Ventilatory changes associated with changes in pulmonary blood flow in dogs

1983 ◽  
Vol 54 (4) ◽  
pp. 997-1002 ◽  
Author(s):  
J. F. Green ◽  
M. I. Sheldon

To examine the influence of pulmonary blood flow (Qp) on spontaneous ventilation (VE), we isolated the systemic and pulmonary circulations and controlled the arterial blood gases and blood flow (Q) in each circuit as we measured VE. Each dog was anesthetized with ketamine and maintained with halothane. Systemic Q was drained from the right atrium and pumped through an oxygenator and heat exchanger and returned to the aorta. An identical bypass was established for the pulmonary circulation, draining blood from the left atrium and pumping it to the pulmonary artery. The heart was fibrillated, all cannulas were brought through the chest wall, and the median sternotomy was closed. The dog was then allowed to breathe spontaneously. The arterial O2 partial pressure (PO2) of both circuits was maintained greater than 300 Torr. Systemic Q was maintained at 0.080 l X min-1 X kg-1. Initially the arterial CO2 partial pressure (PCO2) of both circuits was set at 40 Torr as Qp was varied randomly between approximately 0.025 and 0.175 l X min-1 X kg-1. The average VE-Qp relationship was linear with a slope of 1.45 (P less than 0.0005). Increasing the arterial PCO2 of both circuits to 60 Torr elevated VE an average of 0.37 l X min-1 X kg-1 at each level of Qp (P less than 0.0005). Vagotomy abolished the effect of Qp on VE. Increasing Qp affected the systemic arterial PCO2-VE response curve by shifting it upward without altering its slope. These results demonstrate that increases in Qp are associated with increases in VE. This phenomenon may contribute to exercise hyperpnea.

1987 ◽  
Vol 253 (4) ◽  
pp. H890-H897 ◽  
Author(s):  
R. W. McPherson ◽  
D. Eimerl ◽  
R. J. Traystman

The interaction of hypoxic hypoxia, hypercapnia, and mean arterial blood pressure (MABP) was studied in 15 pentobarbital-anesthetized ventilated dogs. In one group of animals (n = 5) hypercapnia [arterial CO2 partial pressure (PaCO2) approximately 50 Torr] was added to both moderate hypoxia and severe hypoxia. Moderate hypoxia [arterial O2 partial pressure (PaO2) = 36 mmHg] increased MABP and cerebral blood flow (CBF) without changes in cerebral O2 uptake (CMRO2). Superimposed hypercapnia increased CBF and MABP further with no change in CMRO2. In another group of animals (n = 5), a MABP increase of approximately 40 mmHg during moderate hypoxia without hypercapnia did not further increase CBF, suggesting intact autoregulation. Thus, during moderate hypoxia, hypercapnia is capable of increasing CBF. Severe hypoxia (PaO2 = 22 mmHg) increased CBF, but MABP and CMRO2 declined. Superimposed hypercapnia further decreased MABP and decreased CBF from its elevated level and further decreased CMRO2. Raising MABP under these circumstances in another animal group (n = 5) increased CBF above the level present during severe hypoxia alone and increased CMRO2. The change in CBF and CMRO2 during severe hypoxia plus hypercapnia with MABP elevation were not different from that severe hypoxia alone. We conclude that, during hypoxia sufficiently severe to impair CMRO2, superimposed hypercapnia has a detrimental influence due to decreased MABP, which causes a decrease in CBF and cerebral O2 delivery.


1979 ◽  
Vol 46 (6) ◽  
pp. 1171-1177 ◽  
Author(s):  
R. W. Stremel ◽  
B. J. Whipp ◽  
R. Casaburi ◽  
D. J. Huntsman ◽  
K. Wasserman

The ventilatory responses to diminished pulmonary blood flow (Qc), as a result of partial cardiopulmonary bypass (PCB), were studied in chloralose-urethan-anesthetized dogs. Qc was reduced by diverting vena caval blood through a membrane gas exchanger and returning it to the ascending aorta. PCB flows of 400--1,600 ml/min were utilized for durations of 2--3 min. Decreasing Qc, while maintaining systemic arterial blood gases and perfusion, results in a significant (P less than 0.05) decrease in expiratory ventilation (VE) (15.9%) and alveolar ventilation (VA) (31.0%). The ventilatory decreases demonstrated for this intact group persist after bilateral cervical vagotomy (Vx), carotid body and carotid sinus denervation (Cx), and combined Vx and Cx. The changes in VE and VA were significantly (P less than 0.001) correlated with VCO2 changes, r = 0.80 and r = 0.93, respectively. These ventilatory changes were associated with an overall average decrease in left ventricular PCO2 of 2.1 Torr; this decrease was significant (P less than 0.05) only in the intact and Cx groups. Decreasing pulmonary blood flow results in a decrease in ventilation that may be CO2 related; however, the exact mechanism remains obscure but must have a component that is independent of vagally mediated cardiac and pulmonary afferents and peripheral baroreceptor and chemoreceptor afferents.


1985 ◽  
Vol 249 (3) ◽  
pp. H570-H576 ◽  
Author(s):  
S. J. Soifer ◽  
R. D. Loitz ◽  
C. Roman ◽  
M. A. Heymann

The factors responsible for maintaining the normally low pulmonary blood flow and high pulmonary vascular resistance in the fetus are not well understood. Since leukotrienes are potent pulmonary vasoconstrictors in many adult animal species, we determined whether leukotrienes were perhaps involved in the control of the fetal pulmonary circulation by studying the effects of putative leukotriene end organ antagonists in two groups of fetal lambs. In six fetal lambs studied at 130-134 days gestation, FPL 55712 increased pulmonary blood flow by 61% (P less than 0.05) and reduced pulmonary vascular resistance by 45% (P less than 0.05). There was a small increase in heart rate but no changes in pulmonary and systemic arterial pressures and systemic arterial blood gases. In six other fetal lambs studied at 130-140 days gestation, FPL 57231 increased pulmonary blood flow by 580% (P less than 0.05) and decreased pulmonary vascular resistance by 87% (P less than 0.05). Pulmonary and systemic arterial pressures decreased (P less than 0.05), and heart rate increased (P less than 0.05). Leukotriene end organ antagonism significantly increases fetal pulmonary blood flow and decreases pulmonary vascular resistance. Leukotrienes may play a role in the physiological control of the fetal pulmonary circulation.


1998 ◽  
Vol 84 (4) ◽  
pp. 1278-1288 ◽  
Author(s):  
Michael P. Hlastala ◽  
Myron A. Chornuk ◽  
David A. Self ◽  
Harry J. Kallas ◽  
John W. Burns ◽  
...  

This study was undertaken to assess the influence of gravity on the distribution of pulmonary blood flow (PBF) using increased inertial force as a perturbation. PBF was studied in unanesthetized swine exposed to −G x (dorsal-to-ventral direction, prone position), where G is the magnitude of the force of gravity at the surface of the Earth, on the Armstrong Laboratory Centrifuge at Brooks Air Force Base. PBF was measured using 15-μm fluorescent microspheres, a method with markedly enhanced spatial resolution. Each animal was exposed randomly to −1, −2, and −3 G x . Pulmonary vascular pressures, cardiac output, heart rate, arterial blood gases, and PBF distribution were measured at each G level. Heterogeneity of PBF distribution as measured by the coefficient of variation of PBF distribution increased from 0.38 ± 0.05 to 0.55 ± 0.11 to 0.72 ± 0.16 at −1, −2, and −3 G x , respectively. At −1 G x , PBF was greatest in the ventral and cranial and lowest in the dorsal and caudal regions of the lung. With increased −G x , this gradient was augmented in both directions. Extrapolation of these values to 0 G predicts a slight dorsal (nondependent) region dominance of PBF and a coefficient of variation of 0.22 in microgravity. Analysis of variance revealed that a fixed component (vascular structure) accounted for 81% and nonstructure components (including gravity) accounted for the remaining 19% of the PBF variance across the entire experiment (all 3 gravitational levels). The results are inconsistent with the predictions of the zone model.


PEDIATRICS ◽  
1950 ◽  
Vol 6 (4) ◽  
pp. 557-572
Author(s):  
DONALD E. CASSELS ◽  
MINERVA MORSE ◽  
W. E. ADAMS

The effect of the patent ductus arteriosus on the circulation and on the arterial blood gases and pHs has been studied. The pulmonary blood flow diminished 19.6 to 61.8% following ligation in 12 cases examined. The blood volume diminished following closure of the ductus in most cases. Likewise, the heart rate lessened and the pulse pressure was lower after surgery. Arterial oxygen saturation was low preoperatively in some cases and in most instances postoperatively, and this low value sometimes persisted. Some aspects of the data presented have been discussed in detail.


1983 ◽  
Vol 55 (5) ◽  
pp. 1574-1581 ◽  
Author(s):  
J. P. Kiley ◽  
M. R. Fedde

To determine the importance of nonhumoral drives to exercise hyperpnea in birds, we exercised adult White Pekin ducks on a treadmill (3 degrees incline) at 1.44 km X h-1 for 15 min during unidirectional artificial ventilation. Intrapulmonary gas concentrations and arterial blood gases could be regulated with this ventilation procedure while allowing ventilatory effort to be measured during both rest and exercise. Ducks were ventilated with gases containing either 4.0 or 5.0% CO2 in 19% O2 (balance N2) at a flow rate of 12 l X min-1. At that flow rate, arterial CO2 partial pressure (PaCO2) could be maintained within +/- 2 Torr of resting values throughout exercise. Arterial O2 partial pressure did not change significantly with exercise. Heart rate, mean arterial blood pressure, and mean right ventricular pressure increased significantly during exercise. On the average, minute ventilation (used as an indicator of the output from the central nervous system) increased approximately 400% over resting levels because of an increase in both tidal volume and respiratory frequency. CO2-sensitivity curves were obtained for each bird during rest. If the CO2 sensitivity remained unchanged during exercise, then the observed 1.5 Torr increase in PaCO2 during exercise would account for only about 6% of the total increase in ventilation over resting levels. During exercise, arterial [H+] increased approximately 4 nmol X l-1; this increase could account for about 18% of the total rise in ventilation. We conclude that only a minor component of the exercise hyperpnea in birds can be accounted for by a humoral mechanism; other factors, possibly from muscle afferents, appear responsible for most of the hyperpnea observed in the running duck.


1983 ◽  
Vol 55 (3) ◽  
pp. 736-741 ◽  
Author(s):  
R. A. Steinbrook ◽  
V. Fencl ◽  
R. A. Gabel ◽  
D. E. Leith ◽  
S. E. Weinberger

Whether CO2 partial pressure (PCO2) in expired gas may exceed that in arterial blood has been controversial. We measured arterial PCO2 (Paco2) and end-tidal PCO2 (PETco2) in four awake goats during air breathing and during hyperoxic CO2 rebreathing in various conditions of acid-base balance. During air breathing, Paco2 was slightly higher than PETco2; i.e., the mean (+/- SE) difference, Paco2 - PETco2, was positive by + 2.36 +/- 0.53 Torr (P less than 0.001). In contrast, during CO2 rebreathing with the same techniques of measurement, this difference was always negative (mean +/- SE = -11.63 +/- 0.22 Torr, P less than 0.001), and it widened as Paco2 increased with rebreathing. Magnitude of the negative difference during rebreathing was too great to be accounted for by incorrect assumptions or measurement error, even if reasonable contributions from all known sources of error were concurrently invoked. We conclude that during hyperoxic CO2 rebreathing in goats, PETco2 exceeds Paco2.


1982 ◽  
Vol 53 (1) ◽  
pp. 110-116 ◽  
Author(s):  
S. Matalon ◽  
M. S. Nesarajah ◽  
L. E. Farhi

We have measured the effects of normobaric hyperoxia on arterial and mixed venous gas tensions, cardiac output, heart rate, right atrial, pulmonary, and aortic pressures in 12 conscious chronically instrumented sheep. Regional blood flow to brain, heart, kidney, intestines, and respiratory muscles was assessed in five sheep by injecting 15-micrometers microspheres labeled with gamma-emitting isotopes. Survival time ranged from 60 to 120 h (mean = 80 h). All variables except arterial O2 partial pressure (PaO2) and mixed venous O2 partial pressure remained at base-line level during the first 40 h of exposure, after which PaO2 decreased gradually but remained above 200 Torr at death. After this there was a progressive uncompensated respiratory acidosis with terminal arterial CO2 partial pressure values exceeding 90 Torr. There was a considerable rise in the brain blood flow, whereas flow to the other organs either remained unchanged or increased in proportion to cardiac output. Our experiments also showed that systemic hyperoxic vasoconstriction did not occur, and any local changes were not of sufficient magnitude to affect perfusion.


1984 ◽  
Vol 56 (1) ◽  
pp. 150-154 ◽  
Author(s):  
P. J. Feustel ◽  
M. J. Stafford ◽  
J. S. Allen ◽  
J. W. Severinghaus

The H2 clearance technique was used to determine the blood flow of the postulated respiratory chemosensitive areas near the ventrolateral surface of the medulla. In 12 pentobarbital sodium-anesthetized cats, flow (mean +/- SD) was measured from 25-micron Teflon-coated platinum wire electrodes implanted to a depth of 0.3–0.7 mm. Flow (in ml X min-1 X 100 g-1, n = 35) was 52.8 +/- 28.5 in hypocapnia [arterial CO2 partial pressure (PaCO2) = 21.8 +/- 1.6 Torr], 57.8 +/- 27.5 in normocapnia (PaCO2 = 31.9 +/- 2.2 Torr), and 75.0 +/- 31.7 in hypercapnia (PaCO2 = 44.5 +/- 3.0 Torr). Flow determined from 15 electrodes in adjacent pyramidal tracts (white matter) was less at all levels of CO2; 22.9 +/- 12.3 in hypocapnia, 29.1 +/- 15.9 in normocapnia, and 33.9 +/- 13.9 in hypercapnia. In hypoxia [arterial O2 partial pressure (PaO2) = 39.9 +/- 6.3 Torr] ventrolateral surface flow rose to 87.9 +/- 47.6, and adjacent white matter flow was 35.8 +/- 15.6. These results indicate that flow in the postulated central chemoreceptor areas exceeds that of white matter and is sensitive to variations in PaCO2 and PaO2.


1992 ◽  
Vol 73 (5) ◽  
pp. 1756-1761 ◽  
Author(s):  
H. M. Frankel ◽  
E. Garcia ◽  
F. Malik ◽  
J. K. Weiss ◽  
H. R. Weiss

This study investigated the effects 2 h after administration of acetazolamide on cerebral blood flow and the pattern of cerebral capillary perfusion. Arterial blood pressure, heart rate, arterial blood gases, and pH were recorded in two groups of rats along with either regional cerebral blood flow or the percentage of capillary volume per cubic millimeter and number per square millimeter perfused as determined in cortical, thalamic, pontine, and medullary regions of the brain. Blood pressure, heart rate, and arterial PCO2 were not significantly different between the rats receiving acetazolamide (100 mg/kg) and the controls. Arterial blood pH was significantly lower in the acetazolamide rats. Blood flow increased significantly in the cortical (+ 102%), thalamic (+ 89%), and pontine (+ 88%) regions receiving acetazolamide. In control rats, approximately 60% of the capillaries were perfused in all of the examined regions. The percentage of capillaries per square millimeter perfused was significantly greater in the cortical (+ 52%), thalamic (+ 49%), and pontine (+ 47%) regions of acetazolamide rats compared with controls. In the medulla the increases in blood flow and percentage of capillaries perfused were not significant. Thus in the regions that acetazolamide increased cerebral blood flow, it also increased the percentage of capillaries perfused.


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