Hypoxic pulmonary vasoconstriction and gas exchange in acute canine pulmonary embolism

1996 ◽  
Vol 80 (4) ◽  
pp. 1240-1248 ◽  
Author(s):  
M. Delcroix ◽  
C. Melot ◽  
F. Vermeulen ◽  
R. Naeije
Keyword(s):  
Pulmonary Embolism ◽  
Gas Exchange ◽  
Sulfur Hexafluoride ◽  
Blood Clot ◽  
Hypoxic Pulmonary Vasoconstriction ◽  
Autologous Blood ◽  
Response Curves ◽  
Pulmonary Hemodynamics ◽  
Pulmonary Vasoconstriction ◽  
Pulmonary Arterial

Hypoxic pulmonary vasoconstriction (HPV) is inhibited in several models of acute lung injury. Whether HPV is preserved in pulmonary embolism is unknown. We investigated the effects of a reduction in the fraction of inspired O2 (FIO2) on pulmonary hemodynamics and gas exchange in anesthetized dogs before and after autologous blood clot pulmonary embolism. In a first group of 14 dogs, stimulus-response curves for HPV were constructed as pulmonary arterial pressure (Ppa) vs. FIO2 varied between 1.0 and 0.06 at a cardiac output (Q) kept constant at 3.5 l.min-1.m-2. Gas exchange was evaluated by using the multiple inert-gas elimination technique at FIO2 of 1.0, 0.4, and 0.1. Embolism decreased the relative magnitude of HPV, expressed as the gradient between Ppa and pulmonary arterial occluded pressure in hypoxia divided by (Ppa-pulmonary arterial occluded pressure) at FIO2 of 1.0, from 1.8 to 1.2 (P < 0.05). Retention minus excretion gradients for sulfur hexafluoride and ethane were increased by decreased FIO2 (P < 0.005 and P < 0.05, respectively) before but not after embolism. Hypoxia-induced deterioration in gas exchange before embolism was related to the amount of baseline very low ventilation-perfusion (VA/Q) ratios. Similar results were obtained in a second group of seven dogs with Q decreased to maintain Ppa at the same average value as before embolism. However, gas exchange was not affected by inspiratory hypoxia before as well as after embolism in this group, which presented with a lesser amount of baseline very low VA/Q. In both groups of dogs, increase in the FIO2 from 0.4 to 1.0 did not affect gas exchange. We conclude that 1) pulmonary embolism is associated with a partial inhibition of HPV, 2) HPV does not contribute to preserve gas exchange in pulmonary embolism, and 3) a strong HPV may deteriorate gas exchange in severe hypoxia in the presence of minor very low VA/Q inequality.

Effects of hyperoxia on vasoconstriction and VA/Q matching in the neonatal lung

1987 ◽  
Vol 63 (6) ◽  
pp. 2536-2541 ◽  
Author(s):  
W. E. Truog ◽  
G. J. Redding ◽  
T. A. Standaert
Keyword(s):  
Gas Exchange ◽  
Sulfur Hexafluoride ◽  
Hypoxic Pulmonary Vasoconstriction ◽  
Inert Gas ◽  
Control Group ◽  
Pulmonary Hemodynamics ◽  
Neonatal Piglets ◽  
Hyperoxic Exposure ◽  
Neonatal Lung ◽  
Pulmonary Arterial

Exposure of adult animals to 48–72 h of 100% O2 breathing is associated with a blunting of hypoxic pulmonary vasoconstriction (HPV) (Newman et al. J. Appl. Physiol. 54: 1379–1386, 1983). It is unknown whether HPV is also diminished in neonates after hyperoxic exposure and if so to what extent such suppression might interfere with pulmonary gas exchange during hypoxic gas breathing. We tested the possibility that hyperoxia would suppress HPV and interfere with ventilation-perfusion (VA/Q) matching and therefore gas exchange in neonatal piglets. Twelve 2- to 4-wk-old piglets were exposed for an average of 68 h to greater than 90% inspired O2. A control group of eight piglets was exposed to room air for a similar period of time. Immediately after exposure the animals were anesthetized and instrumented. Pulmonary hemodynamics and respiratory and inert gas exchange were assessed while the animals inspired an O2 fraction of 1.0, 0.21, and 0.12. After 20 min of hypoxic gas breathing, pulmonary arterial pressure rose to a lesser degree in the hyperoxia (H)-exposed animals than in the control (C) animals (P less than 0.02). The increase in pulmonary vascular resistance was similarly blunted. Venous admixture of the insoluble inert gas, sulfur hexafluoride, an index of extremely low VA/Q areas, was increased during hypoxic gas breathing compared with room air breathing in the H-preexposed animals (P less than 0.02). Standard deviation of pulmonary blood flow was increased (P less than 0.02), indicating an increase in mismatching of VA/Q during hypoxic breathing in the H-preexposed animals compared with the C animals.(ABSTRACT TRUNCATED AT 250 WORDS)

PEEP inhibits hypoxic pulmonary vasoconstriction in dogs

1991 ◽  
Vol 70 (4) ◽  
pp. 1867-1873 ◽  
Author(s):  
P. Lejeune ◽  
J. L. Vachiery ◽  
J. M. De Smet ◽  
M. Leeman ◽  
S. Brimioulle ◽  
...  
Keyword(s):  
Inferior Vena ◽  
Intact Animal ◽  
Hypoxic Pulmonary Vasoconstriction ◽  
Balloon Catheter ◽  
Vena Cava ◽  
Pulmonary Hemodynamics ◽  
Mean Pulmonary Arterial Pressure ◽  
Pulmonary Vasoconstriction ◽  
Anesthetized Dogs ◽  
Pulmonary Arterial

The effects of an increase in alveolar pressure on hypoxic pulmonary vasoconstriction (HPV) have been reported variably. We therefore studied the effects of positive end-expiratory pressure (PEEP) on pulmonary hemodynamics in 13 pentobarbital-anesthetized dogs ventilated alternately in hyperoxia [inspired O2 fraction (FIO2) 0.4] and in hypoxia (FIO2 0.1). In this intact animal model, HPV was defined as the gradient between hypoxic and hyperoxic transmural (tm) mean pulmonary arterial pressure [Ppa(tm)] at any level of cardiac index (Q). Ppa(tm)/Q plots were constructed with mean transmural left atrial pressure [Pla(tm)] kept constant at approximately 6 mmHg (n = 5 dogs), and Ppa(tm)/PEEP plots were constructed with Q kept constant approximately 2.8 l.min-1.m-2 and Pla(tm) kept constant approximately 8 mmHg (n = 8 dogs). Q was manipulated using a femoral arteriovenous bypass and a balloon catheter in the inferior vena cava. Pla(tm) was held constant by a balloon catheter placed by left thoracotomy in the left atrium. Increasing PEEP, from 0 to 12 Torr by 2-Torr increments, at constant Q and Pla(tm), increased Ppa(tm) from 14 +/- 1 (SE) to 19 +/- 1 mmHg in hyperoxia but did not affect Ppa(tm) (from 22 +/- 2 to 23 +/- 1 mmHg) in hypoxia. Both hypoxia and PEEP, at constant Pla(tm), increased Ppa(tm) over the whole range of Q studied, from 1 to 5 l/min, but more at the highest than at the lowest Q and without change in extrapolated pressure intercepts. Adding PEEP to hypoxia did not affect Ppa(tm) at all levels of Q.(ABSTRACT TRUNCATED AT 250 WORDS)

Relationship of leukotriene C4 and D4 to hypoxic pulmonary vasoconstriction in dogs

1988 ◽  
Vol 64 (6) ◽  
pp. 2538-2543 ◽  
Author(s):  
A. J. Lonigro ◽  
R. S. Sprague ◽  
A. H. Stephenson ◽  
T. E. Dahms
Keyword(s):  
Hypoxic Pulmonary Vasoconstriction ◽  
Lavage Fluid ◽  
Pulmonary Hemodynamics ◽  
Mean Pulmonary Arterial Pressure ◽  
Pulmonary Vasoconstriction ◽  
Time Period ◽  
Pulmonary Arterial ◽  
Synthase Inhibitor ◽  
Leukotriene A4 ◽  
Relationship Of

Leukotrienes C4 and D4 have been implicated as possible mediators of hypoxic pulmonary vasoconstriction. To test this hypothesis, the relationship between pulmonary leukotriene (LT) synthesis in response to hypoxia and alterations in pulmonary hemodynamics was evaluated in pentobarbital sodium-anesthetized, neuromuscular-blocked, male, mongrel dogs. A reduction in the fraction of inspired O2 (FIO2) in vehicle-treated animals (n = 12) from 0.21 to 0.10 was associated with increases in LTC4 and LTD4 in bronchoalveolar lavage fluid (BALF). After 30 min of continuous hypoxia, LTC4 and LTD4 increased from control values of 59.4 +/- 10.4 and 91.7 +/- 18.1 ng/lavage to 142.7 +/- 31.8 (P less than 0.05) and 156.3 +/- 25.3 (P less than 0.01) ng/lavage, respectively. Concomitantly, mean pulmonary arterial pressure (Ppa) and pulmonary vascular resistance (PVR) were increased over control by 67 +/- 7 (P less than 0.001) and 62 +/- 7% (P less than 0.001), respectively. In contrast, in animals treated with diethylcarbamazine (n = 5), a leukotriene A4 synthase inhibitor, identical reductions in FIO2 were not associated with increases in LTC4 and LTD4 in BALF, although at the same time period, Ppa and PVR were increased over control by 60 +/- 13 (P less than 0.05) and 112 +/- 31% (P less than 0.05), respectively. These results, therefore, do not support the contention that leukotrienes mediate hypoxic pulmonary vasoconstriction in dogs.

Pulmonary vascular impedance response to hypoxia in dogs and minipigs: effects of inhaled nitric oxide

1995 ◽  
Vol 79 (4) ◽  
pp. 1156-1162 ◽  
Author(s):  
M. Maggiorini ◽  
S. Brimioulle ◽  
D. De Canniere ◽  
M. Delcroix ◽  
P. Wauthy ◽  
...  
Keyword(s):  
Hypoxic Pulmonary Vasoconstriction ◽  
Characteristic Impedance ◽  
Low Frequency ◽  
Pulmonary Hemodynamics ◽  
Vascular Impedance ◽  
Impedance Response ◽  
Pulmonary Vasoconstriction ◽  
Pulmonary Arterial ◽  
Induced Changes ◽  
Inhaled No

The pig has been reported to present with a stronger hypoxic pulmonary vasoconstriction (HPV) than many other species, including dogs. We investigated [pulmonary arterial pressure (Ppa)-pulmonary arterial occluded pressure (Ppao)] vs. pulmonary blood flow (Q) relationships and pulmonary vascular impedance (PVZ) spectra in nine minipigs and nine weight-matched dogs. The animals were anesthetized and ventilated in hyperoxia [inspired O2 fraction 0.4] or hypoxia (inspired O2 fraction 0.12). PVZ was computed from the Fourier series for Ppa and Q. In hyperoxia, the pigs had a higher Ppa (26 +/- 1 vs. 16 +/- 1 mmHg), a higher first-harmonic impedance (Z1), and a more negative low-frequency phase angle but no different characteristic impedance (Zc) compared with the dogs at the same Q. Hypoxia in the dogs increased (Ppa-Ppao) at all levels of Q studied by an average of 2 mmHg but did not affect Z1 or Zc. Hypoxia in the pigs increased (Ppa-Ppao) at all levels of Q by an average of 13 mmHg and increased Z1 and Zc. Inhaled NO (150 ppm) reversed the hypoxia-induced changes in (Ppa-Ppao)/Q plots and PVZ in the dogs and pigs. However, differences in (Ppa-Ppao)/Q plots and PVZ between the dogs and pigs in hyperoxia and hypoxia were not affected by inhaled NO. We conclude 1) that minipigs present with an elevated pulmonary vascular resistance and impedance in hypoxia more than in hyperoxia and 2) that baseline differences in pulmonary hemodynamics between dogs and minipigs are structural rather than functional.

Embolus size affects gas exchange in canine autologous blood clot pulmonary embolism

1993 ◽  
Vol 74 (3) ◽  
pp. 1140-1148 ◽  
Author(s):  
M. Delcroix ◽  
C. Melot ◽  
P. Vanderhoeft ◽  
R. Naeije
Keyword(s):  
Pulmonary Hypertension ◽  
Gas Exchange ◽  
Blood Clot ◽  
Autologous Blood ◽  
Inert Gas ◽  
Experimental Conditions ◽  
Arterial Ph ◽  
Pulmonary Arterial ◽  
Vascular Obstruction ◽  
Autologous Blood Clot

Embolic pulmonary hypertension is associated with alterations in gas exchange of variable severity, which we hypothesized to be related to embolus size. We therefore examined the effects of different-size autologous blood clot embolization on pulmonary arterial pressure-cardiac output relationships (Ppa/Q) and on the distribution of ventilation-perfusion ratios (VA/Q) in 18 intact anesthetized and ventilated (inspired fraction of O2 0.4) dogs. Multipoint Ppa/Q plots were generated by a manipulation of venous return before and 60 min after sufficient amounts of small (1 mm, n = 6 dogs), medium (5 mm, n = 6 dogs), or large (10 mm, n = 6 dogs) clots to increase Ppa to 50 mmHg. The distribution of VA/Q was determined by the multiple inert gas elimination technique at the same intermediate Q in each of these experimental conditions. All three sizes of emboli resulted in an 82–92% mean angiographic pulmonary vascular obstruction and increased both the extrapolated pressure intercepts and the slopes of the linear Ppa/Q plots. Gas exchange was altered the most after large clots, which were associated with lower arterial pH, higher physiological and inert gas dead spaces, higher dispersion of ventilation, and also lower mean VA/Q of perfusion distributions. In contrast, inert gas dead space was decreased after small clots. We conclude that, in autologous blood clot embolic pulmonary hypertension, Ppa/Q characteristics are unaffected by embolus size but that gas exchange is affected differently, mainly in high-VA/Q regions and most often after the largest clots.

Effects of inhaled nitric oxide on pulmonary hemodynamics and gas exchange in an ovine model of ARDS

1994 ◽  
Vol 76 (1) ◽  
pp. 345-355 ◽  
Author(s):  
I. Rovira ◽  
T. Y. Chen ◽  
M. Winkler ◽  
N. Kawai ◽  
K. D. Bloch ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Acute Lung Injury ◽  
Gas Exchange ◽  
Lung Injury ◽  
Soluble Guanylate Cyclase ◽  
Hypoxic Pulmonary Vasoconstriction ◽  
Pulmonary Hemodynamics ◽  
Pulmonary Vasodilation ◽  
Pulmonary Vasoconstriction ◽  
Selective Pulmonary Vasodilation

Inhaling low concentrations of nitric oxide (NO) gas causes selective pulmonary vasodilation of ventilated lung regions. NO activates soluble guanylate cyclase, increasing guanosine 3′,5′-cyclic monophosphate (cGMP). Inhibition of NO synthesis enhances hypoxic pulmonary vasoconstriction. Therefore we examined independent and combined effects of NO inhalation and infusion of NG-nitro-L-arginine methyl ester (L-NAME), an NO synthesis inhibitor, on pulmonary vascular pressure-flow relationships, gas exchange, and plasma cGMP levels in anesthetized and mechanically ventilated sheep with acute lung injury induced by bilateral lavage. After lavage, inhaling 60 ppm by volume of NO decreased pulmonary arterial pressure (PAP) and resistance without any systemic hemodynamic effects, increased arterial PO2, and decreased venous admixture (Qva/QT; all P < 0.05) without altering cardiac output (QT), mixed venous PO2, or O2 uptake, major determinants of intrapulmonary shunt. During NO inhalation, PAP-left atrial pressure gradient (PAP-LAP) and Qva/QT were reduced (both P < 0.05) independently of QT, which was varied mechanically. L-NAME infusion produced systemic and pulmonary vasoconstriction and increased PAP-LAP gradient across the entire range of QT, whereas Qva/QT, was not changed. NO inhalation after L-NAME infusion produced pulmonary vasodilation and decreased Qva/QT to the same degree as NO inhalation alone. Five to 10 min after inhalation of 60 ppm NO, before and after L-NAME infusion, arterial plasma cGMP levels were increased by 80% (both P < 0.05). With NO breathing after L-NAME, we measured a consistent transpulmonary cGMP arteriovenous gradient [31 +/- 8 and 33 +/- 7 (SE) pmol/ml at 5 and 10 min, respectively; both P < 0.05]. NO inhalation before or after L-NAME administration in this acute lung injury model reduced Qva/QT, most likely by increasing cGMP concentration in ventilated lung regions and causing selective pulmonary vasodilation.

A distensible vessel model applied to hypoxic pulmonary vasoconstriction in the neonatal pig

1993 ◽  
Vol 74 (5) ◽  
pp. 2049-2056 ◽  
Author(s):  
L. D. Nelin ◽  
G. S. Krenz ◽  
D. A. Rickaby ◽  
J. H. Linehan ◽  
C. A. Dawson
Keyword(s):  
Hypoxic Pulmonary Vasoconstriction ◽  
Autologous Blood ◽  
Vessel Diameter ◽  
Flow Data ◽  
Neonatal Pigs ◽  
Pulmonary Vasoconstriction ◽  
Resistance Vessels ◽  
Torr Pressure ◽  
Pulmonary Arterial ◽  
Isolated Lungs

Recently, we presented a simple two-parameter distensible vessel model as a potential tool for characterizing pulmonary vascular pressure vs. flow curves under zone 3 conditions (Linehan et al. J. Appl. Physiol. 73: 987–994, 1992). One parameter, alpha, represents the distensibility of the resistance vessels as the fractional change in vessel diameter per Torr change in pressure, and the other parameter, R0, represents the vascular resistance that would exist if the resistance vessels were at their respective diameters obtained if the vascular pressure were zero. The objective of the present study was to determine whether this distensible vessel model was capable of describing the pressure vs. flow data obtained during hypoxia vasoconstriction and under control conditions in isolated lungs from neonatal pigs. The piglet lungs were perfused with autologous blood, and the pulmonary arterial pressure was measured over a range of flow rates from 15 to 250 ml.min-1 x kg-1 at constant left atrial (3 Torr) pressure. The model provided a reasonable fit to the data under both conditions. Hypoxia resulted in a significant increase in R0, from 0.39 +/- 0.10 Torr.ml-1 x min.kg during control conditions to 1.41 +/- 0.46 Torr.ml-1 x min.kg during hypoxia. alpha was 2.4 +/- 0.4%/Torr under control conditions and 2.0 +/- 0.4%/Torr during hypoxia, but this difference was not statistically significant. The results suggest that the distensible vessel model may be useful for interpreting pressure-flow data in terms of changes in geometry and distensibility of the resistance vessels in response to a vasoconstrictor stimulus such as hypoxia.

Effects of hypoxia on leukotriene activity and vasomotor tone in isolated sheep lungs

1990 ◽  
Vol 68 (6) ◽  
pp. 2457-2465 ◽  
Author(s):  
J. Schnader ◽  
B. Undem ◽  
G. K. Adams ◽  
S. P. Peters ◽  
N. F. Adkinson ◽  
...  
Keyword(s):  
Hypoxic Pulmonary Vasoconstriction ◽  
Autologous Blood ◽  
Vasomotor Tone ◽  
Pulmonary Vasoconstriction ◽  
Period 2 ◽  
Tracheal Pressure ◽  
O2 Concentration ◽  
Pulmonary Arterial ◽  
Lung Lymph

To determine whether hypoxic pulmonary vasoconstriction was associated with release of sulfidopeptide leukotrienes (SPLTs) from the lung, we measured SPLT activity by bioassay (guinea pig ileum) and radioimmunoassay in lymph, perfusate, and bronchoalveolar lavage (BAL) fluid from sheep lungs (n = 20) isolated and perfused in situ with a constant flow of autologous blood (100 ml.kg-1.min-1) containing indomethacin (60 micrograms/ml). The protocol consisted of three periods, each at least 1 h in duration. In experimental lungs, inspired O2 concentration (FIO2) was 28.2% in periods 1 and 3 and 4.2% in period 2. In control lungs, FIO2 was 28.2% throughout. Hypoxia increased pulmonary arterial pressure but did not alter peak tracheal pressure, lung lymph flow, or weight gain measured during the last 30 min of each period. SPLT activity was greatest in lung lymph and least in BAL fluid. Hypoxia did not alter SPLT activity in any fluid. Similar results were obtained in lungs not treated with indomethacin (n = 15). These data do not support the hypothesis that hypoxic pulmonary vasoconstriction is mediated by SPLTs.

Inhibition of hypoxic pulmonary vasoconstriction by antagonists of store-operated Ca2+ and nonselective cation channels

2005 ◽  
Vol 289 (1) ◽  
pp. L5-L13 ◽  
Author(s):  
Letitia Weigand ◽  
Joshua Foxson ◽  
Jian Wang ◽  
Larissa A. Shimoda ◽  
J. T. Sylvester
Keyword(s):  
Hypoxic Pulmonary Vasoconstriction ◽  
Acute Hypoxia ◽  
Pulmonary Arteries ◽  
Cation Channels ◽  
Pulmonary Vasoconstriction ◽  
Nonselective Cation Channels ◽  
Pressor Responses ◽  
Intracellular Ca ◽  
Pulmonary Arterial

Previous studies indicated that acute hypoxia increased intracellular Ca2+ concentration ([Ca2+]i), Ca2+ influx, and capacitative Ca2+ entry (CCE) through store-operated Ca2+ channels (SOCC) in smooth muscle cells from distal pulmonary arteries (PASMC), which are thought to be a major locus of hypoxic pulmonary vasoconstriction (HPV). Moreover, these effects were blocked by Ca2+-free conditions and antagonists of SOCC and nonselective cation channels (NSCC). To test the hypothesis that in vivo HPV requires CCE, we measured the effects of SOCC/NSCC antagonists (SKF-96365, NiCl2, and LaCl3) on pulmonary arterial pressor responses to 2% O2 and high-KCl concentrations in isolated rat lungs. At concentrations that blocked CCE and [Ca2+]i responses to hypoxia in PASMC, SKF-96365 and NiCl2 prevented and reversed HPV but did not alter pressor responses to KCl. At 10 μM, LaCl3 had similar effects, but higher concentrations (30 and 100 μM) caused vasoconstriction during normoxia and potentiated HPV, indicating actions other than SOCC blockade. Ca2+-free perfusate and the voltage-operated Ca2+ channel (VOCC) antagonist nifedipine were potent inhibitors of pressor responses to both hypoxia and KCl. We conclude that HPV required influx of Ca2+ through both SOCC and VOCC. This dual requirement and virtual abolition of HPV by either SOCC or VOCC antagonists suggests that neither channel provided enough Ca2+ on its own to trigger PASMC contraction and/or that during hypoxia, SOCC-dependent depolarization caused secondary activation of VOCC.

Endothelium-derived relaxing factor activity in rat lung during hypoxic pulmonary vascular remodeling

1993 ◽  
Vol 74 (3) ◽  
pp. 1061-1065 ◽  
Author(s):  
L. Zhao ◽  
D. E. Crawley ◽  
J. M. Hughes ◽  
T. W. Evans ◽  
R. J. Winter
Keyword(s):  
Hypoxic Pulmonary Vasoconstriction ◽  
Hypoxic Exposure ◽  
Control Group ◽  
Pulmonary Vascular Remodeling ◽  
Relaxing Factor ◽  
Pulmonary Vasoconstriction ◽  
O2 Concentration ◽  
Pulmonary Arterial ◽  
Endothelium Derived Relaxing Factor

We have investigated the role of endothelium-derived relaxing factor in modulating hypoxic pulmonary vasoconstriction by inhibiting its synthesis with the false substrate NG-monomethyl-L-arginine (L-NMMA) in the isolated blood-perfused lungs of Wistar rats after chronic hypoxia (CH, fractional inspiratory O2 concentration 10%) for 15 h, 2 days, and 7 days. Lungs were perfused with blood of normal hematocrit at constant flow (18 ml/min) ventilated with 1) 95% air-5% CO2 (normoxia) and 2) 2% O2–5% CO2-93% N2 (hypoxia) and were studied in the absence and presence of L-NMMA (30 and 300 microM) or L-arginine (L-Arg, 1 and 6 mM) in separate groups. Pulmonary arterial pressure (Ppa) rose incrementally with hypoxic exposure (all P < 0.05 vs. normoxic control group). Hypoxic pulmonary vasoconstriction (HPV) was markedly reduced after 15 h and 2 days of CH: the mean increases in Ppa (delta Ppa) in hypoxia were 15.3, 3.5, 3.8, and 13.6 mmHg in control rats and rats exposed to 15 h (P < 0.05 vs. control and 7 days of CH), 2 days (P < 0.001 vs. control and 7 days of CH), and 7 days of CH, respectively. Ppa in control rats and rats exposed to 15 h, 2 days, and 7 days of CH were 137, 179, 184, and 166% of control, respectively, after 30 microM L-NMMA (all P < 0.05 when expressed as percent change vs. no L-NMMA). Similar augmentation in HPV was seen after 30 microM L-NMMA, with all hypoxic groups having a greater response than control groups.(ABSTRACT TRUNCATED AT 250 WORDS)

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