Capillary recruitment and transit time in the rat lung

1997 ◽  
Vol 83 (2) ◽  
pp. 543-549 ◽  
Author(s):  
Robert G. Presson ◽  
Thomas M. Todoran ◽  
Bracken J. De Witt ◽  
Ivan F. McMurtry ◽  
Wiltz W. Wagner

Presson, Robert G., Jr., Thomas M. Todoran, Bracken J. De Witt, Ivan F. McMurtry, and Wiltz W. Wagner, Jr.Capillary recruitment and transit time in the rat lung. J. Appl. Physiol. 83(2): 543–549, 1997.—Increasing pulmonary blood flow and the associated rise in capillary perfusion pressure cause capillary recruitment. The resulting increase in capillary volume limits the decrease in capillary transit time. We hypothesize that small species with relatively high resting metabolic rates are more likely to utilize a larger fraction of gas-exchange reserve at rest. Without reserve, we anticipate that capillary transit time will decrease rapidly as pulmonary blood flow rises. To test this hypothesis, we measured capillary recruitment and transit time in isolated rat lungs. As flow increased, transit time decreased, and capillaries were recruited. The decrease in transit time was limited by an increase in the homogeneity of the transit time distribution and an increased capillary volume due, in part, to recruitment. The recruitable capillaries, however, were nearly completely perfused at flow rates and pressures that were less than basal for the intact animal. This suggests that a limited reserve of recruitable capillaries in the lungs of species with high resting metabolic rates may contribute to their inability to raise O2 consumption manyfold above basal values.

1994 ◽  
Vol 76 (4) ◽  
pp. 1701-1711 ◽  
Author(s):  
R. G. Presson ◽  
C. C. Hanger ◽  
P. S. Godbey ◽  
J. A. Graham ◽  
T. C. Lloyd ◽  
...  

The complex morphology of the pulmonary capillary network causes capillary transit times to be dispersed about a mean. It is known that flow-induced decreases in mean capillary transit time are partially offset by capillary recruitment and distension, but the effect of these factors on the rest of the distribution of transit times is unknown. We have studied the relationship between blood flow, capillary recruitment, and the distribution of transit times in isolated canine lungs with videomicroscopy. Doubling baseline lobar blood flow recruited capillaries. All transit times in the distribution decreased, as did relative dispersion. Doubling flow again caused a further decrease in transit times, but neither capillary recruitment nor relative dispersion changed significantly. We conclude that capillary transit times become more homogeneous as lobar flow increases from low to intermediate levels. Further increases in flow across a fully recruited network are associated with decreases in transit times but not with more homogeneous capillary perfusion.


1988 ◽  
Vol 255 (5) ◽  
pp. H1114-H1129 ◽  
Author(s):  
M. J. Davis

Regulation of blood flow depends on changes in the sum of arterial (Ra) and venous (Rv) resistances, whereas regulation of capillary pressure (Pc) depends on the ratio of Rv to Ra. If the myogenic response of the arterial system (i.e., delta Ra) is the primary mechanism for controlling pressure and flow when perfusion pressure is lowered, then Pc and total flow should be regulated to the same degree under these conditions. This hypothesis was tested by making direct measurements of Pc and flow in skin and skeletal muscle in the wings of unanesthetized bats. The box method was used to reduce perfusion pressure to the wing. Pressures were measured with a servo-null system; flows were computed from measurements of vascular diameters and red cell velocities using intravital microscopy. All branching orders of arterioles dilated significantly during decreases in box pressure (Pb). For 0 less than Pb less than or equal to -30 mmHg, total flow (1st-order arteriolar flow) remained nearly constant, whereas Pc was "regulated" only approximately 60%. These results cannot be explained by changes in arteriolar resistance alone and suggest that changes in Rv may be important. The possible consequences of flow redistribution, capillary recruitment, and micropressure sampling procedures are discussed in relationship to local regulation of capillary pressure and flow.


1992 ◽  
Vol 262 (6) ◽  
pp. H1908-H1914 ◽  
Author(s):  
M. Ferrari ◽  
D. A. Wilson ◽  
D. F. Hanley ◽  
R. J. Traystman

This study tested the hypothesis that cerebral blood flow (CBF) is maintained by vasodilation, which manifests itself as a progressive increase in mean transit time (MTT) and cerebral blood volume (CBV) when cerebral perfusion pressure is reduced. Cerebral perfusion pressure was decreased in 10 pentobarbital-anesthetized dogs by controlled hemorrhage. Microsphere-determined CBF was autoregulated in all tested cerebral regions over the 40- to 130-mmHg cerebral perfusion pressure range but decreased by 50% at approximately 30 mmHg. MTT and CBV progressively and proportionately increased in the right parietal cerebral cortex over the 40- to 130-mmHg cerebral perfusion pressure range. Total hemoglobin content (Hb1), measured in the same area by an optical method, increased in parallel with the increases in CBV computed as the (CBF.MTT) product. At 30 mmHg cerebral perfusion pressure, CBV and Hb were still increased and MTT was disproportionately lengthened (690% of control). We conclude that within the autoregulatory range, CBF constancy is maintained by both increased CBV and MTT. Outside the autoregulatory range, substantial prolongation of the MTT occurs. When CBV is maximal, further reductions in cerebral perfusion pressure produce disproportionate increases in MTT that signal the loss of cerebral vascular dilatory hemodynamic reserve.


2001 ◽  
Vol 86 (3) ◽  
pp. 391-398 ◽  
Author(s):  
R. W. J. Junor ◽  
A. R. Benjamin ◽  
D. Alexandrou ◽  
D. V. Walters

1960 ◽  
Vol 199 (6) ◽  
pp. 1192-1194 ◽  
Author(s):  
Robert A. Hardin ◽  
Jerry B. Scott ◽  
Francis Haddy

Perfusion of the dog kidney via the aorta with no interruption of renal blood flow or disturbance of the kidney or its immediate physical surroundings revealed perfusion pressure-blood flow relationships similar to those previously reported for semi-isolated and isolated kidneys. This suggests that the kidney in the completely intact animal has a local mechanism for holding its blood flow constant despite changes of arterial pressure over the approximate range 70–200 mm Hg.


2012 ◽  
Vol 113 (2) ◽  
pp. 328-339 ◽  
Author(s):  
Susan R. Hopkins ◽  
Mark O. Wielpütz ◽  
Hans-Ulrich Kauczor

From the first measurements of the distribution of pulmonary blood flow using radioactive tracers by West and colleagues ( J Clin Invest 40: 1–12, 1961) allowing gravitational differences in pulmonary blood flow to be described, the imaging of pulmonary blood flow has made considerable progress. The researcher employing modern imaging techniques now has the choice of several techniques, including magnetic resonance imaging (MRI), computerized tomography (CT), positron emission tomography (PET), and single photon emission computed tomography (SPECT). These techniques differ in several important ways: the resolution of the measurement, the type of contrast or tag used to image flow, and the amount of ionizing radiation associated with each measurement. In addition, the techniques vary in what is actually measured, whether it is capillary perfusion such as with PET and SPECT, or larger vessel information in addition to capillary perfusion such as with MRI and CT. Combined, these issues affect quantification and interpretation of data as well as the type of experiments possible using different techniques. The goal of this review is to give an overview of the techniques most commonly in use for physiological experiments along with the issues unique to each technique.


2020 ◽  
Vol 129 (6) ◽  
pp. 1413-1421
Author(s):  
Leif Østergaard

The transport of oxygen between blood and tissue is limited by blood’s capillary transit time, understood as the time available for diffusion exchange before blood returns to the heart. If all capillaries contribute equally to tissue oxygenation at all times, this physical limitation would render vasodilation and increased blood flow insufficient means to meet increased metabolic demands in the heart, muscle, and other organs. In 1920, Danish physiologist August Krogh was awarded the Nobel Prize in Physiology or Medicine for his mathematical and quantitative, experimental demonstration of a solution to this conceptual problem: capillary recruitment, the active opening of previously closed capillaries to meet metabolic demands. Today, capillary recruitment is still mentioned in textbooks. When we suspect symptoms might represent hypoxia of a vascular origin, however, we search for relevant, flow-limiting conditions in our patients and rarely ascribe hypoxia or hypoxemia to short capillary transit times. This review describes how natural changes in capillary transit-time heterogeneity (CTH) and capillary hematocrit (HCT) across open capillaries during blood flow increases can account for a match of oxygen availability to metabolic demands in normal tissue. CTH and HCT depend on a number of factors: on blood properties, including plasma viscosity, the number, size, and deformability of blood cells, and blood cell interactions with capillary endothelium; on anatomical factors including glycocalyx, endothelial cells, basement membrane, and pericytes that affect the capillary diameter; and on any external compression. The review describes how risk factor- and disease-related changes in CTH and HCT interfere with flow-metabolism coupling and tissue oxygenation and discusses whether such capillary dysfunction contributes to vascular disease pathology.


2021 ◽  
pp. 1-7
Author(s):  
Daniel Stromberg ◽  
Karen Carvalho ◽  
Alison Marsden ◽  
Carlos M. Mery ◽  
Camille Immanuel ◽  
...  

Abstract Introduction: Cardiopulmonary resuscitation (CPR) in the shunted single-ventricle population is associated with poor outcomes. Interposed abdominal compression-cardiopulmonary resuscitation, or IAC-CPR, is an adjunct to standard CPR in which pressure is applied to the abdomen during the recoil phase of chest compressions. Methods: A lumped parameter model that represents heart chambers and blood vessels as resistors and capacitors was used to simulate blood flow in both Blalock-Taussig-Thomas and Sano circulations. For standard CPR, a prescribed external pressure waveform was applied to the heart chambers and great vessels to simulate chest compressions. IAC-CPR was modelled by adding phasic compression pressure to the abdominal aorta. Differential equations for the model were solved by a Runge-Kutta method. Results: In the Blalock-Taussig-Thomas model, mean pulmonary blood flow during IAC-CPR was 30% higher than during standard CPR; cardiac output increased 21%, diastolic blood pressure 16%, systolic blood pressure 8%, coronary perfusion pressure 17%, and coronary blood flow 17%. In the Sano model, pulmonary blood flow during IAC-CPR increased 150%, whereas cardiac output was improved by 13%, diastolic blood pressure 18%, systolic blood pressure 8%, coronary perfusion pressure 15%, and coronary blood flow 14%. Conclusions: In this model, IAC-CPR confers significant advantage over standard CPR with respect to pulmonary blood flow, cardiac output, blood pressure, coronary perfusion pressure, and coronary blood flow. These results support the notion that single-ventricle paediatric patients may benefit from adjunctive resuscitation techniques, and underscores the need for an in-vivo trial of IAC-CPR in children.


1993 ◽  
Vol 74 (6) ◽  
pp. 2940-2948 ◽  
Author(s):  
J. W. Barnard ◽  
P. S. Wilson ◽  
T. M. Moore ◽  
W. J. Thompson ◽  
A. E. Taylor

Pulmonary vascular resistance decreases with increased cardiac output. Because nitric oxide (NO) and prostacyclin are potent vasodilators that are released with increased shear stress, their roles in the control of pulmonary vascular pressure were evaluated using isolated blood-perfused rat and dog lungs. Lungs were perfused with an initial arteriovenous pressure gradient (Ppa-Ppv) of 15 cmH2O; Ppa and Ppv were increased by the same amount, and the flow was measured. In rat lung (n = 6), the NO synthesis inhibitor NG-nitro-L-arginine methyl ester (L-NAME) decreased pulmonary blood flow by approximately 50% at the same pressure (P < 0.05), whereas the cyclooxygenase inhibitor indomethacin (n = 6) had no effect. In dog lungs (n = 6), indomethacin decreased pulmonary blood flow by approximately 50% at the same pressure gradient (P < 0.05), whereas L-NAME (n = 6) had no effect. Furthermore, the flow increase that occurs as venous and arterial pressures are elevated together (so that Ppa-Ppv is constant) was inhibited by L-NAME in rat lungs and by indomethacin in dog lungs (P < 0.05 for each). Plasma guanosine 3′,5′-cyclic monophosphate (cGMP) rose with increased absolute pressure in rat lung [from 71 +/- 17 to 274 +/- 104 pM (P < 0.05)], and this increase was blocked by L-NAME. Plasma cGMP was unchanged in dog lung, but the ratio of prostacyclin to thromboxane tended to be higher.(ABSTRACT TRUNCATED AT 250 WORDS)


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