Effect Of Pulmonary Blood Flow Research Articles

Drug detection in breath: effects of pulmonary blood flow and cardiac output on propofol exhalation

Breath analysis could offer a non-invasive means of intravenous drug monitoring if robust correlations between drug concentrations in breath and blood can be established. In this study, propofol blood and breath concentrations were determined in an animal model under varying physiological conditions. Propofol concentrations in breath were determined by means of two independently calibrated analytical methods: continuous, real-time proton transfer reaction mass spectrometry (PTR-MS) and discontinuous solid-phase micro-extraction coupled with gas chromatography mass spectrometry (SPME-GC-MS). Blood concentrations were determined by means of SPME-GC-MS. Effects of changes in pulmonary blood flow resulting in a decreased cardiac output (CO) and effects of dobutamine administration resulting in an increased CO on propofol breath concentrations and on the correlation between propofol blood and breath concentrations were investigated in seven acutely instrumented pigs. Discontinuous propofol determination in breath by means of alveolar sampling and SPME-GC-MS showed good agreement (R(2)=0.959) with continuous alveolar real-time measurement by means of PTR-MS. In all investigated animals, increasing cardiac output led to a deterioration of the relationship between breath and blood propofol concentrations (R(2)=0.783 for gas chromatography-mass spectrometry and R(2)=0.795 for PTR-MS). Decreasing pulmonary blood flow and cardiac output through banding of the pulmonary artery did not significantly affect the relationship between propofol breath and blood concentrations (R(2)>0.90). Estimation of propofol blood concentrations from exhaled alveolar concentrations seems possible by means of different analytical methods even when cardiac output is decreased. Increases in cardiac output preclude prediction of blood propofol concentration from exhaled concentrations.

Effects of Pulmonary Blood Flow on Respiratory Mechanics: Measurements by the End-Inflation Occlusion Method in Healthy Rats After Acute Blood Volume Expansion

Effects of Pulmonary Blood Flow on Respiratory Mechanics: Measurements by the End-Inflation Occlusion Method in Healthy Rats After Acute Blood Volume Expansion

Pulmonary blood flow alters nitric oxide production in patients undergoing device closure of atrial septal defects

OBJECTIVETo determine the effect of pulmonary blood flow (Qp) on nitric oxide (NO) production in patients with increased Qp due to an atrial septal defect (ASD).BACKGROUNDAlterations in pulmonary vascular NO production have been implicated in the development of pulmonary hypertension secondary to increased Qp. In vitro, acute changes in flow or shear stress alter NO production. However, the effect of Qp on lung NO production in vivo is unclear.METHODSNineteen patients (2.4–61 years of age, median 17) with secundum ASD undergoing device closure were studied. Before, and 30 min after ASD closure, exhaled NO and plasma nitrate concentration were measured by chemiluminescence (NOA 280, Sievers, Boulder, Colorado).RESULTSBefore ASD closure, all patients had increased Qp (Qp: systemic blood flow [Qs] of 2.0 ± 0.7) and normal mean pulmonary arterial pressure (13.4 ± 3.1 mm Hg). Atrial septal defect device closure decreased Qp from 6.0 ± 2.5 to 3.6 ± 1.3 L/min/m2(p < 0.05). Mean pulmonary arterial pressure was unchanged. Associated with the decrease in Qp, both exhaled NO (−22.1%, p < 0.05) and plasma nitrate concentrations (−17.9%, p < 0.05) decreased.CONCLUSIONSThese data represent the first demonstration that acute changes in Qp alter pulmonary NO production in vivo in humans. Exhaled NO determinations may provide a noninvasive assessment of pulmonary vascular NO production in patients with congenital heart disease. Potential correlations between exhaled NO, pulmonary vascular reactivity and pulmonary hypertension warrant further study.

Pulmonary blood flow regulates plasma tissue plasminogen activator concentrations in patients with congenital heart defects

Objective: The wall shear stress generated by blood flow regulates the expression of fibrinolytic proteins by endothelial cells in vitro. In the present study, the effects of pulmonary blood flow on fibrinolytic activity were studied in patients with congenital heart defects and pulmonary hypertension. Methods: Twenty-seven patients who underwent cardiac operation because of congenital heart defects were divided into four groups according to the severity of pulmonary hypertension. Group I consisted of seven patients with normal pulmonary artery pressure, group II consisted of nine patients with pulmonary hypertension caused by increased pulmonary blood flow, group III consisted of six patients with pulmonary hypertension caused by increased pulmonary vascular resistance, and group IV consisted of five patients with tetralogy of Fallot. Plasma concentrations of tissue plasminogen activator, plasmin, and thrombin were assayed as the inhibitor-bound forms. Results: The preoperative concentration of tissue plasminogen activator was higher in group II than in all other groups ( p = 0.0003). However, the postoperative concentration decreased only in patients in group II when compared with the preoperative value ( p = 0.01). By Pearson's correlation analysis, pulmonary blood flow was found to correlate with the preoperative concentration of tissue plasminogen activator (95% confidence interval = 3.99 to 10.58, p = 0.0001). No definite conclusion was found for the relationship between tissue plasminogen activator and plasmin concentration. Further, the preoperative thrombin concentration was similar in all groups. Conclusions: These findings suggest that pulmonary blood flow may regulate the plasma concentration of tissue plasminogen activator in patients with congenital heart defects. (J Thorac Cardiovasc Surg 1997;113:742-7)

Plasma endothelin-1 in patients with left-to-right shunt

Endothelin-1 (ET-1) has been implicated in the pathogenesis of pulmonary vascular disease in patients with congenital heart disease. We studied the effect of pulmonary blood flow on plasma ET-1 concentrations. Systemic venous, pulmonary arterial, and pulmonary venous blood samples were obtained from 40 patients with atrial septal defect II ( n = 21), ventricular septal defect ( n = 10), persistent ductus arteriosus ( n = 6), and complete ( n = 2) and partial ( n = 1) atrioventricular canal at cardiac catheterization and analyzed by radioimmunoassay. Median age (range) was 5.2 years (8 months to 66 years), and the resistance ratio ( Rp Rs ) was 0.08 (0.03 to 0.67). Pulmonary vein to pulmonary artery ET-1 ratio in patients with “high flow” ( n = 26, Qp Qs ≥ 1.5 ; ET-1 ratio = 0.8) did not differ from those with “low flow” ( n = 14, Qp Qs < 1.5 ; ET-1 ratio = 1.0). We conclude that an increase in pulmonary blood flow alone does not result in an increase in plasma ET-1.

Effect of pulmonary blood flow on microvascular pressure profile determined by micropuncture in perfused cat lungs

To clarify the role of the pulmonary microvasculature in adjusting to increased pulmonary blood flow, we measured arteriolar and venular pressure by the servo-null micropuncture method while changing the pulmonary blood flow in isolated perfused cat lungs. We divided the lung vasculature into three longitudinal segments: 1) arterial (pulmonary artery to 30- to 50-microns arteriole), 2) microvascular (between 30- to 50-microns arteriole and venule), and 3) venous (30- to 50-microns venule to left atrium). The vascular resistance was calculated by dividing the pressure gradient by the flow. The pressure gradient of the microvascular segment did not increase, whereas the pressure gradient of the arterial and venous segments increased simultaneously with flow rate. Total and microvascular resistance decreased with increase of flow rate. Resistances of the arterial and venous segments did not change with increase in flow. We conclude that the microvasculature plays a crucial role in preventing pulmonary hypertension with increases in flow by decreasing microvascular resistance.

Effects of pulmonary blood flow on the fractal nature of flow heterogeneity in sheep lungs

The spatial heterogeneity of pulmonary blood flow can be described by the relative dispersion (RD) of weight-flow histograms (RD = SD/mean). Glenny and Robertson (J. Appl. Physiol. 69: 532-545, 1990) showed that RD of flow in the lung is fractal in nature, characterized by the fractal dimension (D) and RD for the smallest realizable volume element (RDref). We studied the effects of increasing total pulmonary blood flow on D and RDref. In eight in situ perfused sheep lung preparations, 15-microns radio-labeled microspheres were injected into the pulmonary artery at five different blood flows ranging, in random order, from 1.5 to 5.0 l/m. The lungs were in zone 2 at the lower flows and in zone 3 at the higher flows. The lungs were removed, dried, cut into 2 x 2 x 2-cm3 pieces, weighed, and then counted for microsphere radioactivity. Fractal plots of log(weight) vs. log(RD) were constructed by iteratively combining neighboring pieces and then calculating RD with the increasingly larger portion size. D, which is one minus the slope of the fit through this plot, was 1.14 +/- 0.09 and did not change as blood flow increased. However, RDref decreased significantly (P < 0.01) as total flow increased. We conclude that the fractal nature of pulmonary blood flow distribution is not altered by changes in overall flow.

Relation of elevated plasma endothelin in congenital heart disease to increased pulmonary blood flow

Endothelin-1 (ET), a potent vasoconstrictor peptide, has been found to be elevated in children with pulmonary hypertension associated with congenital heart defects. To evaluate the effect of pulmonary blood flow on ET concentrations, 5 ml blood samples were obtained peripherally at cardiac catheterization from 35 patients, ages 0.13 to 17 years (median 2). Plasma was extracted and ET measured by radioimmunoassay. Patients were classified into 2 groups based on the presence (group A) or absence (group B) of increased pulmonary blood flow defined as a Qp Qs ≥1.5 . When the 13 patients (37%) in group A were compared with the 22 patients (63%) in group B there were no significant differences in age, cardiac index, or pulmonary and systemic resistances. ET concentrations were significantly higher in group A patients (median 3.25, range 0 to 16.5 vs median 0, range 0 to 6.35 pg/ml; p ≤ 0.05). Pulmonary Mood flow and pulmonary artery pressure were also higher in group A patients (p ≤ 0.01). When patients within group A were subdivided into those with and without pulmonary hypertension, no difference was present in their ET concentrations ( mean/SD: 4.4 4.3 vs 4.0 6.4 pg/ml, p = NS ). Thus, ET is elevated in patients with congenital heart disease associated with left-to-right shunts and it appears that this increase is related to increased pulmonary blood flow independent of pulmonary artery pressure.

Effect of pulmonary blood flow on measurements of respiratory mechanics using the interrupter technique.

The relationship between respiratory mechanics, changes in pulmonary blood flow (PBF), pulmonary arterial pressure, and left atrial pressure is unclear. Conventional methods for the measurement of respiratory mechanics model the respiratory system as a single compartment, which may not adequately represent the respiratory system in a diseased state. The interrupter technique models the respiratory system as two compartments, with the "flow resistance" of the conducting airways and chest wall (Raw) considered separately from Pdif, a measure of the viscoelastic properties of the lung and chest wall, together with any pendelluft present. The respiratory mechanics of 15 infants in the first year of life were studied during cardiac catheterization with the use of conventional methods and the interrupter technique. The infants had a PBF-to-systemic blood flow ratio ranging from 0.6 to 4.0:1. The specific dynamic compliance of the respiratory system was not related to the PBF; however, there was a significant relationship between PBF and the total resistance of the respiratory system (Rrs) [analysis of variance (ANOVA) F = 5.69, P < 0.05], Raw (ANOVA, F = 12.30, P < 0.01), and Pdif (ANOVA, F = 3.79, P < 0.05). Rrs increased significantly with an increase in mean left atrial pressure (ANOVA, F = 6.92, P < 0.05); however, dynamic compliance, Raw, and Pdif did not. These results suggest that the relationship between Rrs and PBF is due an increase in the resistive properties of the conducting airways and tissue components.

The effect of blood flow and left atrial pressure on the D lCO in lambs and sheep

Previous studies suggest that pulmonary capillary distensibility and recruitment may differ in lambs and sheep. To study the effect of pulmonary blood flow (PBF) and vascular pressure on capillary hemodynamics in lambs and sheep we measured the diffusing capacity for carbon monoxide (D l CO) as an index of pulmonary capillary blood volume during a baseline period, after increasing PBF, and during left atrial hypertension. In the lamb, D l CO did not change significantly either with a 65% increase in PBF or with an increase in left atrial pressure (Pla) of 1.33 kPa at constant PBF. In the sheep on the other hand, doubling PBF led to a 28% increase in D l CO ( P < 0.02), and an increase in Pla of 1.87 kPa at constant PBF led to a 19% increase in D l CO ( P < 0.01). These results suggest that the neonatal lamb has a nearly fully recruited and relatively non-compliant pulmonary capillary bed at rest, unlike the adult sheep which can respond to hemodynamic changes with distension and recruitment of the pulmonary capillary bed.

Effect of Pulmonary Blood Flow on Lung Water and Pulmonary Hemodynamics in the Canine Lung Lobe

The isolated left middle lobes of canine lungs were perfused in situ, by stepwise elevation of the blood flow. The weight gain of the lung lobe per initial bloodless dry lung weight (delta w g/min.IdQ1) showed a significant (p less than 0.001) correlation with the blood flow per body weight (F, ml/min.kg) with a regression line of delta w = 8.3 X 10-4F2.3. The pulmonary venous pressure (Pv) correlated significantly (p less than 0.001) with the pulmonary artery pressure (Pa), i.e. Pa = 11.2 + 1.3 Pv, with a constant left atrial pressure (Pla). The total pulmonary vascular resistance [TPVR = (Pa - Pla)/F] and the small pulmonary artery resistance [SR = (Pa-Pv)/F] decreased by steps with a constant pulmonary venous resistance (VR = TPVR-SR), and VR/TPVR increased by steps as the flow was increased. By incremental blood flow through the restricted lung tissue, we conclude that fluid filtration into the interstitium was flow-dependent, the pulmonary capillaries and precapillaries provided a large capacity for blood flow and the resistance to the flow was directed to the postcapillary site.

Effect of pulmonary blood flow on leukocyte uptake and release by dog lung.

The effect of pulmonary blood flow on leukocyte uptake and release by the lung was examined in 10 anesthetized spontaneously breathing dogs. Pulmonary arterial and pulmonary venous blood was sampled with catheters placed into the right ventricle and aorta, respectively. Pulmonary blood flow was lowered by inflating a balloon catheter located in the inferior vena cava. In five experiments simultaneous blood samples were drawn from the right ventricle and aorta at 10-s intervals during a control period, a 2- to 3-min period of low flow, and a recovery period. In five additional experiments, less frequent samples were taken over periods of 15-60 min. Total leukocyte concentrations and differential counts were determined for each blood sample. The study shows that large numbers of leukocytes become sequestered within the lung when pulmonary blood flow is low and that an equivalent number of cells are released from the lung after deflation of the balloon catheter. Both the polymorphonuclear leukocytes and the lymphocytes were taken up by the lung when pulmonary blood flow was reduced. We conclude that pulmonary blood flow has a marked effect on the uptake and release of leukocytes by the dog lung.

Pulmonary blood flow: A potential factor in the pathogenesis of pulmonary edema

The purpose of this study is to examine the hemodynamics of the pulmonary circulation and the potential role of pulmonary blood flow in the pathogenesis of cardiogenic pulmonary edema. To do so, the pulmonary circulation was isolated and controlled such that, within a closed circuit, pulmonary blood flow and left atrial pressure (LAP) could be regulated independently: the first by a constant flow pump, the second by a variable height reservoir. The effect of pulmonary blood flow on pulmonary artery pressure and intravascular blood volume was then determined at different LAPs. Contrary to our expectations, the results indicate that (1) pulmonary vascular resistance does not change appreciably as flow increases, (2) the microcirculation comprises the major capacitance vessels of the lung, and (3) increased pulmonary flow in the normal lung causes little change in intravascular pulmonary blood volume, whereas, by contrast, major changes in pulmonary blood volume occur as LAP rises. Next, the effect of pulmonary blood flow on edema formation in the lungs was examined. Below a critical level of LAP (15 mm Hg in these experiments), pulmonary blood flow up to 5 L/min did not produce pulmonary edema. Above this level, however, such an effect was clear. Thus, at an LAP of 20 mm Hg, edema did not develop if pulmonary flow was low (0.7 L/min) but did if flow was increased to 2 L/min. As well, if the LAP was 17.5 mm Hg and pulmonary flow 3.5 L/min, severe pulmonary edema also resulted.

Effects of pulmonary blood flow and mixed venous O2 tension on gas exchange in dogs.

The authors investigated whether the increases in venous admixture and intrapulmonary shunt which occur with increases in cardiac output (Qt) results from an effect mediated by mixed venous PO2 (PVO2) or an effect mediated by the increase in pulmonary blood flow. Using a veno-venous bypass system thay were able to alter PVO2 independent of variations in Qt and vice versa. During room air ventilation of dogs with normal lungs at constant Qt, an increase in PVO2 from 33 +/- 7 (mean +/- SD) to 54 +/- 9 mmHg (P less than 0.05) resulted in a decrease in venous admixture from 22 +/- 11 to 13 +/- 4% (P less than 0.05). During room air ventilation of normal dogs at a constant PVO2, raising Qt from 2.16 +/- .53 to 3.49 +/- 0.91 l/min (P less than 0.05) increased venous admixture from 10 +/- 5 to 16 +/- 5% (P less than 0.05). During oxygen ventilation in these two groups of dogs, changes in PVO2 and Qt had no effect on shunt. During oxygen ventilation of dogs with significant shunts from oleic-acid-induced pulmonary edema, independent increases in either PVO2 or pulmonary blood flow resulted in increased shunt. At constant Ot, an increase in PVO2 from 30 +/- 8 to 52 +/- 3 mmHg (P less than 0.05) resulted in an increase in shunt from 39 +/- 12 to 43 +/- 12% (P less than 0.05). When PVO2 remained constant, increasing Qt from 1.97 pm 0.42 to 3.61 +/- 0.50 l/min (P less than 0.05) resulted in an increase in shunt from 47 +/- 17 to 53 +/- 15% (P less than 0.05). The authors conclude that during oxygen ventilation, normal dogs have shunts which are unaffected by changes in blood flow or PVO2. Increases in pulmonary blood flow increase venous admixture during room air ventilation, while increases in PVO2 decrease venous admixture during air ventilation. In edematous lungs, increases in either PVO2 or pulmonary blood flow increase shunt.

The effects of pulmonary circulation pulsatility on the impedance cardiogram.

To study the effects of pulmonary blood flow on the impedance cardiogram, the pattern of pulmonary blood flow was alternated from pulsatile to non pulsatile, or the reverse, using our extracorporeal bypass-method on anaesthetized dogs. The thoracic impedance cardiogram was recorded from band electrodes placed around the neck and upper abdomen. During nonpulsatile pulmonary blood flow, the height of the diastolic phase of the delta Z wave was lower than that during pulsatile pulmonary blood flow. The area under the impedance curve decreased during nonpulsatile pulmonary blood flow. This appeared to be more obvious as the pulmonary arterial flow was reduced. The results suggest that the pulmonary blood flow might have substantial effects on the impedance cardiogram.

Effect of pulmonary blood flow on the exchange between the circulating and marginating pool of polymorphonuclear leukocytes in dog lungs.

The effect of pulmonary blood flow on the exchange between the circulating was marginating pool of polymorphonuclear leukocytes (PMN) was examined in three sets of experiments. In the first we used the double indicator dilution technique with labeled PMN and erythrocytes (RBC) to calculate the percent extraction and percent recovery of PMN at different levels of cardiac output (CO). In the second group of experiments we took advantage of the wide range of blood flow in the lung to determine the effect of regional blood flow on regional PMN retention, and in the third set we measured total leukocyte (WBC) and PMN counts in simultaneous samples from the pulmonary artery and aorta over a wide range of cardiac output. The studies showed that 80-90% of the labeled PMN were removed in a single pass through the lung and that regional retention of labeled PMN and A-V differences for unlabeled PMN increased with decreasing blood flow. The data for regional retention of labeled PMN and the A-V differences observed for unlabeled cells both fit the equation Y = A + Be-cx (where A + B = 100), which showed that PMN accumulate in the lung as blood flow is reduced. We conclude that a dynamic equilibrium exists between the circulating and marginating pools of leukocytes in the lung and that blood flow primarily effects the reentry of cells into the circulating pool so that the marginating pool of PMN within the lung accumulates cells when blood flow is reduced below 7 ml/min per g.

Effect of pulmonary blood flow on the elimination of fibrin from the lungs

Effect of pulmonary blood flow on the elimination of fibrin from the lungs

Effect of pulmonary blood flow upon lung mechanics.

Airway pressure was continuously recorded in an isolated horizontally mounted canine heart-lung preparation during abrupt, stepwise 100-200 ml inflations to 20-25 cm water pressure, and subsequent deflations. With each change in volume there was a steep rise or fall in pressure, followed by stress relaxation to a static equilibrium airway pressure. Comparison was made between the nonperfused state and during perfusion with whole blood at 100 ml/kg dog wt per min, and left atrial pressure of 10 mm Hg. Pressure tracings were similar during deflation in the perfused and the nonperfused lung. During inflation, in the middle range of lung inflation volumes, the peak inflation and equilibrium airway pressures were greater in the nonperfused state; maximum difference of static pressures in nine preparations averaged 146% of perfused values and the average stress relaxation difference from eight of these was 276%. Lung distensibility was the same with packed red cells or plasma perfusates and was not changed by varying the perfusion rate up to 220 ml/kg per min. During cyclic ventilation, dynamic compliance was similarly greater in the perfused than in the nonperfused state in the middle range of inflation volumes. Static distention of the vascular bed produced similar results with progressive improvement in distensibility in mid-inflation range up to a hydrostatic pressure of 15 cm blood. These data suggest that the distended pulmonary vascular bed provides structural airway support which facilitates entry of gas into the terminal respiratory units at diminished pressure.

Effects of Pulmonary Blood Flow and Distention on the Capacity of Intrapulmonary Vessels

Effects of Pulmonary Blood Flow and Distention on the Capacity of Intrapulmonary Vessels