Effect of increase of pulmonary blood flow on segmental pulmonary vascular resistance--with special emphasis on the pulmonary capillary bed]

The decrease of pulmonary vascular resistance with increase of pulmonary blood flow has been attributed to the function of the pulmonary vascular bed, consisting of capillary recruitment or dilatation. However, experimental evidence of a decrease of capillary resistance is lacking. To clarify this phenomenon, we perfused isolated cat lungs with diluted autologous blood and measured pulmonary microvascular pressure while changing pulmonary blood flow rate. We set the initial flow rate to achieve Ppa of 20 cmH2O and changed the flow rate while keeping left atrial pressure (Pla) and alveolar pressure (Palv) constant at 10 cmH2O and 9 cmH2O, respectively. Thereafter, pulmonary flow rate was increased 2 to 3 fold, and pulmonary arterial pressure (Ppa) and venular pressure (Pvo) were measured by venous occlusion method. The initial flow rate was 150 to 270 ml/min and the achieved maximum flow rate was from 300 to 543 ml/min. There was a linear correlation between Ppa, Pvo, and flow rate, in which the slope (rate of increase of pressure with flow) of Ppa was slightly steeper than that of Pvo. We calculated total and segmental pulmonary vascular resistance from the mean pressure-flow relationship. The total and upstream resistance involving arterial and capillary segments decreased hyperbolically with increase in flow rate. The mean upstream resistance decreased about 54%, from 35.20 x 10(-3) (cmH2O/ml/min) at a flow rate of 150 ml/min to 16.27 x 10(-3) (cmH2O/ml/min) at a flow rate of 450 ml/min. The degree of this decrease was similar to the result observed by micropuncture method (Nagasaka, 1990). Downstream resistance, which represents venous resistance, did not change significantly with the flow rate.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of alveolar hypoxia during partial mitral valve obstruction in unanesthetized sheep

The effects of elevated left atrial pressure (Pla) on the pulmonary hemodynamic responses to hypoxia and infused prostaglandin-H2 analog (PGH2-A) were studied in 10 chronically instrumented unanesthetized sheep. Sheep were studied with isocapnic hypoxia (fraction of inspired O2, 0.12) or infused PGH2-A (0.2 to 1.0 micrograms X kg-1 X min-1 adjusted to increase pulmonary artery pressure (Ppa) by approximately 15 cm H2O) when Pla was normal or elevated to 10 or 20 cm H2O. The Pla was elevated by inflating a Foley catheter positioned in the mitral valve orifice. Elevation of Pla did not block the increase in Ppa or cardiac output (CO) caused by hypoxia but did block the increase in pulmonary vascular resistance (PVR). When Pla was elevated to 10 or 20 cm H2O, hypoxia caused Pla to increase further, and PGH2-A caused Ppa and PVR to increase whether Pla was elevated or not; PGH2-A did not cause CO to increase or Pla to increase further under any experimental condition. Neither hypoxia nor PGH2-A had any effect on left ventricular end-diastolic pressure under any experimental condition. We hypothesize that when Pla is elevated, the increase in CO may dilate the pulmonary circulation, obscuring hypoxic vasoconstriction. When Pla is elevated, the direct effects of hypoxic pulmonary vasoconstriction cannot overcome the increased intraluminal pressure, and PVR does not increase. The pulmonary vessels are still able to respond to a potent vasoconstrictor such as PGH2-A when Pla is elevated. We conclude that the further increase in Pla caused by hypoxia when Pla is elevated is primarily due to increased flow across a mitral valve behaving as a relatively fixed resistor.     

Effects of alveolar hypoxia on lung fluid and protein transport in unanesthetized sheep.

To determine whether hypoxia directly affects pulmonary microvascular filtration of fluid or permeability to plasma proteins, we measured steady state lung lymph flow and protein transport in eight unanesthetized sheep breathing 10% O2 in N2 for 4 hours. We also studied three sheep breathing the same gas mixture for 48 hours. We surgically prepared the sheep to isolate and collect lung lymph and to measure average pulmonary arterial (Ppa) and left atrial (Pla) pressures. We placed a balloon catheter in the left atrium to elevate Pla. After recovery, the sheep breathed air through a tracheostomy for 2-4 hours, followed by 4 or 48 hours of hypoxia. In 13 4-hour studies, the average arterial PO2 fell from 97 to 38 torr; Ppa rose from 20 to 33 cm H2O; and lung lymph flow and lymph protein flow were unchanged. We also found that during 48-hour hypoxia, with a sustained elevation in Ppa and a decline in Pla, lymph flow and protein flow did not increase. In four sheep, we also raised Pla for 4 hours, followed by 4 hours of hypoxia with elevated Pla. Again, despite the added stress of elevated Pla, we found that lymph flow and lymph protein flow remained constant during hypoxia. We conclude that severe alveolar hypoxia, for 4 or 48 hours, alone or with increased pulmonary microvascular pressure, produced no change in lung fluid filtration or protein permeability, a finding supported by normal postmortem histology and extravascular lung water content.     

Factors affecting bronchial blood flow through bronchopulmonary anastomoses in dogs

Most of the bronchial arterial blood flow (Qbr) drains through bronchopulmonary anastomoses into the pulmonary circulation, and the remainder goes into the systemic venous system via the bronchial veins. We studied the relationship between blood flow through bronchopulmonary anastomoses, and alveolar pressure and pulmonary vascular pressures as well as hydrostatic pressure in the bronchial veins in 10 adult dogs. The pulmonary artery and vein of the experimental left lower lobes (LLL) of open-chested, anesthetized dogs were isolated and connected to reservoirs. That part of the Qbr that flowed through bronchopulmonary anastomoses into the reservoirs was continuously measured at constant pulmonary vascular pressures of 0 cm H2O relative to the lung base. Any bronchial blood volume that retained within the LLL was estimated from changes in lobe weight. The lobe was distended with 5% CO2 and air, at alveolar pressures of 5, 10, or 20 cm H2O in a random sequence. Because bronchial veins drain into the azygos vein, the bronchial venous pressure was elevated by snaring the azygos vein. The mean anastomotic Qbr was 4.4 +/- 1.1 (mean +/- SEM) ml/min and it decreased by 23 and 39% when alveolar pressure was raised from 5 cm H2O to 10 and 20 cm H2O respectively (p less than 0.05). Approximately 75% of the total anastomotic Qbr was collected from the pulmonary venous reservoir at all alveolar pressures. When both pulmonary artery and venous pressures were increased higher than the alveolar pressure (zone III), azygos snaring increased the anastomotic Qbr by 13 and 31% at alveolar pressures of 10 and 20 cm H2O, respectively (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)     

Vascular conductance and critical closing pressure in the isolated canine lung in situ. Its natural history

The vascular pressure-flow relationship (P-QL) in West's zone II condition were studied in isolated, in situ, canine, left lower lobe (ISLL) in order to characterize the total resistance in the pulmonary vascular bed (Rp), the normal values for pulmonary vascular conductance (Cv) and for critical closing pressure (PLc). After the basal parameters were obtained, measurements of Cv and PLc were done every 30' in order to know the natural history (NH) of this canine ISLL preparation. The P-QL relationship of the pulmonary vasculature of the ISLL preparation, perfused under classical zone II conditions, can be characterized by a rectilinear segment at high flow, a curvilinear segment at low flow and a pulmonary arterial pressure that exceeds alveolar (PA) pressure at zero flow. This demonstrates the existence of critical closing pressure (PLc) in the pulmonary vascular bed. The mean control Cv and PLc were 38.5 +/- 14 (ml. min)/mmHg and 7.9 +/- 2.2 mmHg respectively; those parameters did not change through the observation of the experiment. PLc was found to be independent of bronchial flow and it was not related to PA when the values for this pressure were less than 5 cm H20. On the contrary, higher levels of PA pressure were significantly related to PLc (r = 0.94, p less than 0.05). We conclude that in this model of ISLL in West's zone II condition it is possible to study the two components of Rp, one given by vessels that determine changes in flow resistance and for the other vessels disclosing critical closure. The values of these components remained stable over 180' of observation.     

The effect of dextran solution on pulmonary plasma-lymph barrier in awake sheep

We investigated the effect of dextran solution on lung lymph flow in awake sheep with chronic lung lymph fistulas. Ten percent of dextran (molecular weight 40,000) solution or normal saline were infused at 1000 ml/h for 2 h through left atrial catheter. We measured pulmonary arterial pressure (Ppa), left atrial pressure (Pla), aortic pressure (Psa), cardiac output (CO), oncotic pressures of both plasma (IImv) and lung lymph (IIpmv), lung lymph flow rate (Qlym), and lymph-to-plasma ratio of total protein (L/P). Infusion of dextran solution caused significant increases in Ppa, Pla and CO and decrease in plasma-lung lymph oncotic pressure gradient (IImv-IIpmv), without changes in L/P. Infusion of normal saline caused significant increases in Ppa and Pla and no changes in IImv-IIpmv and CO, and slight decrease in L/P. The calculated filtration coefficients increased by 2.2 fold after dextran infusion and 1.7 fold after normal saline infusion. Moreover, an apparent increase in protein transport across microvessels as evidenced by the normal L/P despite increases in hydrostatic pressure occurred after dextran solution infusion. These results suggest that dextran solution may increase permeability of microvascular wall, as well as effective net pressure gradient across microvessels, both of which result in a large net fluid filtration from microvessels to perimicrovascular compartment.     

Relationship of arterial wedge pressure to closing pressure in the pulmonary circulation

We studied the relationship between the pulmonary artery wedge pressure (Pw) and pulmonary venous pressure (Ppv) at 2 alveolar pressures (PA) in 7 isolated perfused dog lobes. If PA were the critical pressure in the pulmonary circulation, one would expect Pw to equal Ppv for all Ppv greater than PA. Relative to the hilum, the average critical pressure in these lobes was 15.07 +/- 0.40 cmH2O at PA = 5 cmH2O and increased significantly to 17.23 +/- 0.82 cmH2O at PA = 7 cmH2O. Because the critical pressure in fact exceeded PA, Pw was found to be relatively constant and independent of Ppv even when Ppv exceeded PA by 5 cmH2O or more. For example, at PA = 5.13 +/- 0.04 cmH2O and Ppv = 9.64 +/- 0.28, the mean value for Pw was 13.30 +/- 0.59 cmH2O. Pw is equal neither to the average critical pressure nor to PA, but instead lies between these two values. It is determined by the spectrum of closing pressures in the pulmonary circulation, and the time-constants for drainage of beds downstream from the occluded pulmonary arterial branch.     

The effect of bronchial venous pressure on pulmonary edema in the dog

We examined the effect of elevating systemic venous pressure on the rate of edema formation in the left lower lobes (LLL) of anesthetized, open-chested dogs. The pulmonary circulation of the LLL was isolated using cannulae in the artery and vein which were attached to blood-filled reservoirs. The LLL was distended to an alveolar pressure of 25 cm H2O with 5% CO2 and air, and suspended from a strain gauge which allowed continuous weight recording. The pulmonary vascular pressures were raised so all of the LLL was in zone III. The rate of weight change occurring over the last 4 minutes of a 6 minute period of this pulmonary vascular pressure rise was taken to represent the control transvascular fluid flux. The rate of weight gain of the LLL was then determined with the same pulmonary vascular pressure elevation only when downstream bronchial venous pressure alone, downstream lymphatic pressure alone, or when both downstream lymphatic and bronchial venous pressures were elevated. The transvascular fluid flux was increased when downstream bronchial venous pressure was elevated. When only downstream lymphatic pressure was elevated there was no augmentation of transvascular fluid flux. These findings suggest that when a lung is already subjected to raised pulmonary vascular pressure sufficient to cause edema, acute elevation of bronchial systemic venous pressure augments the net rate of outward fluid flux, while downstream lymphatic pressure elevation does not.     

The effect of positive end-expiratory pressure on the coronary blood flow

Positive end-expiratory pressure (PEEP) is used liberally whenever a ventilated patient shows signs of increased pulmonary venous shunting. Clinicians using PEEP to improve blood oxygenation may face the cardiovascular side effects which limit utilization of the desired respiratory effects of PEEP. We measured the pressure flow characteristics of the cardiovascular system and the coronary arterial system as a function of PEEP, using closed-chest surgically instrumented dogs, in order to assess its effects on myocardial blood flow with respect to the left ventricular energy demands. The aortic left ventricular blood pressure as well as the aortic blood flow decreased with increasing PEEP values. The coronary blood flow decreased by 5% for PEEP values of 4 cm H2O, and by 25% for 14 cm H2O of PEEP. PEEP values under 10 cm H2O reduced the left ventricular end-diastolic pressure (LVEDP), while higher PEEP values caused an increase in LVEDP. The relation between the alterations of coronary and aortic blood flows changed with PEEP values. Low PEEP values (less than 10 cm H2O) had a tendency for higher relative reduction of aortic blood flow, whereas higher PEEP values (higher than 10 cm H2O) reduced the coronary blood flow more than the reduction occurring in the aortic blood flow. Our results suggest that low PEEP values may have beneficial effects on the relation between aortic blood flow and coronary blood flow, therefore low PEEP application may minimize hypoxic myocardial alterations. Further studies that will measure left ventricular workload or another metabolic index for estimating myocardial perfusion relative to its metabolic demand are essential before clinical conclusions can be drawn from our results.     

Lung edema caused by high peak inspiratory pressures in dogs. Role of increased microvascular filtration pressure and permeability

Mechanical ventilation with high peak airway pressures (Paw) has been shown to induce pulmonary edema in animal experiments, but the relative contributions of transvascular filtration pressure and microvascular permeability are unclear. Therefore, we examined the effects of positive-pressure ventilation on two groups of open-chest dogs ventilated for 30 min with a peak Paw of 21.8 +/- 2.3 cm H2O (Low Paw) or 64.3 +/- 3.5 cm H2O (High Paw). No hemodynamic changes were observed in the Low Paw group during ventilation, but mean pulmonary artery pressure (Ppa) increased by 9.9 cm H2O, peak inspiratory Ppa by 24.6 cm H2O, and estimated mean microvascular pressure by 12.5 cm H2O during High Paw ventilation. During the same period, lung lymph flow increased by 435% in the High Paw and 35% in the Low Paw groups, and the terminal extravascular lung water/blood-free dry weight ratios were 5.65 +/- 0.27 and 4.43 +/- 0.13 g/g, respectively, for the two groups. Lung lymph protein clearances and minimal lymph/plasma ratios of total protein were significantly higher (p less than 0.05) after 2 h of increased left atrial pressure (PLA) in the High Paw group versus the Low Paw group, which indicates a significant increase in microvascular permeability. Lymph prostacyclin concentration in pulmonary lymph, measured as the stable metabolite 6-0-PGF1 alpha, was increased significantly by 70 to 150% from baseline (p less than 0.05) in both groups during the periods of increased Paw and increased PLA, but it was not significantly different between the groups.(ABSTRACT TRUNCATED AT 250 WORDS)     

Alveolar pressure magnitude and asynchrony during high-frequency oscillations of excised rabbit lungs

One possible advantage of high-frequency ventilation (HFV) over conventional mechanical ventilation is that adequate pulmonary ventilation may be established with lower pressure swings. Pressure swings measured at the airway opening may not accurately reflect pressure swings in the alveoli, however. Furthermore, little is known about the synchrony of alveolar filling during HFV. We have assessed the magnitude of alveolar pressure swings (PA) relative to those at the airway opening (Pao) and investigated asynchrony of alveolar filling during small tidal volume (less than 1.0 ml), high-frequency (1 to 60 Hz) oscillations (HFO) in 8 excised rabbit lungs. The PA was measured in several capsules glued to the pleural surface and communicating with alveolar gas via pleural punctures. The peak value of the ratio [PA/Pao] occurred near the resonant frequency and was 1.90, 1.45, and 1.0 at distending pressures of 25, 10, and 5 cm H2O, respectively. Temporal asynchrony of PA between sampled lung regions was quantified by measuring the interregional standard deviation of alveolar pressure phase angles, delta phi. The delta phi increased with increasing frequency and decreasing transpulmonary pressure. The maximal observed delta phi was 30 degrees. These results, when compared with earlier results on excised canine lungs, show that the amplification of PA during HFO is lung-size dependent. The observed degree of phase differences in pressure swings between peripheral alveolar locations implies substantial asynchrony of alveolar filling. This in turn suggests interregional gas transport as an important contributor to gas mixing during HFV.     

Reactivity and site of vasomotion in pulmonary vessels of chronically hypoxic rats: relation to structural changes

The high pressure muscular pulmonary circulation of chronically hypoxic (CH) rats was compared with the low pressure circuit in control (C) rats; differences were found in the effects of lung inflation, in pressure/flow relations during lung inflation, in reactivity to autocoids, and in responses to pulmonary dilator drugs. Isolated blood-perfused lungs of CH rats (2 to 3 wk in 10% O2) were compared with those of C rats kept in air. High inflation (alveolar) pressure (Palv) caused a rise in pulmonary artery pressure (Ppa) close to delta Palv in both groups; in CH rats, Ppa continued to rise, whereas it adapted to a lower level in C rats. Pressure-flow (P/Q) lines were measured at high and low Palv, all in Zone 2 state. In normoxia, high Palv caused a parallel shift in the P/Q line close to delta Palv in both C and CH rats. However, during hypoxic pulmonary vasoconstriction (HPV), high Palv caused a shift in the P/Q line less than delta Palv in C rats and greater than delta Palv in CH rats. Similar differences between C and CH rats were seen during constriction caused by almitrine, a drug that simulates HPV. Thus, these stimuli affect vessels that are functionally "extra-alveolar" in C rats but functionally "alveolar" in CH rats. We consider whether vasoconstriction by hypoxia and almitrine moves peripherally to the newly muscularized alveolar arterioles that are found in CH rats. Reactivity of lung vessels to bradykinin, angiotensin-1, and platelet-activating factor was greater in CH than in C rats, possibly also associated with muscularization of arterioles in the former.(ABSTRACT TRUNCATED AT 250 WORDS)     

Relationship of ultrafiltration and anastomotic flow in isolated rat lungs.

OBJECTIVE: When arterial and venous pressures are increased to equal values in "stop-flow" studies, perfusate continues to enter the pulmonary vasculature from the arterial and venous reservoirs. Losses of fluid from the pulmonary vasculature are due to ultrafiltration and flow through disrupted anastomotic (bronchial) vessels. This study compared the relative sites of ultrafiltration and anastomotic flows at low and high intravascular pressures. METHODS: Isolated rat lungs were perfused for 10 minutes with FITC-dextran, which was used to detect ultrafiltration. Arterial and venous catheters were then connected to reservoirs containing radioactively labeled dextrans at 20 or 30 cm H2O for 10 minutes. The vasculature was subsequently flushed into serial vials, and ultrafiltration and vascular filling during the equal-pressure interval were calculated. RESULTS: Ultrafiltration equaled 0.43 +/- 0.11 mL at 20 cm H2O and was similar to the volume of fresh arterial and venous perfusate which entered and remained in the pulmonary vasculature during the equal-pressure interval (0.45 +/- 0.10 mL). At 30 cm H2O, 0.80 +/- 0.23 mL entered and remained in the vasculature during the equal-pressure interval, replacing the original perfusate, and calculated transudation (0.56 +/- 0.09 mL) was not significantly more than at 20 cm H2O. Fluid also entered the airspaces at 30 cm H2O but not at 20 cm H2O. CONCLUSIONS: At 20 cm H2O, flow through anastomotic vessels occurs at sites that are at the arterial and venous ends of the microcirculation. Flow in exchange vessels remains minimal, permitting measurements of ultrafiltration and exchange. Losses of perfusate from the pulmonary vessels complicate measurements of ultrafiltration at 30 cm H2O.     

Vasodilators do not abolish pulmonary vascular critical closing pressure

To examine whether the critical closing pressure (Pcrit) of the pulmonary vasculature is dependent upon vasomotor tone, we measured Pcrit in six dog lobes before and after the administration of vasodilators. We evaluated the pressure-flow (P-Q) relationship in zone 2 flow conditions in situ perfused dog lobe (control period). We calculated Pcrit as the mean extrapolated zero-flow pressure intercepts for the P-Q relationship. We also used arterial and venous occlusions under zone 3 conditions to partition pulmonary vascular resistance into arterial, middle and venous segment resistances. We then repeated all measurements following administration of papaverine (150 micrograms/ml) and sodium nitroprusside (200 micrograms/min) into the venous reservoir (vasodilator period). Resistance in all three vascular segments was significantly reduced during vasodilator conditions. Pcrit decreased from 3.68 +/- 0.76 cm H2O to 2.53 +/- 0.92 cm H2O during control and vasodilator periods respectively (P less than 0.05). The slopes of the P-Q relationships were similar during both conditions. Our data support a model in which vasomotor tone normally sets Pcrit but in which the pulmonary vasculature can exhibit the phenomenon of critical closure even with vasomotor tone pharmacologically ablated.     

Improvement in gas exchange with nasal continuous positive airway pressure in pulmonary alveolar microlithiasis.

A 37-yr-old man with pulmonary alveolar microlithiasis (PAM) presented with respiratory failure and cor pulmonale. The FEV1/FVC was 1.4/1.8 L with total lung capacity of 3.2 L using the helium dilution method (54% predicted) and 6.1 L using body plethysmography (102% predicted), indicating large noncommunicating regions. The KCO (transfer factor per liter lung volume) was 3.05 ml/min/mm Hg/L (47% predicted). Despite home oxygen (3 L/min) and diuretic therapy, the patient remained hypoxic (PaO2, 55 mm Hg) and incapacitated with dyspnea. Nasal continuous positive airway pressure (nCPAP) at 12 cm H2O and oxygen at 1 L/min improved his oxygenation (PaO2, 93 mm Hg), and introduction of this regimen at night resulted in subjective improvement in daytime function. A Grandjean right heart catheter was introduced at the bedside, and the multiple inert gas elimination technique (MIGET) was used to measure ventilation and blood flow distributions at ambient pressure and with the addition of 10 cm H2O nCPAP. The patient had severe pulmonary hypertension (mean Ppa, 57 mm Hg) and severe hypoxemia (PaO2 37 mm Hg), which was mainly due to shunt (16% of cardiac output) and a broadening of the main mode of the ventilation-perfusion (VA/Q) distribution (log SD Q, 0.94). There was a significant reduction in shunt during nCPAP to 6% of cardiac output without increasing Ppa, and this effect appeared to extend past the period of application. We conclude that nCPAP reduces intrapulmonary shunt in this rare condition and allows for correction of hypoxemia with a smaller oxygen flow rate.     

Interpretation of pulmonary artery wedge pressure and pullback blood gas determinations during positive end-expiratory pressure ventilation and after exclusion of the bronchial circulation in the dog

Left atrial pressure (LAP) and pulmonary artery wedge pressure (PWP) were measured at different heights during graded increases in positive end-expiratory pressure (PEEP). Six healthy anesthetized dogs were placed in lateral decubitus positions with a balloon-tipped pulmonary artery catheter inserted in each lung. PWP in the gravitationally superior lung overestimated LAP at 15 and at 20 cm H2O PEEP (p less than 0.05). PWP in the dependent lung was virtually identical to LAP at all degrees of PEEP. Wedge blood could be aspirated through the distal lumen of the pulmonary artery catheters during balloon inflation at all degrees of PEEP except for 3 attempts. PCO2 in wedge blood in both the nondependent and dependent lungs at all degrees of PEEP was consistently lower than PCO2 in arterial blood (p less than 0.05). Wedge blood was arterialized, i.e., oxygen saturation greater than 95%, in all but 4 specimens. Surgical elimination of the bronchial artery supply to the lung in 3 dogs did not affect PWP or blood gas measurements. We conclude that in this animal model: (1) the tip of a pulmonary artery catheter must be below the level of the left atrium, Zone III location, to accurately reflect LAP at high degrees of PEEP; (2) arterialization of wedge blood samples does not guarantee that PWP reflects LAP; (3) bronchial artery blood supply does not affect PWP or wedge blood gas measurements, even at high degrees of PEEP.     

Effect of lung surface tension on pulmonary vascular mechanics in excised dog lungs

We measured pulmonary vascular pressure (Pvas)-volume (Vvas) relationships in excised air and oil-filled dog lungs. First, pulmonary vessels were perfused with dextran and Pvas-Vvas curves of the total pulmonary circulation were measured. Second, air was perfused into the artery or vein, and the arterial or venous extra-alveolar Pvas-Vvas curves were measured. Alveolar vessel Pvas-Vvas curve was obtained by the substraction of both the arterial and venous extra-alveolar Pvas-Vvas curves from the total vascular Pvas-Vvas curves. When lung recoil pressure (PL) was reduced by filling the lung with oil at a given lung volume (VL), the determinants of pulmonary vascular dimensions and compliances were compared in terms of PL and VL. The arterial vascular area (Avas) was correlated with PL, while venous Avas was correlated with both PL and VL. Alveolar vessel Vvas at high Pvas reached its peak at PL 5 cm H2O. Compliance of arteries, veins, and alveolar vessels were correlated with PL. We concluded that lung surface tension contributes to the lung parenchyma's radial traction to the extra-alveolar vessels and that it also contributes to the stabilization of the alveolar vessels.     

Plasma levels of atrial natriuretic peptide under acute hypoxia in normal subjects

To investigate whether the acute hypoxia can be a stimulus for atrial natriuretic peptide (ANP) secretion, plasma levels of ANP were determined under three different hypoxic conditions in six normal subjects. During 15% O2 breathing for 10 min, no significant change in plasma ANP level was observed. Severe hypoxia induced by 10% O2 breathing increased the mean pulmonary arterial pressure (Ppa) by 11.6 mm Hg within 10 min (P less than 0.01), accompanying a slight but significant rise in plasma ANP level of pulmonary artery (PA) from 24.3 +/- 5.3 to 28.2 +/- 4.6 pg/ml (P less than 0.05). There was a tendency for the ANP level of PA to rise under hypoxic hypobaria at 515 Torr for 10 min, followed by a decrease of that level during 100% O2 breathing under hypobaric condition. These changes, however, still remained in the normal range. No significant changes were observed both in right atrial pressure and in pulmonary capillary wedge pressure under any of the three hypoxic conditions. From these results we conclude that ANP can be released in response to the elevation of Ppa caused by acute hypoxia in normal subjects, but the changes in plasma ANP level may be too small to play a significant physiological role in hemodynamic responses to acute hypoxia.     

Estimating left ventricular filling pressure during positive end-expiratory pressure in humans

In the critically ill, accurate measurements of left ventricular (LV) filling pressure using pulmonary artery occlusion pressure (Ppao) are important for diagnostic and therapeutic purposes. In patients receiving positive end-expiratory pressure (PEEP), Ppao may not reflect LV filling pressure because of elevated pericardial pressure (Ppc). It has been proposed that in humans, Ppc and right atrial pressure (PRA) are equal, so that referencing Ppao to PRA may improve the assessment of LV filling pressure when Ppc is elevated. Similarly, it has also been shown in the dog that nadir Ppao immediately after airway disconnection from PEEP (nadir Ppao), accurately reflects LV filling pressure when LV filling pressure is greater than or equal to 10 mm Hg. We examined methods of estimating LV filling pressure using Ppao measurements under conditions in which increases in Ppc were the primary determinants of differences in the two measurements. Using left atrial pressure (PLA) relative to Ppc, called transmural PLA (PLAtm), as LV filling pressure, we compared the accuracy of Ppao, nadir Ppao, and Ppao relative to PRA to reflect PLAtm in 15 postoperative cardiac surgery patients in whom an air-filled pericardial balloon catheter and a left atrial catheter were inserted during surgery. PEEP was sequentially increased from zero to 15 cm H2O. We found that PRA always exceeded Ppc (p less than 0.01) and increased less with PEEP than did Ppc (p less than 0.05). At less than or equal to 5 cm H2O PEEP, both Ppao and nadir Ppao were similar to each other and to PLAtm.(ABSTRACT TRUNCATED AT 250 WORDS)     

Hemodynamic effects of bilevel nasal positive airway pressure ventilation in patients with heart failure

AIMS: Benefits of nasal continuous positive airway pressure (CPAP) in patients presenting with chronic heart failure (CHF) are controversial. The purpose of this study was to compare the hemodynamic effects of CPAP and bilevel positive airway pressure (BiPAP) in patients with or without CHF. METHODS AND RESULTS: Twenty patients with CHF and 7 with normal left ventricular function underwent cardiac catheterization. Measurements were made before and after three 20-min periods of BiPAP: expiratory positive airway pressure (EPAP) = 8 cm H2O and inspiratory positive airway pressure (IPAP) = 12 cm H2O, EPAP = 10 cm H2O and IPAP = 15 cm H2O, and CPAP = EPAP = IPAP = 10 cm H2O administered in random order. Positive pressure ventilation decreased cardiac output (CO) and stroke volume. No change was observed in either pulmonary or systemic arterial pressure. There was no difference in the hemodynamic effects of the three ventilation settings. Only mean pulmonary wedge pressure (MPWP) and heart rate were lower with CPAP than with BiPAP. CO decreased only in patients with low MPWP (相似文献