogenesis. Many studies of HAPE have estimated systolic pulmonary arterial pressure (SPAP) with Doppler echocardiography. Whereas at low altitude, Doppler echocardiographic estimation of SPAP correlates closely with its invasive measurement, no such evidence exists for estimations obtained at high altitude, where alterations of blood viscosity may invalidate the simplified Bernoulli equation. We measured SPAP by Doppler echocardiography and invasively in 14 mountaineers prone to HAPE and in 14 mountaineers resistant to this condition at 4,559 m. Mountaineers prone to HAPE had more pronounced pulmonary hypertension (57 +/- 12 and 58 +/- 10 mmHg for noninvasive and invasive determination, respectively; means +/- SD) than subjects resistant to HAPE (37 +/- 8 and 37 +/- 6 mmHg, respectively), and the values measured in the two groups as a whole covered a wide range of pulmonary arterial pressures (30-83 mmHg). Spearman test showed a highly significant correlation (r = 0.89, P < 0.0001) between estimated and invasively measured SPAP values. The mean difference between invasively measured and Doppler-estimated SPAP was 0.5 +/- 8 mmHg. At high altitude, estimation of SPAP by Doppler echocardiography is an accurate and reproducible method that correlates closely with its invasive measurement.

Adult↗
PubMed2000

Permissive hypercapnia impairs pulmonary gas exchange in the acute respiratory distress syndrome.

Current recommendations for mechanical ventilation in the acute respiratory distress syndrome (ARDS) include the use of small tidal volumes (VT), even at the cost of respiratory acidosis. We evaluated the effects of this permissive hypercapnia on pulmonary gas exchange with the multiple inert gas elimination technique (MIGET) in eight patients with ARDS. After making baseline measurements, we induced permissive hypercapnia by reducing VT from 10 +/- 2 ml/kg to 6 +/- 1 ml/kg (mean +/- SEM) at constant positive end-expiratory pressure. After restoration of initial VT, we infused dobutamine to increase cardiac output (Q) by the same amount as with hypercapnia. Permissive hypercapnia increased Q by an average of 1.4 L. min(-)(1). m(2), decreased arterial oxygen tension from 109 +/- 10 mm Hg to 92 +/- 11 mm Hg (p < 0.05), markedly increased true shunt (Q S/Q T), from 32 +/- 6% to 48 +/- 5% (p < 0.0001), and had no effect on the dispersion of VA/Q.VA/Q. On reinstatement of baseline V T with maintenance of a high Q, Q S/Q T remained increased, to 38 +/- 6% (p < 0.05), and Pa(O(2 ))remained decreased, to 93 +/- 4 mm Hg (p < 0. 05). These results agreed with effects of changes in VT and Q predicted by the mathematical lung model of the MIGET. We conclude that permissive hypercapnia increases pulmonary shunt, and that deterioration in gas exchange is explained by the combined effects of increased Q and decreased alveolar ventilation.

Adolescent↗
PubMed2000

Continuous versus pulsatile pulmonary hemodynamics in canine oleic acid lung injury.

Pulmonary hypertension occurs commonly in the acute respiratory distress syndrome (ARDS), but associated right ventricular failure is relatively rare. We tested the hypothesis that this apparent contradiction is explained by a peripheral location of the increased pulmonary vascular resistance (Rpva). Experimental ARDS was induced in eight dogs by injection of oleic acid (0.07 ml/kg). Changes in Rpva were evaluated by measurements of pulmonary artery pressure (Ppa) at several levels of flow (Q), which was altered by manipulation of venous return. The analysis of Ppa decay curves after arterial balloon occlusion was used to partition Rpva into arterial and venous segments. Right ventricular afterload was evaluated by determination of pulmonary vascular impedance (Zpva), which was calculated from spectral analysis of Ppa and Q waves. Oleic acid lung injury was associated with an increase in both the slope and the extrapolated pressure intercept of Ppa/Q plots, no change in the partitioning of Rpva, no change in time-domain indices in wave reflection or in pulmonary arterial compliance, and a decrease in both the characteristic impedance and pulsatile component of total right ventricular hydraulic load. We conclude that the site of increased Rpva in oleic acid lung injury is the smallest pulmonary arterioles, which, together with a decreased characteristic impedance, contributes to minimize right ventricular afterload.

Animals↗
PubMed1999

Cerebral blood flow velocity responses to hypoxia in subjects who are susceptible to high-altitude pulmonary oedema.

Cerebral blood flow increases on exposure to high altitude, and perhaps more so in subjects who develop acute mountain sickness. We determined cerebral blood flow by transcranial Doppler ultrasound of the middle cerebral artery at sea level, in normoxia (fraction of inspired O2, F(I)O2 0.21), and during 15-min periods of either hypoxic (F(I)O2 0.125) or hyperoxic (F(I)O2 1.0) breathing, in 7 subjects with previous high-altitude pulmonary oedema, 6 climbers who had previously tolerated altitudes between 6000 m and 8150 m, and in 20 unselected controls. Hypoxia increased mean middle cerebral artery flow velocity from 69 (3) to 83 (4) cm x s(-1) (P<0.001) in the controls, from 63 (3) to 75 (3) cm x s(-1) (P<0.001) in the high-altitude pulmonary-oedema-susceptible subjects, and from 58 (4) to 70 (4) cm x s(-1) (P<0.001) in the successful high-altitude climbers. Hyperoxia decreased mean middle cerebral flow velocity to 60 (3) cm x s(-1) (P<0.001), 53 (3) cm x s(-1) (P<0.01), and 49 (3) cm x s(-1) (P<0.01) in the controls, high-altitude pulmonary-oedema-susceptible, and high-altitude climbers, respectively. We conclude that a transcranial Doppler-based estimate of cerebral blood flow is affected by hypoxic and hyperoxic breathing, and that it is not predictive of tolerance to high altitude.

Adult↗
PubMed1999

Effects of low flow on pulmonary vascular flow-pressure curves and pulmonary vascular impedance.

OBJECTIVE: Flow-pressure curves and vascular impedance are commonly used to investigate pulmonary circulation, but they may be affected at low flow by reflex neurohumoral activation. We therefore investigated the mechanical effects and the reflex effects of decreased flow on pulmonary vascular resistance and impedance. METHODS: In ten anaesthetized dogs, we compared flow-pressure curves generated in less than 10 s to prevent sympathetic activation (fast curves), or generated over 20-30 min to allow neurohumoral equilibration (slow curves), in hyperoxia (inspired oxygen, 40%) and in hypoxia (inspired oxygen, 10%), before and after adrenergic blockade by phentolamine and propranolol. Resistance was assessed from the flow-pressure relationship. Impedance was computed from instantaneous flow and pressure obtained with an ultrasonic flowmeter and a micromanometer-tipped catheter. RESULTS: At baseline, fast flow-pressure curves were steeper and had a lower pressure intercept. Transient low flow did not affect heart rate or pulmonary arterial elastance. Sustained low flow increased heart rate, resistance and elastance, suggesting baroreceptor-induced sympathetic stimulation. After adrenergic blockade, no difference persisted between effects of transient and sustained low flow. In hypoxia, slow and fast flow-pressure curves were similar. Hypoxia increased heart rate and resistance but did not decrease elastance, suggesting chemoreceptor-induced sympathetic stimulation. In hypoxia, differences between transient and sustained low flow were no longer significant, and were completely suppressed by adrenergic blockade. In two additional dogs, epinephrine infusion increased pulmonary vascular resistance and elastance. CONCLUSIONS: We conclude that (1) compared to transient low flow, sustained low flow is associated with increases in distal resistance and proximal elastance due to sympathetic stimulation and (2) these differences between the effects of transient and sustained low flow do not persist in hypoxia, because of an already present chemoreceptor-induced sympathetic stimulation.

Adrenergic alpha-Antagonists↗
PubMed1999

Hydrostatic pulmonary edema: evaluation with thin-section CT in dogs.

PURPOSE: To identify the hemodynamic determinants of ground-glass opacification on thin-section computed tomographic (CT) scans of hydrostatic pulmonary edema and to compare attenuation and subjective assessments of ground-glass opacification with extravascular lung water. MATERIALS AND METHODS: Left atrial pressure, pulmonary arterial pressure, effective pulmonary capillary pressure, and extravascular lung water were measured in six dogs before and during progressive increase of effective pulmonary capillary pressure. A thin-section CT scan was obtained at each step. Lung attenuation and subjective assessments of ground-glass opacification were compared with hemodynamic variables and extravascular lung water. RESULTS: Ground-glass opacification was identified when effective pulmonary capillary pressure equaled critical pulmonary capillary pressure. Extravascular lung water increased, and the distribution curve of lung attenuation coefficients shifted to higher attenuation from the second measurement at an effective pulmonary capillary pressure greater than the critical pulmonary capillary pressure. Attenuation was highly correlated (r = 0.98, P < .001) with extravascular lung water; ground-glass opacification was detected before a significant (P = .615, analysis of variance) increase in extravascular lung water. CONCLUSION: Thin-section CT depicts ground-glass opacification when effective pulmonary capillary pressure equals critical pulmonary capillary pressure and before a detectable increase in extravascular lung water. Attenuation reflects extravascular lung water.

Animals↗
PubMed1999

Pulmonary arterial compliance in dogs and pigs: the three-element windkessel model revisited.

In six dogs and six weight-matched miniature pigs at baseline and after pulmonary embolization, pulmonary arterial compliance was determined using the pulse pressure method (C(PPM)), the three-element windkessel model (C(WK-3)), and the ratio of stroke volume to pulse pressure (SV/PP). C(PPM) was lower in pigs than in dogs at baseline (0.72 +/- 0.23 vs. 1.14 +/- 0.29 ml/mmHg, P < 0.05) and after embolism (0.37 +/- 0.14 vs. 0.54 +/- 0.16 ml/mmHg, P = 0. 07) at matched flow, but not at matched flow and pressure. C(PPM) showed the expected inverse relation with pressure and a direct relation with flow. C(WK-3) was closely correlated with C(PPM), except for all dogs at baseline where C(WK-3) was up to 100% higher than C(PPM). Excluding these data, regression analysis yielded C(WK-3) = -0.01 + 1.30. C(PPM) (r(2) = 0.97). C(WK-3) was found to be unreliable when input impedance first harmonic modulus was close to characteristic impedance, i.e., when reflections were small. SV/PP correlated well with C(PPM) (SV/PP = -0.10 + 1.76. C(PPM), r(2) = 0.89). We conclude that 1) C(PPM) is a consistent estimate of pulmonary arterial compliance in pigs and dogs, 2) C(WK-3) and SV/PP overestimate compliance, and 3) C(WK-3) is unreliable when wave reflections are small.

Animals↗
PubMed1999

Inhibition of cyclooxygenase and nitric oxide synthase in hypoxic vasoconstriction and oleic acid-induced lung injury.

Cyclooxygenase (COX) products and nitric oxide (NO) inhibit hypoxic pulmonary vasoconstriction (HPV), and their release could contribute to alterations in gas exchange in lung injury. We tested the hypothesis that combined blockade of COX and NO synthase (NOS) could further increase HPV and better protect gas exchange in lung injury than could blockade of either COX or NOS alone. We determined pulmonary vascular pressure-flow relationships in pentobarbital-anesthetized and ventilated dogs submitted to hypoxic challenges before and after administration of solvent (n = 4), indomethacin alone (2 mg/kg intravenously, n = 8), Nomega-nitro-L-arginine (L-NA) alone (10 mg/kg intravenoulsy, n = 8), indomethacin followed by L-NA (n = 8), and L-NA followed by indomethacin (n = 8). All of the dogs so treated then received oleic acid (0.06 ml/kg intravenously) to induce lung injury. Blood flow was manipulated by establishing a femoral arteriovenous bypass or by inflating an inferior vena caval balloon. Gas exchange was evaluated by measuring arterial PO2 and intrapulmonary shunt (using the inert gas sulfur hexafluoride) at identical cardiac outputs. The magnitude of HPV was not affected by solvent. Indomethacin and L-NA given separately enhanced HPV. L-NA added to indomethacin further enhanced HPV, as did indomethacin added to L-NA. After oleic acid-induced lung injury, gas exchange deteriorated less in dogs pretreated with indomethacin than in dogs pretreated with solvent or with L-NA alone. These results suggest that in pentobarbital-anesthetized dogs: (1) the magnitude of HPV is limited by the corelease of COX metabolites and of NO; and (2) inhibition of COX, but not of NOS, attenuates the deterioration of gas exchange in oleic acid-induced lung injury.

Animals↗
PubMed1999

[Point of view on doping].

Doping is defined as the administration of or use by competing athletes of any substance foreign to the body or of any physiological substance taken in abnormal quantity or taken by an abnormal route of entry into the body with the sole intention of increasing in an artificial and unfair manner his/her performance in competition. The prevalence of doping has been estimated by rigorous methods to be 5-15%. The only two dopings of established efficacy are: anabolic steroids for resistive performance, and blood doping for endurance performance. Although medical control of athletes is reputably poor, reported accidents attributable to doping have been until now very rare. Doping is unfair, and must as such be banned from competitions. Medicalized doping is unethical. More studies are required to improve knowledge of doping as a public health issue. Sports medicine is in need of scientific and moral revalorization.

Anabolic Agents↗
PubMed1999

[Physiopathology of pulmonary arterial hypertension and gas exchange in acute pulmonary embolism].

Pulmonary embolism alters the distribution of ventilation/perfusion relationships, and increases pulmonary vascular resistance. These changes lead to hypoxemia and hypocapnia, and eventually, to right heart failure. The thin-walled and compliant right ventricle adapts to any increase in afterload by dilatation and decreased stroke volume, but this is largely prevented or delayed by the pulmonary circulation being a low resistance, recruitable and distensible circuit. Pulmonary embolism cannot be associated with a mean pulmonary artery pressure higher than 40 mmHg. More severe pulmonary hypertension indicates the presence of a hypertrophied right ventricle in the context of preexistent cardiac or pulmonary disease. Gas exchange is initially affected because of increased ventilation/perfusion ratios in embolized lung areas, and decreased ventilation/perfusion ratios in remaining non embolized lung areas. Both physiologic shunt and physiologic dead space increase accordingly, resulting in hypoxemia and hypocapnia. However, these changes are rapidly affected by an increase in ventilation, and by a "pneumoconstriction" which decreases physiologic dead space in embolized areas. In addition, a series of secondary alterations contribute to increase perfusion to lung units with low ventilation/perfusion ratios, thereby aggravating hypoxemia, while hypocapnia persists.

Acute Disease↗
PubMed1998

Pulmonary vascular resistance in dogs and minipigs--effects of hypoxia and inhaled nitric oxide.

The pig has been reported to present with a stronger hypoxic pulmonary vasoconstriction than many other species, including the dog, but it is not known whether this is associated with a different longitudinal partitioning of pulmonary vascular resistance (PVR). We investigated the relationships between cardiac output (Q) and mean pulmonary artery pressure (Ppa) minus occluded Ppa (Ppao), and effective pulmonary capillary pressure (Pc') minus Ppao, in seven minipigs and in seven dogs in hyperoxia (FI(O2) 0.4) and hypoxia (FI(O2) 0.1), first without, then with the inhalation of 80 ppm nitric oxide (NO) to inhibit any reversible component of PVR. Pc' was estimated from the Ppa decay curve following pulmonary artery balloon occlusion. In hyperoxia, minipigs compared to dogs had (Ppa - Ppao)/Q and (Pc' - Ppao)/Q plots shifted to higher pressures. Hypoxia at each level of Q increased Ppa - Ppao in minipigs more than in dogs, and Pc' - Ppao in minipigs only. Inhaled NO reversed hypoxia-induced changes in (Ppa - Ppao)/(Q and (Pc' - Ppao)/Q plots. We conclude that the minipig, compared to the dog, presents with higher PVR and reactivity including vessels downstream to the site of Pc' as determined by the arterial occlusion technique.

Administration, Inhalation↗