Effect of furosemide on pulmonary blood flow distribution in resting and exercising horses

1999 ◽  
Vol 86 (6) ◽  
pp. 2034-2043 ◽  
Author(s):  
Howard H. Erickson ◽  
Susan L. Bernard ◽  
Robb W. Glenny ◽  
M. Roger Fedde ◽  
Nayak L. Polissar ◽  
...  

We determined the spatial distribution of pulmonary blood flow (PBF) with 15-μm fluorescent-labeled microspheres during rest and exercise in five Thoroughbred horses before and 4 h after furosemide administration (0.5 mg/kg iv). The primary finding of this study was that PBF redistribution occurred from rest to exercise, both with and without furosemide. However, there was less blood flow to the dorsal portion of the lung during exercise postfurosemide compared with prefurosemide. Furosemide did alter the resting perfusion distribution by increasing the flow to the ventral regions of the lung; however, that increase in flow was abated with exercise. Other findings included 1) unchanged gas exchange and cardiac output during rest and exercise after vs. before furosemide, 2) a decrease in pulmonary arterial pressure after furosemide, 3) an increase in the slope of the relationship of PBF vs. vertical height up the lung during exercise, both with and without furosemide, and 4) a decrease in blood flow to the dorsal region of the lung at rest after furosemide. Pulmonary perfusion variability within the lung may be a function of the anatomy of the pulmonary vessels that results in a predominantly fixed spatial pattern of flow distribution.

1991 ◽  
Vol 71 (6) ◽  
pp. 2244-2254 ◽  
Author(s):  
H. J. Toivonen ◽  
J. D. Catravas

The parameter Amax/Km (product of reactant enzyme mass in perfused microvessels and the constant kcat/Km), calculated from in vivo assays of pulmonary endothelial ectoenzymes (e.g., angiotensin-converting enzyme, ACE), can provide estimates of the perfused pulmonary microvascular surface area (PMSA) in the absence of enzyme dysfunction. We examined the relationship between PMSA and pulmonary blood flow (Qb) in anesthetized rabbits placed on total heart bypass, using [3H]benzoyl-Phe-Ala-Pro (BPAP) as the ACE substrate. When Qb was increased from 250 to 1,100 ml/min, at zone 3 conditions, pulmonary arterial pressure increased, pulmonary vascular resistance (PVR) decreased, and Amax/Km increased linearly, reflecting increasing PMSA. When only the left lung was perfused, increasing Qb from 250 to 636 +/- 17 ml/min (the last value representing fully recruited and/or distended vascular bed), PVR decreased, while Amax/Km increased. When Qb was further increased to 791 +/- 44 ml/min, both PVR and Amax/Km remained unchanged, confirming the lack of additional changes in PMSA. We conclude that Amax/Km provides a sensitive indication of PMSA, because it 1) increases with increasing Qb and decreasing PVR, 2) reaches a maximum at Qb values that correspond to the minimal values in PVR, and 3) like PVR, did not change with further increases in Qb. Compared with predicted changes in PMSA produced by either microvascular recruitment alone or distension alone, our data indicate that recruitment is a larger contributor to the observed increase in PMSA.


1983 ◽  
Vol 54 (1) ◽  
pp. 225-233 ◽  
Author(s):  
H. Maeda ◽  
H. Itoh ◽  
Y. Ishii ◽  
G. Todo ◽  
T. Mukai ◽  
...  

Distributions of pulmonary blood flow per unit lung volume were measured with subjects in the prone, supine, and sitting positions by means of radionuclide-computed tomography of intravenously administered 99mTc-labeled macroaggregates of human serum albumin. The blood flow was greater in the direction of gravity in all 31 subjects except one with severe mitral valve stenosis. With the subject in a sitting position, four different types of distribution were distinguished. One type had a three-zonal blood flow distribution as previously reported by West and co-workers (J. Appl. Physiol. 19: 713–724, 1964). Pulmonary arterial pressure and venous pressure estimated from this model showed reasonable agreement with pulmonary arterial pressure and capillary wedge pressure measured by Swan-Ganz catheter in 17 supine patients and in 2 sitting patients. The method makes possible noninvasive assessment of pulmonary vascular pressures.


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.


1999 ◽  
Vol 14 (3) ◽  
pp. 154-160 ◽  
Author(s):  
Masao Tayama ◽  
Nobuaki Hirata ◽  
Tohru Matsushita ◽  
Tetsuya Sano ◽  
Norihide Fukushima ◽  
...  

1986 ◽  
Vol 61 (6) ◽  
pp. 2136-2143 ◽  
Author(s):  
D. C. Curran-Everett ◽  
K. McAndrews ◽  
J. A. Krasney

The effects of acute hypoxia on regional pulmonary perfusion have been studied previously in anesthetized, artificially ventilated sheep (J. Appl. Physiol. 56: 338–342, 1984). That study indicated that a rise in pulmonary arterial pressure was associated with a shift of pulmonary blood flow toward dorsal (nondependent) areas of the lung. This study examined the relationship between the pulmonary arterial pressor response and regional pulmonary blood flow in five conscious, standing ewes during 96 h of normobaric hypoxia. The sheep were made hypoxic by N2 dilution in an environmental chamber [arterial O2 tension (PaO2) = 37–42 Torr, arterial CO2 tension (PaCO2) = 25–30 Torr]. Regional pulmonary blood flow was calculated by injecting 15-micron radiolabeled microspheres into the superior vena cava during normoxia and at 24-h intervals of hypoxia. Pulmonary arterial pressure increased from 12 Torr during normoxia to 19–22 Torr throughout hypoxia (alpha less than 0.049). Pulmonary blood flow, expressed as %QCO or ml X min-1 X g-1, did not shift among dorsal and ventral regions during hypoxia (alpha greater than 0.25); nor were there interlobar shifts of blood flow (alpha greater than 0.10). These data suggest that conscious, standing sheep do not demonstrate a shift in pulmonary blood flow during 96 h of normobaric hypoxia even though pulmonary arterial pressure rises 7–10 Torr. We question whether global hypoxic pulmonary vasoconstriction is, by itself, beneficial to the sheep.


2001 ◽  
Vol 11 (4) ◽  
pp. 420-430 ◽  
Author(s):  
Elisabeth V. Stenbøg ◽  
Daniel A. Steinbrüchel ◽  
Anne Bloch Thomsen ◽  
Ulrik Baandrup ◽  
Lene Heickendorff ◽  
...  

Introduction: Hypertension and hyperperfusion of the pulmonary vascular bed in the setting of congenital cardiac malformations may lead to progressive pulmonary vascular disease. To improve the understanding of the basic mechanisms of this disease, there is a need for clinically relevant animal models which reflect the disease process. Material and Results: We randomly allocated 45 newborn pigs, at the age of 48 hrs, to groups in which there was either construction of a 3 mm central aorto-pulmonary shunt, undertaken in 9, or ligation of the left pulmonary artery, achieved in 13. Controls included sham operations in 13, or no operations in 10 pigs. Follow-up was continued for three months. The interventions were compatible with survival in most pigs. The shunts resulted in an acute 85% increase in systolic pulmonary arterial pressure, and a more than twofold increase in pulmonary blood flow. By three months of age, nearly all shunts had closed spontaneously, and haemodynamics were normal. Ligation of the left pulmonary artery resulted in a normal total pulmonary blood flow, despite only the right lung being perfused, and a 33% increase in systolic pulmonary arterial pressure. These haemodynamic changes were maintained throughout the period of study. In both groups, histomorphometry revealed markedly increased muscularity of the intra-acinar pulmonary arteries. Circulating levels of endothelin were normal in the shunted animals, and elevated in those with ligation of the left pulmonary artery. Conclusion: In neonatal porcine models of pulmonary vascular disease, created by construction of 3 mm central aorto-pulmonary shunts and ligation of one pulmonary artery, we observed histopathological changes of the pulmonary vasculature similar to early hypertensive pulmonary vascular disease in humans. Elevated circulating levels of endothelin were associated with abnormal haemodynamics rather than abnormal pathology. These findings could be valuable for future studies on the pathogenesis of hypertensive pulmonary vascular disease associated with congenital cardiac malformations.


1988 ◽  
Vol 255 (5) ◽  
pp. H1004-H1010 ◽  
Author(s):  
D. E. Mohrman ◽  
R. R. Regal

We pump-perfused gastrocnemius-plantaris muscle preparations at constant pressure to study the relationship of muscle blood flow (Q) to muscle oxygen consumption (VO2), venous oxygen tension (PVO2), and venous carbon dioxide tension (PVCO2) during steady-state exercise at different rates. Tests were performed under four experimental conditions produced by altering the perfusate blood-gas status with a membrane lung. The consistency of the relationship of Q to other variables was evaluated by statistical analysis of fitted curves. Not one of the above listed variables had the same relationship with Q in all four of the experimental conditions we tested. However, we did find that a consistent relationship existed among Q, PVO2, and PVCO2 in our data. That relationship is well described by the equation (Q-23).[PVO2 - (0.5.PVCO2) - 3] = 105 (when Q is expressed in ml.100 g-1.min-1 and PVO2 and PVCO2 in mmHg). One interpretation of this result is that both PO2 and PCO2 are important variables in the control of blood flow in skeletal muscle the combined influence of which could account for nearly all of the hyperemia response to steady-state muscle exercise.


1961 ◽  
Vol 200 (6) ◽  
pp. 1169-1176 ◽  
Author(s):  
William E. Huckabee

Veno-arterial differences of pyruvate and lactate across the myocardium in chloralose-anesthetized dogs were very variable; in any one animal they changed continually with time despite constant blood flow and arterial blood concentrations. There was a systematic tendency of v-a lactate to vary with v-a pyruvate, as expressed in the calculated "Δ excess lactate," which remained nearly constant (or, if blood flow changed, bore a constant ratio to (a-v)O2). No change in Δ excess lactate from control values occurred in nonhypoxic experiments despite marked changes in v-a differences, arterial blood composition, and coronary flow. Cardiac Δ excess lactate became positive in most animals breathing 10% O2 in N2; output of excess lactate was also observed in all those in which moderate muscular exercise was induced. This anaerobic metabolism, or change in the relationship between pyruvate and lactate exchanges, was interpreted as an indication that O2 delivery response was not adequate to meet cardiac tissue requirements during such mild stresses when judged by the standards of adequacy of the basal state.


1963 ◽  
Vol 18 (4) ◽  
pp. 781-785 ◽  
Author(s):  
Leo C. Senay ◽  
Leon D. Prokop ◽  
Leslie Cronau ◽  
Alrick B. Hertzman

The relationship of local skin temperature and the onset of sweating to the local cutaneous blood flow was studied in the forearm and calf. The purpose of the investigation was to appraise the possible relation of sweat gland activity to the cutaneous vasodilatation which has been attributed to bradykinin or to intracranial temperatures. The onset of sweating was not marked by any apparently related increases in the rate of cutaneous blood flow. On the contrary, the onset of sweating was followed often by a stabilization or even a decrease in the level of cutaneous blood flow. The relations of the latter to the local skin temperature were complex, particularly in the forearm. There appeared to be additional unidentified influences, possibly vasomotor, operating on the skin vessels during transitional phases in the relation of skin temperature to blood flow. Submitted on October 15, 1962


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