Decreased pulmonary vascular responses in dogs with increased pulmonary blood flow' Can. J. Physiol. Pharmacol. Downloaded from www.nrcresearchpress.com by ACQ Service/Serials (A) on 01/02/15 For personal use only.
ALANTUCKER,^ JOHN T. REEVES, DON L. JACKSON, AND ROBERT F. GROVER Curdiovascular Pulmonary Research Lnborarory, University ):f Colorado Meclical Center, Denver, CO, U.S.A. 80220 Received hlay 5, 1978 R. F. 1978. Decreased puln~onary TUCKER, A., REEVES, J. T., JACKSON, D. L., and GROVER, vascular responses in dogs with increased pulmonary blood flow. Can. J. 13hysiol.Pharmacol. 56, 1011-1016. We wished to determine whether high pulmonary blood flow alters the pulmonary vascular responses to the vasoconstrictors, hypoxia and prostaglandin Fa, (PGF,,). Acute or chronic left pulmonary artery (PA) occlusion was performed in dogs in order to create high pulmoilary blood flow conditions. Right lung puln~onaryvascular resistance (PVR) during normoxia was reduced by both acute and chronic left PA occlusion, suggesting passive vasodilatation. Increases in right lung PVR induced by hypoxia (10-15Tc 0 2 ) and PGF2, (0.8-4 pg kg-' min-l) were attenuated both in acute and chronic left PA occluded dogs. Since the reductions in responsiveness were similar with acute and chronic increases in blood flow, the attenuating effect of high blood flow was not dependent upon morphologic changes in the vasculature. Puln~onary vascular responsiveness was probably reduced in these animals due to their dilated pulmonary vascular beds, consequent to the increased puln~onaryblood flow, thereby decreasing the effectiveness of smooth muscle contraction. D. L., et GROVER, R. F. 1978. Decreased pulmonary TUCKER, A., REEVES, J. T., JACKSON, vascular responses in dogs with increased pulmonary blood flow. Can. J. Physiol. Pharmacol. 56, 1011-1016. On cherche h dkternliner si la rCponse vasculaire pulmonaire aux vasoconstricteurs, $I l'hypoxie et ti la prostaglandine F2, (PGF2,) est altQCe ou non par un debit sanguin pulmonaire ClevC. On a procCdC ii l'occlusion aigue ou chronique de l'artkre pulmonaire gauche (PA) chez le chien dans le but de crCer des coilditions de debit pulmoiiaire ClevC. L'occlusion PA gauche tant aigue que chronique, rCduit la resistance vasculaire pulmonaire droite (PVR) en normoxie, ce qui sugpttre une \~asodilatationpassive. Des augmentations de la PVR du pournon droit induites par hypoxie (10-15',6 d'O2) et par PGFiL, (0.8-4 pg kg-' min-I) sont attenuks chez les chiens ayant subi une occlusion Vant aigue que chroniclue. L'effet attCnuateur d'un dCbit sanguin ClevC n'est pas dependant des changements rnorphologiques du systkme vasculaire, puisque les dinlinutions des reponses sont sen~blableslorsque l'on a des augmentations aigues et chroniquzs du debit sanguin. La rCponse vasculaire pulmonaire est probablenlent reduite chez ces anirnaux du fait de leurs lits vasculaires pulnlonaires dilates, consCc~uen~ment B l'augmentation du dCbit sanguin pulmonaire. ditninuant ainsi l'efficacite de la contraction des muscles lisses. [Traduit par le journal]
Introduction Increased pulmonary blood flow, produced by ligation of a single pulmonary artery, aorto-pulmonary shunt, or pneumonectomy, causes chronic morphologic-pathologic changes in the pulmoilary vasculature (Ferguson et al. 1953; Muller et al. 1953; Rudolph et al. 1961 Pool et al. 1962; McCradey et al. 1968; Kato et al. 1971; Friedli et al. 1975), but these changes have not been considered to alter the reactivity of the pulmonary vascular bed. Friedli et al. (1975) observed that chronic increases in Aow, ABBREVIATIONS: PVR, pullnonary vascular resistance; PGF2,, prostaglandin F2,; PA. pulmbnary artery. lSupported in part NIH Grants HL-14985 and HL-01798. PPresent address: Department of Physiology, Wright State University School of Medicine, Dayton, OH, U.S.A. 45435.
due to pneurnonectomy, dilated the PA9s in most experiments, although in some animals both dilated and hypertrophied lung vessels were seen. These dilated vessels might be expected to be less reactive to constrictor stimuli for several reasons, but particularly because of the mechanical disadvantage caused by the decreased ratio of wall thickness t o vessel diatneter. Therefore, the aim of this study was to determine the influence of increased blood flow on the response of lung vessels t o vasoconstrictor stimuli. Beinonstration of an eff-ect of vessel dilation would emphasize the importance of the magnitude of both blood pressure a d flow in the determination of pulmonary ;ascular responses to various stimuli. If dilation of blood is a primary factor in altering vascular reactivity, then similar results may be expected with both acute and chronic increases in
1012
CAN. J. PHYSIOL. PHARMACOL. VOL. 56, 1978
Can. J. Physiol. Pharmacol. Downloaded from www.nrcresearchpress.com by ACQ Service/Serials (A) on 01/02/15 For personal use only.
pulmonary blood flow. Therefore, we compared the hemodynamic responses with acute and chronic unilateral PA occlusion, using both hypoxia and prostaglandin F2a as pulmonary vasoconstrictors. Calves and pigs have been used extensively in studies on the effects of unilateral PA occlusion. However, since these animals develop moderate t o severe pulmonary hypertension at Denver's altitude (1600 m) following PA ligation (Vogel et al. 1967; Rosenkrantz et al. 1973) we used a less reactive species, the dog (Tucker et al. 1975). The results obtained in this study are compatible with the hypothesis that pulmonary vascular res~onsivenessis reduced as blood flow is increased. 1
Methods
Chronic Left PA Ligation In 10 adult dogs of either sex (mean weight 17 -t 1 kg) anesthesia was induced with sodium thiopental ( 15-20 mg/kg, iv) and maintained with halothane. A left thoracotomy was performed and the left branch of the main PA was isolated and doubly ligated with umbilical tape. Subsequent fluoroscopic examination with the injection of contrast medium confirmed that complete occlusion was achieved in all of the animals. These dogs comprised the left PA ligation group with increased blood flow through the right lung. At least 20 days (mean of 34 -t 2 days) elapsed prior to further experimentation. Ten adult dogs (mean weight 23 -t 1 kg), comprising the control group, were not subjected to any surgical intervention prior to experimentation. Following the recovery period, each animal was anesthetized with intravenous sodium pentobarbital (30 mg/kg) and intubated with a cuffed endotracheal tube. The dogs breathed 305; 0 2 (Denver's P, = 630 mmHg, Pro2 = 175 mmHg) spontaneously through a low resistance respiratory valve. Polyethylene catheters were positioned in the main PA and in the abdominal aortil, for pressure determinations, and an infusion catheter was placed in the superior vena cava. Pulmonary arterial wedge pressure was determined using a Swan-Ganz flow-directed catheter positioned in a peripheral pulmonary artery. Mean blood pressures, cardiac output (dye dilution), PVR (mean pulmonary arterial - wedge pressure/cardiac output), and systemic vascular resistance (mean systemic arterial pressure/cardiac output) were computed as previously described (Tucker and Reeves 1975). Right lung PVR in control dogs was calculated by dividing the pulmonary perfusion pressure by 55% of the cardiac output. In four dogs we measured wet lung weights and found the right lung to be 55(,;j of total lung weight (see also Rahn et al. 1956). We assumed, therefore, that 5556 of the cardiac output perfused the right lung under normal conditions. End-tidal carbon dioxide was monitored with an infrared CO2 analyzer (Beckman, model LB-1) and was maintained at the control level by manual addition of 100(,1C 0 2 to the inspired gas during the hyperventilation induced by acute hypoxia. Cardiovascular responses to hypoxia were determined during 20-min exposures to 10C,i, 12'j,, and 157h O z in Nz, administered in random sequence, following control measurements obtained while the dogs breathed 30(,; 0 2 . With the onset of hypoxia, heart rate and mean blood pressures were recorded each minute, and cardiac output, total and right lung PVR, and systemic vascular resistance were determined at 5, 10, 15, and 20 min of hypoxia. Arterial blood gas tensions and pH
were measured with appropriate electrodes (Radiometer blood gas analyzer) during both normoxia and hypoxia. Cardiovascular responses to PGFz, were also determined for both control (tz = 10) and left PA ligated dogs 01 = 9). During normoxia (30(; 04 each dog was administered PGFz, ininfusions (0.8, 2, and 4 pg kg-' min-') for 3 min. Cardiac output, total and right lung PVR, systemic vascular resistance, and arterial blood gas tensions and pH were determined prior to and at 3 min of the infusions. Acute Left PA Obstruction Since any changes in pulmonary vascular reactivity with chronic left PA ligation might have been due to either increased blood flow or morphological changes of the vasculature, we studied four dogs (mean weight 26 2 kg) with acute left PA obstruction. With this maneuver we hoped to dissociate the effects of increased pulmonary blood flow from morphological changes of the vasculature. The dogs were anesthetized and catheterized as described above. They were then exposed to 20-min hypocapnic hypoxic exposures (10yo and 155; 0 2) and to PGFz, infusions (0.8, 2, and 4 pg kg-' min-I) before and 10-20 mill after obstruction of the left PA with a balloontipped catheter. Placement of the catheter and verification of left PA obstruction were determined by injecting contrast medium during fluoroscopic observation. Statistical evaluation was obtained with t tests, and significance was accepted at the P < 0.05 level.
+
Results
Chronic Left P A Ligation (Table 1 ) Cardiac output was unchanged by left PA ligation (3.2 k 0.3 t/min in control, 3.4 & 0.3 t/min in ligated dogs), resulting in a nearly doubled pulmonary blood flow through the right lung. Mild pulmonary arterial hypertension developed in the left PA ligated dogs (14 +_ 1 mmHg in control, 18 +_ 1 mmHg in ligated dogs) but pulmonary wedge pressure was not different (4 0.4 mmHg in control, 4 +_ 0.4 mmHg in ligated dogs). Total P V R was higher in the left PA ligated dogs compared with the P V R values obtained in control dogs. However, when resistance to flow in only the perfused right lung was compared, the PA-ligated animals exhibited lower right lung P V R than the control animals (5.8 & 0.4 mmHg e-I min-I (units) in control, 4.4 k 0.4 mmHg t - I min-l (units) in ligated dogs). Systemic arterial pressures were similar in control (137 mmHg) and PA-ligated (138 mmHg) dogs. Similarly, arterial pH (7.33) and oxygen tension (96 mmHg) were unchanged by left PA ligation. Arterial carbon dioxide tension was significantly lower in the 1.2 mmHg in control, 37 PA-ligated dogs (41 1.0 mmHg in ligated dogs) ( P < 0.05). The pulmonary pressor response to acute hypoxia was unchanged by left PA ligation. However, the increase in right lung P V R induced by hypoxia was reduced in the ligated dogs (Fig. 1). The degree of arterial hypoxemia was similar in the control and left PA ligated dogs for all three hypoxic exposures.
+
+
+
1013
TUCKER ET AL.
Can. J. Physiol. Pharmacol. Downloaded from www.nrcresearchpress.com by ACQ Service/Serials (A) on 01/02/15 For personal use only.
TABLE 1. Pulmonary vascular and arterial blood gas tension responses to hypoxja in control and chronic left PA ligated clogs --Control %,eftPA ligation Normoxia Hypoxia ({A Nsrmuxia Hygoxia '(A 8 O';o 02 PAP, nzmHg CO, Elmin PVR, units Right lung PVR Pa,,, mmHg Pac029 mmHg
I F4,Q 2 PAP GO P VR
Right lung P V R Pooz paco2
15q; O 2 PAP CO P VR Right lung PVR Po,, P~c02
( n = 10)
14~-1 3.2k0.3 3.0k0.2 5.5k0.3 93+3 43 k B (n
14f 1 3.220.3 3.650.3 6.5k0.5 95 5 3 41 e% (n
14k l 3.650.6 3.1 50.3 5 0 66 0 . 6 9954 41 t l
-
-
(II
26kI 3.5k0.3 6.9k0.7 1 2 . 6 + 1.2 39+l 37 & 2 10) 252 I 3.7k0.3 6.250.4 11.3-bI.O 4351 36k2 6) 22k1 3.8k0.6 5.450.7 9 . 8 5 1.2 5752 4052
86;;
=
10) 3022 4.2k0.4 6.6t0.6 6.6+_0.6* 39rf.1 31 +2*
18+1*
-
3.4+0.4 4 . 3 -&0.4* 4.350.4* 95C5 37*1*
1305: 1309; -
(N =
79':c
18p1* 3.450.4 4.3 k 0 . 5 4.3 i 0 . 5 " 94+6 39 k 1
-
73:; 73(,; -
-
(la
57' , 74 (/, 74%
-
+
29 2* 4.0+0.4 7.0 _+0. 6 7.0~0.6* 45 i 1 34f I =
1851 3.5k0.3 4 . 4 f Oe4* 3.4tO.4" 90k6 38 + I
-
10)
64' 53' ;* 5 j r ,* (
-
6 I f(
63'' 63(
-
10) 25 f 2 3.9-tO.3 6.0 t O . 3 6.0t0.5* 54 1: 2 34+1
39'
;
36'
1'
36' * 4
NOTE: PAP, pulmonary arterial pressure, CO, c ~ r d ~ noutput, c P V K . pulmonary v,~scul,lr resist.lnce. Pabao,,arterl,ll 0 1 ten
ALANTUCKER,^ JOHN T. REEVES, DON L. JACKSON, AND ROBERT F. GROVER Curdiovascular Pulmonary Research Lnborarory, University ):f Colorado Meclical Center, Denver, CO, U.S.A. 80220 Received hlay 5, 1978 R. F. 1978. Decreased puln~onary TUCKER, A., REEVES, J. T., JACKSON, D. L., and GROVER, vascular responses in dogs with increased pulmonary blood flow. Can. J. 13hysiol.Pharmacol. 56, 1011-1016. We wished to determine whether high pulmonary blood flow alters the pulmonary vascular responses to the vasoconstrictors, hypoxia and prostaglandin Fa, (PGF,,). Acute or chronic left pulmonary artery (PA) occlusion was performed in dogs in order to create high pulmoilary blood flow conditions. Right lung puln~onaryvascular resistance (PVR) during normoxia was reduced by both acute and chronic left PA occlusion, suggesting passive vasodilatation. Increases in right lung PVR induced by hypoxia (10-15Tc 0 2 ) and PGF2, (0.8-4 pg kg-' min-l) were attenuated both in acute and chronic left PA occluded dogs. Since the reductions in responsiveness were similar with acute and chronic increases in blood flow, the attenuating effect of high blood flow was not dependent upon morphologic changes in the vasculature. Puln~onary vascular responsiveness was probably reduced in these animals due to their dilated pulmonary vascular beds, consequent to the increased puln~onaryblood flow, thereby decreasing the effectiveness of smooth muscle contraction. D. L., et GROVER, R. F. 1978. Decreased pulmonary TUCKER, A., REEVES, J. T., JACKSON, vascular responses in dogs with increased pulmonary blood flow. Can. J. Physiol. Pharmacol. 56, 1011-1016. On cherche h dkternliner si la rCponse vasculaire pulmonaire aux vasoconstricteurs, $I l'hypoxie et ti la prostaglandine F2, (PGF2,) est altQCe ou non par un debit sanguin pulmonaire ClevC. On a procCdC ii l'occlusion aigue ou chronique de l'artkre pulmonaire gauche (PA) chez le chien dans le but de crCer des coilditions de debit pulmoiiaire ClevC. L'occlusion PA gauche tant aigue que chronique, rCduit la resistance vasculaire pulmonaire droite (PVR) en normoxie, ce qui sugpttre une \~asodilatationpassive. Des augmentations de la PVR du pournon droit induites par hypoxie (10-15',6 d'O2) et par PGFiL, (0.8-4 pg kg-' min-I) sont attenuks chez les chiens ayant subi une occlusion Vant aigue que chroniclue. L'effet attCnuateur d'un dCbit sanguin ClevC n'est pas dependant des changements rnorphologiques du systkme vasculaire, puisque les dinlinutions des reponses sont sen~blableslorsque l'on a des augmentations aigues et chroniquzs du debit sanguin. La rCponse vasculaire pulmonaire est probablenlent reduite chez ces anirnaux du fait de leurs lits vasculaires pulnlonaires dilates, consCc~uen~ment B l'augmentation du dCbit sanguin pulmonaire. ditninuant ainsi l'efficacite de la contraction des muscles lisses. [Traduit par le journal]
Introduction Increased pulmonary blood flow, produced by ligation of a single pulmonary artery, aorto-pulmonary shunt, or pneumonectomy, causes chronic morphologic-pathologic changes in the pulmoilary vasculature (Ferguson et al. 1953; Muller et al. 1953; Rudolph et al. 1961 Pool et al. 1962; McCradey et al. 1968; Kato et al. 1971; Friedli et al. 1975), but these changes have not been considered to alter the reactivity of the pulmonary vascular bed. Friedli et al. (1975) observed that chronic increases in Aow, ABBREVIATIONS: PVR, pullnonary vascular resistance; PGF2,, prostaglandin F2,; PA. pulmbnary artery. lSupported in part NIH Grants HL-14985 and HL-01798. PPresent address: Department of Physiology, Wright State University School of Medicine, Dayton, OH, U.S.A. 45435.
due to pneurnonectomy, dilated the PA9s in most experiments, although in some animals both dilated and hypertrophied lung vessels were seen. These dilated vessels might be expected to be less reactive to constrictor stimuli for several reasons, but particularly because of the mechanical disadvantage caused by the decreased ratio of wall thickness t o vessel diatneter. Therefore, the aim of this study was to determine the influence of increased blood flow on the response of lung vessels t o vasoconstrictor stimuli. Beinonstration of an eff-ect of vessel dilation would emphasize the importance of the magnitude of both blood pressure a d flow in the determination of pulmonary ;ascular responses to various stimuli. If dilation of blood is a primary factor in altering vascular reactivity, then similar results may be expected with both acute and chronic increases in
1012
CAN. J. PHYSIOL. PHARMACOL. VOL. 56, 1978
Can. J. Physiol. Pharmacol. Downloaded from www.nrcresearchpress.com by ACQ Service/Serials (A) on 01/02/15 For personal use only.
pulmonary blood flow. Therefore, we compared the hemodynamic responses with acute and chronic unilateral PA occlusion, using both hypoxia and prostaglandin F2a as pulmonary vasoconstrictors. Calves and pigs have been used extensively in studies on the effects of unilateral PA occlusion. However, since these animals develop moderate t o severe pulmonary hypertension at Denver's altitude (1600 m) following PA ligation (Vogel et al. 1967; Rosenkrantz et al. 1973) we used a less reactive species, the dog (Tucker et al. 1975). The results obtained in this study are compatible with the hypothesis that pulmonary vascular res~onsivenessis reduced as blood flow is increased. 1
Methods
Chronic Left PA Ligation In 10 adult dogs of either sex (mean weight 17 -t 1 kg) anesthesia was induced with sodium thiopental ( 15-20 mg/kg, iv) and maintained with halothane. A left thoracotomy was performed and the left branch of the main PA was isolated and doubly ligated with umbilical tape. Subsequent fluoroscopic examination with the injection of contrast medium confirmed that complete occlusion was achieved in all of the animals. These dogs comprised the left PA ligation group with increased blood flow through the right lung. At least 20 days (mean of 34 -t 2 days) elapsed prior to further experimentation. Ten adult dogs (mean weight 23 -t 1 kg), comprising the control group, were not subjected to any surgical intervention prior to experimentation. Following the recovery period, each animal was anesthetized with intravenous sodium pentobarbital (30 mg/kg) and intubated with a cuffed endotracheal tube. The dogs breathed 305; 0 2 (Denver's P, = 630 mmHg, Pro2 = 175 mmHg) spontaneously through a low resistance respiratory valve. Polyethylene catheters were positioned in the main PA and in the abdominal aortil, for pressure determinations, and an infusion catheter was placed in the superior vena cava. Pulmonary arterial wedge pressure was determined using a Swan-Ganz flow-directed catheter positioned in a peripheral pulmonary artery. Mean blood pressures, cardiac output (dye dilution), PVR (mean pulmonary arterial - wedge pressure/cardiac output), and systemic vascular resistance (mean systemic arterial pressure/cardiac output) were computed as previously described (Tucker and Reeves 1975). Right lung PVR in control dogs was calculated by dividing the pulmonary perfusion pressure by 55% of the cardiac output. In four dogs we measured wet lung weights and found the right lung to be 55(,;j of total lung weight (see also Rahn et al. 1956). We assumed, therefore, that 5556 of the cardiac output perfused the right lung under normal conditions. End-tidal carbon dioxide was monitored with an infrared CO2 analyzer (Beckman, model LB-1) and was maintained at the control level by manual addition of 100(,1C 0 2 to the inspired gas during the hyperventilation induced by acute hypoxia. Cardiovascular responses to hypoxia were determined during 20-min exposures to 10C,i, 12'j,, and 157h O z in Nz, administered in random sequence, following control measurements obtained while the dogs breathed 30(,; 0 2 . With the onset of hypoxia, heart rate and mean blood pressures were recorded each minute, and cardiac output, total and right lung PVR, and systemic vascular resistance were determined at 5, 10, 15, and 20 min of hypoxia. Arterial blood gas tensions and pH
were measured with appropriate electrodes (Radiometer blood gas analyzer) during both normoxia and hypoxia. Cardiovascular responses to PGFz, were also determined for both control (tz = 10) and left PA ligated dogs 01 = 9). During normoxia (30(; 04 each dog was administered PGFz, ininfusions (0.8, 2, and 4 pg kg-' min-') for 3 min. Cardiac output, total and right lung PVR, systemic vascular resistance, and arterial blood gas tensions and pH were determined prior to and at 3 min of the infusions. Acute Left PA Obstruction Since any changes in pulmonary vascular reactivity with chronic left PA ligation might have been due to either increased blood flow or morphological changes of the vasculature, we studied four dogs (mean weight 26 2 kg) with acute left PA obstruction. With this maneuver we hoped to dissociate the effects of increased pulmonary blood flow from morphological changes of the vasculature. The dogs were anesthetized and catheterized as described above. They were then exposed to 20-min hypocapnic hypoxic exposures (10yo and 155; 0 2) and to PGFz, infusions (0.8, 2, and 4 pg kg-' min-I) before and 10-20 mill after obstruction of the left PA with a balloontipped catheter. Placement of the catheter and verification of left PA obstruction were determined by injecting contrast medium during fluoroscopic observation. Statistical evaluation was obtained with t tests, and significance was accepted at the P < 0.05 level.
+
Results
Chronic Left P A Ligation (Table 1 ) Cardiac output was unchanged by left PA ligation (3.2 k 0.3 t/min in control, 3.4 & 0.3 t/min in ligated dogs), resulting in a nearly doubled pulmonary blood flow through the right lung. Mild pulmonary arterial hypertension developed in the left PA ligated dogs (14 +_ 1 mmHg in control, 18 +_ 1 mmHg in ligated dogs) but pulmonary wedge pressure was not different (4 0.4 mmHg in control, 4 +_ 0.4 mmHg in ligated dogs). Total P V R was higher in the left PA ligated dogs compared with the P V R values obtained in control dogs. However, when resistance to flow in only the perfused right lung was compared, the PA-ligated animals exhibited lower right lung P V R than the control animals (5.8 & 0.4 mmHg e-I min-I (units) in control, 4.4 k 0.4 mmHg t - I min-l (units) in ligated dogs). Systemic arterial pressures were similar in control (137 mmHg) and PA-ligated (138 mmHg) dogs. Similarly, arterial pH (7.33) and oxygen tension (96 mmHg) were unchanged by left PA ligation. Arterial carbon dioxide tension was significantly lower in the 1.2 mmHg in control, 37 PA-ligated dogs (41 1.0 mmHg in ligated dogs) ( P < 0.05). The pulmonary pressor response to acute hypoxia was unchanged by left PA ligation. However, the increase in right lung P V R induced by hypoxia was reduced in the ligated dogs (Fig. 1). The degree of arterial hypoxemia was similar in the control and left PA ligated dogs for all three hypoxic exposures.
+
+
+
1013
TUCKER ET AL.
Can. J. Physiol. Pharmacol. Downloaded from www.nrcresearchpress.com by ACQ Service/Serials (A) on 01/02/15 For personal use only.
TABLE 1. Pulmonary vascular and arterial blood gas tension responses to hypoxja in control and chronic left PA ligated clogs --Control %,eftPA ligation Normoxia Hypoxia ({A Nsrmuxia Hygoxia '(A 8 O';o 02 PAP, nzmHg CO, Elmin PVR, units Right lung PVR Pa,,, mmHg Pac029 mmHg
I F4,Q 2 PAP GO P VR
Right lung P V R Pooz paco2
15q; O 2 PAP CO P VR Right lung PVR Po,, P~c02
( n = 10)
14~-1 3.2k0.3 3.0k0.2 5.5k0.3 93+3 43 k B (n
14f 1 3.220.3 3.650.3 6.5k0.5 95 5 3 41 e% (n
14k l 3.650.6 3.1 50.3 5 0 66 0 . 6 9954 41 t l
-
-
(II
26kI 3.5k0.3 6.9k0.7 1 2 . 6 + 1.2 39+l 37 & 2 10) 252 I 3.7k0.3 6.250.4 11.3-bI.O 4351 36k2 6) 22k1 3.8k0.6 5.450.7 9 . 8 5 1.2 5752 4052
86;;
=
10) 3022 4.2k0.4 6.6t0.6 6.6+_0.6* 39rf.1 31 +2*
18+1*
-
3.4+0.4 4 . 3 -&0.4* 4.350.4* 95C5 37*1*
1305: 1309; -
(N =
79':c
18p1* 3.450.4 4.3 k 0 . 5 4.3 i 0 . 5 " 94+6 39 k 1
-
73:; 73(,; -
-
(la
57' , 74 (/, 74%
-
+
29 2* 4.0+0.4 7.0 _+0. 6 7.0~0.6* 45 i 1 34f I =
1851 3.5k0.3 4 . 4 f Oe4* 3.4tO.4" 90k6 38 + I
-
10)
64' 53' ;* 5 j r ,* (
-
6 I f(
63'' 63(
-
10) 25 f 2 3.9-tO.3 6.0 t O . 3 6.0t0.5* 54 1: 2 34+1
39'
;
36'
1'
36' * 4
NOTE: PAP, pulmonary arterial pressure, CO, c ~ r d ~ noutput, c P V K . pulmonary v,~scul,lr resist.lnce. Pabao,,arterl,ll 0 1 ten
