Vasomotor tone does not affect perfusion heterogeneity and gas exchange in normal primate lungs during normoxia

2000 ◽  
Vol 89 (6) ◽  
pp. 2263-2267 ◽  
Author(s):  
Robb W. Glenny ◽  
H. Thomas Robertson ◽  
Michael P. Hlastala

To determine whether vasoregulation is an important cause of pulmonary perfusion heterogeneity, we measured regional blood flow and gas exchange before and after giving prostacyclin (PGI2) to baboons. Four animals were anesthetized with ketamine and mechanically ventilated. Fluorescent microspheres were used to mark regional perfusion before and after PGI2 infusion. The lungs were subsequently excised, dried inflated, and diced into ∼2-cm3 pieces ( n = 1,208–1,629 per animal) with the spatial coordinates recorded for each piece. Blood flow to each piece was determined for each condition from the fluorescent signals. Blood flow heterogeneity did not change with PGI2 infusion. Two other measures of spatial blood flow distribution, the fractal dimension and the spatial correlation, did not change with PGI2 infusion. Alveolar-arterial O2 differences did not change with PGI2 infusion. We conclude that, in normal primate lungs during normoxia, vasomotor tone is not a significant cause of perfusion heterogeneity. Despite the heterogeneous distribution of blood flow, active regulation of regional perfusion is not required for efficient gas exchange.

1998 ◽  
Vol 85 (6) ◽  
pp. 2337-2343 ◽  
Author(s):  
William A. Altemeier ◽  
H. Thomas Robertson ◽  
Steve McKinney ◽  
Robb W. Glenny

To explore mechanisms of hypoxemia after acute pulmonary embolism, we measured regional pulmonary blood flow and alveolar ventilation before and after embolization with 780-μm beads in five anesthetized, mechanically ventilated pigs. Regional ventilation and perfusion were determined in ∼2.0-cm3 lung volumes by using 1-μm-diameter aerosolized and 15-μm-diameter injected fluorescent microspheres. Hypoxemia after embolization resulted from increased perfusion to regions with low ventilation-to-perfusion ratios. Embolization caused an increase in perfusion heterogeneity and a fall in the correlation between ventilation and perfusion. Correlation between regional ventilation pre- and postembolization was greater than correlation between regional perfusion pre- and postembolization. The majority of regional ventilation-to-perfusion ratio heterogeneity was attributable to changes in regional perfusion. Regional perfusion redistribution without compensatory changes in regional ventilation is responsible for hypoxemia after pulmonary vascular embolization in pigs.


2006 ◽  
Vol 101 (2) ◽  
pp. 583-589 ◽  
Author(s):  
A. Cortney Henderson ◽  
David L. Levin ◽  
Susan R. Hopkins ◽  
I. Mark Olfert ◽  
Richard B. Buxton ◽  
...  

Head-down tilt has been shown to increase lung water content in animals and alter the distribution of ventilation in humans; however, its effects on the distribution of pulmonary blood flow in humans are unknown. We hypothesized that head-down tilt would increase the heterogeneity of pulmonary blood flow in humans, an effect analogous to the changes seen in the distribution of ventilation, by increasing capillary hydrostatic pressure and fluid efflux in the lung. To test this, we evaluated changes in the distribution of pulmonary blood flow in seven normal subjects before and after 1 h of 30° head-down tilt using the magnetic resonance imaging technique of arterial spin labeling. Data were acquired in triplicate before tilt and at 10-min intervals for 1 h after tilt. Pulmonary blood flow heterogeneity was quantified by the relative dispersion (standard deviation/mean) of signal intensity for all voxels within the right lung. Relative dispersion was significantly increased by 29% after tilt and remained elevated during the 1 h of measurements after tilt (0.84 ± 0.06 pretilt, 1.09 ± 0.09 calculated for all time points posttilt, P < 0.05). We speculate that the mechanism most likely responsible for our findings is that increased pulmonary capillary pressures and fluid efflux in the lung resulting from head-down tilt alters regional blood flow distribution.


2004 ◽  
Vol 97 (6) ◽  
pp. 2104-2111 ◽  
Author(s):  
William A. Altemeier ◽  
Steve McKinney ◽  
Melissa Krueger ◽  
Robb W. Glenny

Although recent high-resolution studies demonstrate the importance of nongravitational determinants for both pulmonary blood flow and ventilation distributions, posture has a clear impact on whole lung gas exchange. Deterioration in arterial oxygenation with repositioning from prone to supine posture is caused by increased heterogeneity in the distribution of ventilation-to-perfusion ratios. This can result from increased heterogeneity in regional blood flow distribution, increased heterogeneity in regional ventilation distribution, decreased correlation between regional blood flow and ventilation, or some combination of the above (Wilson TA and Beck KC, J Appl Physiol 72: 2298–2304, 1992). We hypothesize that, although repositioning from prone to supine has relatively small effects on overall blood flow and ventilation distributions, regional changes are poorly correlated, resulting in regional ventilation-perfusion mismatch and reduction in alveolar oxygen tension. We report ventilation and perfusion distributions in seven anesthetized, mechanically ventilated pigs measured with aerosolized and injected microspheres. Total contributions of pulmonary structure and posture on ventilation and perfusion heterogeneities were quantified by using analysis of variance. Regional gradients of posture-mediated change in ventilation, perfusion, and calculated alveolar oxygen tension were examined in the caudocranial and ventrodorsal directions. We found that pulmonary structure was responsible for 74.0 ± 4.7% of total ventilation heterogeneity and 63.3 ± 4.2% of total blood flow heterogeneity. Posture-mediated redistribution was primarily oriented along the caudocranial axis for ventilation and along the ventrodorsal axis for blood flow. These mismatched changes reduced alveolar oxygen tension primarily in the dorsocaudal lung region.


1999 ◽  
Vol 86 (2) ◽  
pp. 623-632 ◽  
Author(s):  
Robb W. Glenny ◽  
Susan Bernard ◽  
H. Thomas Robertson ◽  
Michael P. Hlastala

Original studies leading to the gravitational model of pulmonary blood flow and contemporary studies showing gravity-independent perfusion differ in the recent use of laboratory animals instead of humans. We explored the distribution of pulmonary blood flow in baboons because their anatomy, serial distribution of vascular resistances, and hemodynamic responses to hypoxia are similar to those of humans. Four baboons were anesthetized with ketamine, intubated, and mechanically ventilated. Different colors of fluorescent microspheres were given intravenously while the animals were in the supine, prone, upright (repeated), and head-down (repeated) postures. The animals were killed, and their lungs were excised, dried, and diced into ∼2-cm3 pieces with the spatial coordinates recorded for each piece. Regional blood flow was determined for each posture from the fluorescent signals of each piece. Perfusion heterogeneity was greatest in the upright posture and least when prone. Using multiple-stepwise regression, we estimate that 7, 5, and 25% of perfusion heterogeneity is due to gravity in the supine, prone, and upright postures, respectively. Although important, gravity is not the predominant determinant of pulmonary perfusion heterogeneity in upright primates. Because of anatomic similarities, the same may be true for humans.


1982 ◽  
Vol 60 (12) ◽  
pp. 1436-1443 ◽  
Author(s):  
Louis Dumont ◽  
Claudette Lamoureux ◽  
Jacques Lelorier ◽  
Paul Stanley ◽  
Claude Chartrand

We have studied both central and peripheral hemodynamic changes induced by infusion of nitroglycerin (55 μg/kg per minute) over a 15-min period in conscious dogs to clarify its mechanism of action. Dogs were prepared with an electromagnetic flow probe positioned at the root of the aorta, and microspheres (9 μm) were used to measure regional blood flow distribution before and after 15 min of infusion. Controlled hypotension (−15 to −20 mmHg (1 mmHg = 133.322 Pa)) was maintained throughout the infusion period and this hypotensive state was associated with a significant decrease in stroke volume (−30%), cardiac index (−20%), and left ventricular work (−43%). Regional blood flow studies showed that at the 15th min of infusion, nitroglycerin induced significant decrease in blood flow to all components of the myocardium (range −12 to −20%) while their vascular resistances were not affected significantly. Blood perfusion to liver (hepatic artery), spleen, and intestine was also modified significantly (−22, −18, and −16%, respectively) while their vascular resistances remained close to control values. By the time measurements were made, blood flow and vascular resistance of cerebral and renal tissues remained normal. For each organ studied, blood perfusion was uniform. These results indicate that nitroglycerin elicits both central and peripheral hemodynamic changes and that local reflex adjustments modify the vasodilator effect of the drug in most vascular beds that we have studied.


1999 ◽  
Vol 87 (1) ◽  
pp. 132-141 ◽  
Author(s):  
Steven Deem ◽  
Richard G. Hedges ◽  
Steven McKinney ◽  
Nayak L. Polissar ◽  
Michael K. Alberts ◽  
...  

Severe anemia is associated with remarkable stability of pulmonary gas exchange (S. Deem, M. K. Alberts, M. J. Bishop, A. Bidani, and E. R. Swenson. J. Appl. Physiol. 83: 240–246, 1997), although the factors that contribute to this stability have not been studied in detail. In the present study, 10 Flemish Giant rabbits were anesthetized, paralyzed, and mechanically ventilated at a fixed minute ventilation. Serial hemodilution was performed in five rabbits by simultaneous withdrawal of blood and infusion of an equal volume of 6% hetastarch; five rabbits were followed over a comparable time. Ventilation-perfusion (V˙a/Q˙) relationships were studied by using the multiple inert-gas-elimination technique, and pulmonary blood flow distribution was assessed by using fluorescent microspheres. Expired nitric oxide (NO) was measured by chemiluminescence. Hemodilution resulted in a linear fall in hematocrit over time, from 30 ± 1.6 to 11 ± 1%. Anemia was associated with an increase in arterial [Formula: see text] in comparison with controls ( P < 0.01 between groups). The improvement in O2 exchange was associated with reducedV˙a/Q˙heterogeneity, a reduction in the fractal dimension of pulmonary blood flow ( P = 0.04), and a relative increase in the spatial correlation of pulmonary blood flow ( P = 0.04). Expired NO increased with anemia, whereas it remained stable in control animals ( P < 0.0001 between groups). Anemia results in improved gas exchange in the normal lung as a result of an improvement in overallV˙a/Q˙matching. In turn, this may be a result of favorable changes in pulmonary blood flow distribution, as assessed by the fractal dimension and spatial correlation of blood flow and as a result of increased NO availability.


1995 ◽  
Vol 221 (5) ◽  
pp. 531-542 ◽  
Author(s):  
John J. Ferrara ◽  
D. Lynn Dyess ◽  
Guy L. Peeples ◽  
D. Paul Christenberry ◽  
W. Scott Roberts ◽  
...  

2003 ◽  
Vol 10 (2) ◽  
pp. 128-138 ◽  
Author(s):  
Anne V Clough ◽  
Steven T Haworth ◽  
David L Roerig ◽  
Eric A Hoffman ◽  
Christopher A Dawson

1980 ◽  
Vol 48 (1) ◽  
pp. 147-153 ◽  
Author(s):  
W. Nixon ◽  
A. Pack

Experimental studies have established that alveolar gas exchange is inversely relation to the molecular diffusivity of gas in the lung airways. The mechanism underlying this relationship is, however, unclear. To investigate this phenomenon, the conditions relevant to the experimental studies are simulated using a computational model of pulmonary gas transport. Results from these simulations suggest that the inverse relationship found experimentally can largely be explained on the basis of the intra-acinar stratification of blood flow and gas concentrations. Gas having a relatively low molecular diffusivity is not transported as far into the acinus as gas having a higher diffusivity. When these relative intra-acinar gas distributions interact with the blood flow distribution, which has been shown experimentally to be weighted towards the proximal alveoli, more gas exchange occurs in the low molecular diffusivity mixture. Consideration of the various other mechanisms that have been proposed to explain the experimental findings.he inverse dependence suggests that they are of little significance. In particular, our studies remove the need to invoke Taylor diffusion to explain the experimental findings.


1996 ◽  
Vol 80 (1) ◽  
pp. 341-344 ◽  
Author(s):  
M. Scuri ◽  
V. McCaskill ◽  
A. D. Chediak ◽  
W. M. Abraham ◽  
A. Wanner

The reported effects of cholinergic agonists on bronchial blood flow (Qbr) have been inconsistent. The aim of the present study was to determine whether the inconsistency could be due to the mode of agonist administration (systemic vs. aerosol) or the anatomic site of blood flow in the bronchus (mucosal vs. deep wall). In 10 anesthetized mechanically ventilated adult sheep, we measured Qbr in main bronchi by color-coded microspheres, systemic and pulmonary arterial pressures, cardiac output, and lung resistance (RL) before and after acetylcholine (ACh) administered either as an aerosol (nebulized dose 100 micrograms) or as an intravenous bolus (2 micrograms/kg). Before drug administration, 72% of mean Qbr was distributed to the bronchial mucosa and the remainder was distributed to the deep bronchial wall. For a comparable increase in mean RL (150% for intravenous ACh and 205% for aerosol ACh), mean total Qbr normalized for systemic arterial pressure increased by 291% after intravenous ACh (P < 0.05) and decreased by 9% after aerosol ACh (not significant). Mucosal and deep wall Qbr increased proportionally. Atropine (0.2 microgram/kg) prevented the changes in Qbr and RL after intravenous ACh. Thus intravenous but not aerosol ACh increased blood flow in the mucosa and deep wall of extrapulmonary bronchi. This suggests that the muscarinic receptors mediating vasodilation are more accessible to intravascular than intrabronchial ACh.


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