Effects of prostaglandin F2 alpha and prostacyclin on pulmonary microcirculation in the cat

1987 ◽  
Vol 62 (3) ◽  
pp. 1124-1132 ◽  
Author(s):  
K. Sada ◽  
M. Shirai ◽  
I. Ninomiya
Keyword(s):  
Flow Velocity ◽  
Pulmonary Arteries ◽  
Volume Flow ◽  
Internal Diameter ◽  
Dependent Manner ◽  
Television System ◽  
Small Arteries ◽  
Prostaglandin F2 Alpha ◽  
Transit Times ◽  
Pulmonary Microcirculation

In pulmonary microcirculation, using a new X-ray television system, we measured the effects of prostaglandin F2 alpha (PGF2 alpha) and prostacyclin on the internal diameter (ID), flow velocity, volume flow, and transit times of a contrast medium in small arteries (Ta) and veins (Tv) in anesthetized cats. The ID of the arteries and veins ranged from 100 to 500 micron. PGF2 alpha, 0.3, 1, and 3 micrograms/kg, predominantly decreased ID on the arterial side in a dose-dependent manner but increased flow velocity 27–62%. Consequently, volume flow was kept relatively constant. With PGF2 alpha, Ta and Tv were decreased 18–41% and 4–15%, respectively. Prostacyclin, 2 and 4 micrograms/kg, uniformly dilated the ID of small arteries 9–16% but did not change small veins. With prostacyclin, flow velocity was unchanged or decreased, whereas volume flow was increased significantly, 27–32%. No significant changes of Ta and Tv were observed in response to prostacyclin. When both prostaglandins, PGF2 alpha and prostacyclin, were administered, they canceled each other with respect to the ID of small pulmonary arteries. Prostacyclin also prevented the PGF2 alpha-induced vasoconstriction of the pulmonary venous microcirculation.

Diameter and flow velocity changes in small pulmonary vessels due to microembolization

1988 ◽  
Vol 65 (1) ◽  
pp. 288-296 ◽  
Author(s):  
M. Shirai ◽  
K. Sada ◽  
I. Ninomiya
Keyword(s):  
Flow Velocity ◽  
Pulmonary Arterial Pressure ◽  
Pulmonary Arteries ◽  
Volume Flow ◽  
Internal Diameter ◽  
Vascular Bed ◽  
Small Doses ◽  
Mechanical Factors ◽  
Pulmonary Arterial ◽  
Velocity Changes

The pulmonary vascular bed was embolized with glass beads in small doses that induced no significant changes in pulmonary arterial pressure in anesthetized cats. We analyzed changes in internal diameter (ID), flow velocity, and volume flow of embolized and nonembolized arteries simultaneously with ID changes of small veins. In embolized arteries, with 180-, 300-, and 500-microns beads, ID constricted maximally in just proximal portions of the plug by 22, 23, and 17%, respectively, but with 840-microns beads, no ID constriction occurred. With 50-microns beads, the maximum ID constriction occurred in arteries of 200-300 microns but not in those of 100-200 microns. The constriction decreased in the upstream larger arteries and disappeared in those greater than 800 microns ID. In the nonembolized arteries no ID change occurred. Veins constricted slightly compared with arteries. By heparin pretreatment, ID constriction was slightly attenuated in arteries and was almost abolished in veins, whereas it was not affected with hexamethonium bromide. At a branching site, volume flow to an embolized artery decreased because of a decrease in ID and flow velocity, whereas volume flow to a nonembolized artery increased because of an increase in flow velocity. We concluded that pulmonary microembolization induced a vasoconstriction chiefly in small pulmonary arteries upstream to the plug. After embolization, blood flow was locally redistributed from an embolized to a nonembolized artery at a branching site. Arterial vasoconstriction may be mediated chiefly by local mechanical factors.

X-ray TV system for measuring microcirculation in small pulmonary vessels

1985 ◽  
Vol 59 (3) ◽  
pp. 1013-1018 ◽  
Author(s):  
K. Sada ◽  
M. Shirai ◽  
I. Ninomiya
Keyword(s):  
Flow Velocity ◽  
Volume Flow ◽  
Internal Diameter ◽  
Local Circulation ◽  
Cross Sectional ◽  
Pulmonary Vessels ◽  
X Ray ◽  
Transit Times ◽  
Time Required ◽  
Processing Device

We developed a new system that consists of 1) a specially designed X-ray apparatus, 2) an X-ray-sensitive 1-in. Vidicon camera, and 3) a digital image-processing device. The picture element is approximately 20 micron in size, and the time required for one frame is 1/30 s. Using this system, we measured the internal diameter (ID), the cross-sectional area, flow velocity, volume flow, and transit time of small pulmonary vessels of approximately 100–500 micron at control and with serotonin in anesthetized cats. Flow velocity and volume flow from large [458 +/- 22 (SE) micron] to small (340 +/- 32 micron) arteries were 5.4 +/- 0.4 cm/s and 0.53 +/- 0.06 ml/min, respectively. Transit times of the contrast medium from large to small arteries (Ta) and to large veins (Tv) were 0.68 +/- 0.04 and 3.71 +/- 0.25 s, respectively. Serotonin injection (20–30 micrograms/kg iv) decreased ID, flow velocity, and volume flow of arteries by 8–48, 32, and 76%, respectively, whereas Ta and Tv increased by 91 and 69%, respectively. The system can provide useful information regarding the local circulation in the lung.

Effects of regional alveolar hypoxia and hypercapnia on small pulmonary vessels in cats

1986 ◽  
Vol 61 (2) ◽  
pp. 440-448 ◽  
Author(s):  
M. Shirai ◽  
K. Sada ◽  
I. Ninomiya
Keyword(s):  
Flow Velocity ◽  
Volume Flow ◽  
The Other ◽  
Internal Diameter ◽  
Lung Region ◽  
Pulmonary Vessels ◽  
Small Arteries ◽  
X Ray ◽  
Other Hand ◽  
Alveolar Hypoxia

Using an X-ray TV system, we analyzed responses in the internal diameter (ID), flow velocity, and volume flow in small pulmonary vessels (100–600 microns ID) during unilobar hypoxia and hypercapnia in cats. In the hypoxic and hypercapnic lobes, the ID reduced in proportion to the degree of hypoxia and hypercapnia, respectively. The ID reduction was larger in the arteries than in the veins for a given stimulus. In the arteries, the ID reduced nonuniformly in the series-arranged vessels in response to both stimuli. The percentage ID reduction was maximal in the arteries of 200–300 microns ID, in which it was 21, 26, 28, and 36% with 5% O2, 0% O2, 5% CO2, and 10% CO2 inhalations, respectively. On the other hand, in the veins, uniform ID reduction occurred for a given stimulus. In the contralateral normoxic lobe, the ID did not change significantly. In both hypoxic and hypercapnic lobes, the flow velocity and volume flow of the small arteries decreased, with 5% O2, by 18 and 40%, respectively, and, with 5% CO2, by 23 and 50%, respectively. In contrast, in the normoxic lobe, they increased significantly during 5% O2 and 5% CO2 inhalations. We concluded that regional alveolar hypoxia and hypercapnia induced a local vasoconstriction particularly in the small arteries of 200–300 microns ID and decreased the flow velocity and volume flow in the same lung region.

Nonuniform effects of histamine on small pulmonary vessels in cats

1987 ◽  
Vol 62 (2) ◽  
pp. 451-458 ◽  
Author(s):  
M. Shirai ◽  
K. Sada ◽  
I. Ninomiya
Keyword(s):  
Flow Velocity ◽  
Pulmonary Arteries ◽  
Flow Distribution ◽  
Volume Flow ◽  
Beta Blockade ◽  
Internal Diameter ◽  
Vascular Walls ◽  
Beta Receptors ◽  
Arteries And Veins

In in vivo cat lung, using an X-ray TV system, we analyzed responses in internal diameter (ID), flow velocity, and volume flow of arteries and veins (100–500 microns ID) to histamine (8–15 micrograms/kg iv) under three conditions. With histamine alone, three types of ID response (constriction, dilatation, and no change) occurred in parallel-arranged arteries. Relative frequency and magnitude of constriction were maximum in arteries of 300–400 micron ID, whereas those of dilatation were maximum in arteries of 100–200 micron ID. In veins, relatively uniform constriction occurred. Under H2-blockade, histamine caused greater constriction than that with histamine alone in arteries and veins of 300–500 micron ID. Under beta-blockade, with histamine, ID of all vessels decreased significantly below the ID sizes under the above two conditions, and no dilatation occurred. In two parallel arteries that showed opposite ID changes to histamine, flow velocity increased, but volume flow decreased in a constricted artery while it increased in a dilated one. Those data indicated that, with histamine, qualitatively and quantitatively nonuniform ID response was induced in both parallel- and series-arranged small pulmonary arteries and, in turn, produced heterogeneous flow distribution. Factors to cause the nonuniformity may be partly explained by difference in density of H2- and beta-receptors in vascular walls.

beta-Adrenergic mechanisms attenuated hypoxic pulmonary vasoconstriction during systemic hypoxia in cats

1994 ◽  
Vol 266 (5) ◽  
pp. H1777-H1785 ◽  
Author(s):  
M. Shirai ◽  
T. Shindo ◽  
I. Ninomiya
Keyword(s):  
Nervous System ◽  
Autonomic Nervous System ◽  
Hypoxic Pulmonary Vasoconstriction ◽  
Pulmonary Arteries ◽  
Internal Diameter ◽  
Television System ◽  
Autonomic Nervous ◽  
Pulmonary Vasoconstriction ◽  
Alveolar Hypoxia

In this study, we examined how locally mediated hypoxic pulmonary vasoconstriction is modulated by autonomic nervous system activation during global alveolar hypoxia (GAH) accompanied by systemic hypoxemia. Using an X-ray television system on the in vivo cat lung, we measured changes in the internal diameter (ID) during GAH and regional alveolar hypoxia (RAH) without systemic hypoxemia in identical small pulmonary arteries and veins (100-600 microns ID). We also analyzed the effects of the autonomic nervous system blockade on the hypoxic ID changes. During GAH the ID of the arteries reduced by 5 +/- 1 and 3 +/- 1% with 10 and 5% O2 inhalations, respectively, whereas during RAH the arterial ID reduced by 12 +/- 1 and 18 +/- 1% with 10 and 5% O2 inhalations, respectively. The magnitude of the ID reduction was significantly smaller during GAH than during RAH. After pretreatment with propranolol, however, GAH induced large ID reductions (16 +/- 1 and 23 +/- 1% with 10 and 5% O2 inhalations) with patterns very similar to those seen during RAH. Phentolamine and atropine had no effect on the response during GAH. The ID reductions during RAH, on the other hand, were unaffected by all the blockers. The results indicate that, in the cat, alveolar hypoxia per se acts locally to constrict the small pulmonary vessels and that the hypoxic vasoconstriction is attenuated by a beta-receptor-mediated vasodilator effect during GAH with systemic hypoxemia. In addition, we found that, after adrenalectomy plus ganglion blockade with hexamethonium bromide, the GAH-induced ID reduction with 5% O2 inhalation was enhanced from 3 to 19%.(ABSTRACT TRUNCATED AT 250 WORDS)

Hypoxic vasoconstriction in rat pulmonary and mesenteric arteries

1994 ◽  
Vol 266 (3) ◽  
pp. L223-L231 ◽  
Author(s):  
R. M. Leach ◽  
T. P. Robertson ◽  
C. H. Twort ◽  
J. P. Ward
Keyword(s):  
Phase 1 ◽  
Pulmonary Arteries ◽  
Mesenteric Arteries ◽  
Phase 2 ◽  
Biphasic Response ◽  
Small Arteries ◽  
Prostaglandin F2 Alpha ◽  
Mechanical Disruption ◽  
Hypoxic Vasoconstriction ◽  
Rat Experiments

Hypoxic vasoconstriction was investigated in isolated pulmonary and mesenteric arteries of the rat. Experiments were performed on large (approximately 2 mm pulmonary, approximately 0.8 mm mesenteric) and small (100-350 microns) arteries. Hypoxia [oxygen partial pressure (PO2) approximately 33 mmHg] elicited a biphasic response in arteries precontracted with prostaglandin F2 alpha (10 microM). A transient contraction reaching a peak within 2-3 min was observed in both large and small pulmonary and mesenteric arteries (phase 1). In pulmonary arteries, this was followed by a slowly developing contraction over 45 min (phase 2). In mesenteric arteries, there was no phase 2 but instead a profound relaxation. Mechanical disruption of the endothelium had no significant effect on phase 1 in preconstricted large pulmonary arteries but reduced phase 1 in small arteries by 40%. Phase 2 was abolished in both large and small arteries. Inhibition of endothelium-derived relaxing factor synthesis or cyclooxygenase pathways had no effect on either phase. Verapamil substantially reduced phase 1 but abolished phase 2. In conclusion, we have found a clear biphasic response to hypoxia in pulmonary arteries of the rat, but, in contrast to some previous reports, phase 1 was only partially dependent on the endothelium, whereas phase 2 was entirely dependent on the endothelium. Small and large arteries had qualitatively similar responses. These results are consistent with the involvement of at least two mechanisms for hypoxic vasoconstriction, one of which may involve release of an as yet unidentified endothelium-derived constrictor factor.

Inhaled nitric oxide: diameter response patterns in feline small pulmonary arteries and veins

1996 ◽  
Vol 270 (3) ◽  
pp. H974-H980 ◽  
Author(s):  
M. Shirai ◽  
A. Shimouchi ◽  
A. T. Kawaguchi ◽  
K. Sunagawa ◽  
I. Ninomiya
Keyword(s):  
Nitric Oxide ◽  
Pulmonary Arteries ◽  
Internal Diameter ◽  
Response Patterns ◽  
Television System ◽  
X Ray ◽  
Small Vessels ◽  
Pulmonary Vasoconstriction ◽  
Arteries And Veins

Using an X-ray television system on the in vivo cat lung, we directly measured internal diameter (ID) changes in the small pulmonary arteries and veins (100-1,100 microns ID) in response to 5, 15, and 40 ppm nitric oxide (NO) inhalations. We also measured to what extent 40 ppm NO inhalation can attenuate large ID constrictions at the different serial segments of the small vessels due to unilobar anoxic (0% O2) exposure. Under normoxic conditions, 5-40 ppm NO inhalations significantly increased the ID of both arteries and veins less than approximately 900 microns dose dependently but caused no significant, or only slight, ID increases in the vessels larger than this, if any at all. The ID increase in the serially connected arteries was nonuniform (4-18, 8-28, and 7-35% with 5, 15, and 40 ppm NO inhalations, respectively), whereas that for the veins was relatively uniform (4-9, 6-17, and 7-18% with 5, 15, and 40 ppm NO, respectively). The maximum ID increase occurred in the 200- to 500- and 200- to 700-microns arteries in response to 5-15 and 40 ppm NO, respectively. Unilobar anoxic exposure significantly decreased the ID of the 100- to 700-microns arteries and veins, but not the ID of the other-sized vessels. The ID decrease in the serially connected arteries was nonuniform (13-29%) but relatively uniform in the veins (8-12%). The maximum ID decrease occurred in the 200- to 300-microns arteries. However, adding 40 ppm NO to the lobe completely eradicated the ID decreases at all segments of the arteries and veins and, instead, caused significant ID increase (11-21%) in the arteries and (10-12%) in the veins. The data indicate that, according to dosage, 5-40 ppm NO inhalations cause selective dilation of approximately 100- to 900-microns pulmonary arteries and veins, particularly the 200- to 700-microns arteries. During anoxic exposure, the vasodilator effect of NO is preserved and can completely reverse the marked pulmonary vasoconstriction.

Physiological neutrophil sequestration in the lung: visual evidence for localization in capillaries

1987 ◽  
Vol 62 (3) ◽  
pp. 1236-1243 ◽  
Author(s):  
D. C. Lien ◽  
W. W. Wagner ◽  
R. L. Capen ◽  
C. Haslett ◽  
W. L. Hanson ◽  
...  
Keyword(s):  
Dynamic Equilibrium ◽  
Pulmonary Arteries ◽  
Fluorescein Isothiocyanate ◽  
Wide Distribution ◽  
Neutrophil Sequestration ◽  
Pulmonary Capillaries ◽  
Transit Times ◽  
Wide Range ◽  
Pass Through ◽  
Pulmonary Microcirculation

Although the lung is known to be a major site of neutrophil margination, the anatomic location of these sequestered cells within the lung is controversial. To determine the site of margination and the kinetics of neutrophil transit through the pulmonary microvasculature, we infused fluorescein isothiocyanate-labeled canine neutrophils into the pulmonary arteries of 10 anesthetized normal dogs and made fluorescence videomicroscopic observations of the subpleural pulmonary microcirculation through a window inserted into the chest wall. The site of fluorescent neutrophil sequestration was exclusively in the pulmonary capillaries with a total of 951 labeled cells impeded in the capillary bed for a minimum of 2 s. No cells were delayed in the arterioles or venules. Transit times of individual neutrophils varied over a wide range from less than 2 s to greater than 20 min with an exponential distribution skewed toward rapid transit times. These observations indicate that neutrophil margination occurs in the pulmonary capillaries with neutrophils impeded for variable periods of time on each pass through the lung. The resulting wide distribution of transit times may determine the dynamic equilibrium between circulating and marginated neutrophils.

Thromboxane A2/endoperoxide receptors mediate cholinergic constriction of rabbit lung microvessels

1992 ◽  
Vol 72 (3) ◽  
pp. 1179-1185 ◽  
Author(s):  
M. Shirai ◽  
I. Ninomiya ◽  
K. Sada
Keyword(s):  
Muscarinic Receptors ◽  
Pulmonary Arteries ◽  
Thromboxane A2 ◽  
Cyclooxygenase Inhibitors ◽  
Internal Diameter ◽  
Receptor Antagonists ◽  
Rabbit Lung ◽  
Small Arteries ◽  
Prostaglandin Endoperoxide ◽  
Tp Receptor

Using an X-ray television system, we directly measured the internal diameter (ID; 100–1,000 microns) of small pulmonary arteries and analyzed the effects of cyclooxygenase inhibition and thromboxane A2/prostaglandin endoperoxide (TP) receptor blockade on the ID reductions in response to vagal nerve stimulation (VNS; 16 Hz) and injection of acetylcholine (ACh; 0.3 micrograms) in anesthetized rabbits. The ID reductions of the small arteries in response to VNS and ACh were completely abolished by pretreatment with cyclooxygenase inhibitors indomethacin and meclofenamate. Those reductions were also eliminated by pretreatment with TP receptor antagonists AA-2414 and Ono 3708. Both TP receptor antagonists abolished the ID reduction to thromboxane A2 mimetic U-46619 but did not affect the reduction to norepinephrine. The ID reductions in response to VNS and ACh were eliminated by atropine. The reduction in response to VNS was abolished by hexamethonium bromide, whereas the reduction in response to ACh was not altered by hexamethonium bromide. The results indicate that vasoconstrictions of the rabbit small pulmonary arteries in response to VNS and exogenous ACh are mediated by TP receptors as well as muscarinic receptors. The data suggest that during VNS endogenous ACh acts on muscarinic receptors to constrict the small arteries mainly by generating thromboxane A2 or prostaglandin endoperoxide.

Proproliferative phenotype of pulmonary microvascular endothelial cells

2007 ◽  
Vol 292 (3) ◽  
pp. L671-L677 ◽  
Author(s):  
Victor Solodushko ◽  
Brian Fouty
Keyword(s):  
Endothelial Cells ◽  
Barrier Function ◽  
Pulmonary Arteries ◽  
D1 Protein ◽  
Coagulation Cascade ◽  
Microvascular Endothelial Cells ◽  
Significant Heterogeneity ◽  
Pulmonary Microvascular Endothelial Cells ◽  
Microvascular Endothelial ◽  
Pulmonary Microcirculation

Endothelial cells perform a number of important functions including release of vasodilators, control of the coagulation cascade, and restriction of solutes and fluid from the extravascular space. Regulation of fluid balance is of particular importance in the microcirculation of the lung where the loss of endothelial barrier function can lead to alveolar flooding and life-threatening hypoxemia. Significant heterogeneity exists between endothelial cells lining the microcirculation and cells from larger pulmonary arteries, however, and these differences may be relevant in restoring barrier function following vascular injury. Using well-defined populations of rat endothelial cells harvested from the pulmonary microcirculation [pulmonary microvascular endothelial cells (PMVEC)] and from larger pulmonary arteries [pulmonary artery endothelial cells (PAEC)], we compared their growth characteristics in low serum conditions. Withdrawal of serum inhibited proliferation and induced G0/G1 arrest in PAEC, whereas PMVEC failed to undergo G0/G1 arrest and continued to proliferate. Consistent with this observation, PMVEC had an increased cdk4 and cdk2 kinase activity with hyperphosphorylated (inactive) retinoblastoma (Rb) relative to PAEC as well as a threefold increase in cyclin D1 protein levels; overexpression of the cdk inhibitors p21Cip1/Waf1 and p27Kip1 induced G0/G1 arrest. While serum withdrawal failed to induce G0/G1 arrest in nonconfluent PMVEC, confluence was associated with hypophosphorylated Rb and growth arrest; loss of confluence led to resumption of growth. These data suggest that nonconfluent PMVEC continue to proliferate independently of growth factors. This proliferative characteristic may be important in restoring confluence (and barrier function) in the pulmonary microcirculation following endothelial injury.

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