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  • American Physiological Society  (16)
  • 1
    Online Resource
    Online Resource
    Effects of embolus size on hemodynamics and gas exchange in canine embolic pulmonary hypertension
    American Physiological Society ; 1990
    In:  Journal of Applied Physiology Vol. 69, No. 6 ( 1990-12-01), p. 2254-2261
    Details
    In: Journal of Applied Physiology, American Physiological Society, Vol. 69, No. 6 ( 1990-12-01), p. 2254-2261
    Abstract: We examined the effects of different-sized glass-bead embolization on pulmonary hemodynamics and gas exchange in 12 intact anesthetized dogs. Pulmonary hemodynamics were evaluated by multipoint pulmonary arterial pressure (Ppa)/cardiac output (Q) plots before and 60 min after sufficient amounts of 100-microns (n = 6 dogs) or 1,000-microns (n = 6 dogs) glass beads to triple baseline Ppa were given and again 20 min after 5 mg/kg hydralazine in all the animals. Gas exchange was assessed using the multiple inert gas elimination technique in each of these experimental conditions. Embolization increased both the extrapolated pressure intercepts (by 6 mmHg) and the slopes (by 5 mmHg.l-1.min.m2) of the linear Ppa/Q plots, together with an 80% angiographic pulmonary vascular obstruction. These changes were not significantly different in the two subgroups of dogs. However, arterial PO2 was most decreased after the 100-microns beads, and arterial PCO2 was most increased after the 1,000-microns beads. Both bead sizes deteriorated the distribution of ventilation (VA)/perfusion (Q) ratios, with development of lung units with higher as well as with lower than normal VA/Q. Only 100-microns beads generated a shunt. Only 1,000-microns beads generated a high VA/Q mode and increased inert gas dead space. Hydralazine increased the shunt and decreased the slope of the Ppa/Q plots after 100-microns beads and had no effect after 1,000-microns beads. We conclude that in embolic pulmonary hypertension, Ppa/Q characteristics are unaffected by embolus size up to 1,000 microns.(ABSTRACT TRUNCATED AT 250 WORDS)
    Type of Medium: Online Resource
    ISSN: 8750-7587 , 1522-1601
    URL: Article
    DOI: 10.1152/jappl.1990.69.6.2254
    RVK:
    WA 15000
    RVK:
    XA 52094
    Language: English
    Publisher: American Physiological Society
    Publication Date: 1990
    detail.hit.zdb_id: 219139-8
    detail.hit.zdb_id: 1404365-8
    SSG: 12
    SSG: 31
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  • 2
    Online Resource
    Online Resource
    Inhibition of hypoxic pulmonary vasoconstriction by increased left atrial pressure in dogs
    American Physiological Society ; 1990
    In:  American Journal of Physiology-Heart and Circulatory Physiology Vol. 259, No. 1 ( 1990-07-01), p. H93-H100
    Details
    In: American Journal of Physiology-Heart and Circulatory Physiology, American Physiological Society, Vol. 259, No. 1 ( 1990-07-01), p. H93-H100
    Abstract: To further explore the mechanism of hypoxic pulmonary vasoconstriction, we studied the mean pulmonary arterial pressure (Ppa)/left atrial pressure (Pla) relationship at fixed cardiac index (Q) and the Ppa/Q relationship at several levels of fixed Pla in pentobarbital sodium-anesthetized dogs ventilated alternately in hyperoxia [fraction of inspired O2 (FIO2) 0.4 or 1.0] and in hypoxia (FIO2 0.1). In all experimental conditions, Ppa/Q plots were linear with extrapolated pressure intercepts (Pi) not significantly different from Pla. Hypoxia increased the slope of Ppa/Q plots and did not affect Pi. In hyperoxia, increasing Pla (3 to 26 mmHg) induced approximately equal increases in Ppa at fixed Q and shifted Ppa/Q plots toward higher pressures in a parallel manner. In hypoxia, increasing Pla (4 to 25 mmHg) did not affect Ppa at fixed Q until Pla exceeded 16 mmHg and shifted Ppa/Q plots toward higher pressures with a decrease in slope. Consequently, the hypoxia-induced increases in Ppa at constant Q and constant Pla were attenuated at higher Pla. Thus, in anesthetized dogs, hypoxia increases the slope of Ppa/Q plots without affecting Pi at fixed Pla, and an increase in Pla inhibits hypoxic pulmonary vasoconstriction. These results can be explained without invoking a hypoxia-induced Starling resistor mechanism in the pulmonary circulation.
    Type of Medium: Online Resource
    ISSN: 0363-6135 , 1522-1539
    URL: Article
    DOI: 10.1152/ajpheart.1990.259.1.H93
    RVK:
    WA 15000
    Language: English
    Publisher: American Physiological Society
    Publication Date: 1990
    detail.hit.zdb_id: 603838-4
    detail.hit.zdb_id: 1477308-9
    SSG: 12
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  • 3
    Online Resource
    Online Resource
    Starling resistor vs. distensible vessel models for embolic pulmonary hypertension
    American Physiological Society ; 1995
    In:  American Journal of Physiology-Heart and Circulatory Physiology Vol. 268, No. 2 ( 1995-02-01), p. H817-H827
    Details
    In: American Journal of Physiology-Heart and Circulatory Physiology, American Physiological Society, Vol. 268, No. 2 ( 1995-02-01), p. H817-H827
    Abstract: We investigated whether the Starling resistor model (Mitzner et al. J. Appl. Physiol. 51: 1065–1071, 1981) or a distensible vessel model (Haworth et al. J. Appl. Physiol. 70: 15–26, 1991) best describes pulmonary vascular pressure-flow (Q) relationships in embolic pulmonary hypertension. Mean pulmonary arterial pressure (Ppa)-Q plots at constant left atrial pressure (Pla) and Ppa-Pla plots at constant Q were investigated in seven dogs before and after 500-micron glass bead pulmonary embolism. Embolization to a mean angiographic obstruction of 78% increased the slope and extrapolated pressure intercept (P(i)) of Ppa-Q plots and increased the inflection point of Ppa-Pla plots, above which an increase in Pla is transmitted to Ppa in a ratio of approximately 1:1. The Starling resistor and the distensible vessel model provided a reasonably good fit to the Ppa-Q and Ppa-Pla coordinates before and after embolism. However, contrary to the prediction of the Starling resistor model, no correlation was found between the inflection point of Ppa-Pla plots and P(i). We therefore conclude that an increased closing pressure is unlikely to contribute to embolic pulmonary hypertension.
    Type of Medium: Online Resource
    ISSN: 0363-6135 , 1522-1539
    URL: Article
    DOI: 10.1152/ajpheart.1995.268.2.H817
    RVK:
    WA 15000
    Language: English
    Publisher: American Physiological Society
    Publication Date: 1995
    detail.hit.zdb_id: 603838-4
    detail.hit.zdb_id: 1477308-9
    SSG: 12
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  • 4
    Online Resource
    Online Resource
    Increased left atrial pressure inhibits hypoxic pulmonary vasoconstriction
    American Physiological Society ; 1994
    In:  Journal of Applied Physiology Vol. 76, No. 4 ( 1994-04-01), p. 1502-1506
    Details
    In: Journal of Applied Physiology, American Physiological Society, Vol. 76, No. 4 ( 1994-04-01), p. 1502-1506
    Abstract: An increase in left atrial pressure (Pla) has been reported to either inhibit or not affect hypoxic pulmonary vasoconstriction in intact dogs. We investigated mean pulmonary arterial pressure (Ppa)-flow (Q) relationships at low and high fixed Pla and Ppa-Pla relationships at fixed Q in piglets, which are known to present with a stronger hypoxic pulmonary pressor response than dogs. Seven piglets were anesthetized; equipped with balloon catheters in inferior vena cava and left atrium to control Q and Pla, respectively; and ventilated alternatively in hyperoxia [fractional concn of O2 in inspired air (FIO2) 0.4] and hypoxia (FIO2 0.12). In all experimental conditions, Ppa-Q plots were best described by a linear approximation with extrapolated pressure intercepts (Pi) not different from Pla. Hypoxia increased slope but not Pi of Ppa-Q plots. An increase in Pla from 8 to 17 mmHg induced a parallel shift of Ppa-Q plots to higher Ppa in hyperoxia but did not affect Ppa-Q plots in hypoxia. In hyperoxia, an increase in Pla at constant Q induced an approximately equal increase in Ppa, whereas in hypoxia there was no effect. The hypoxia-induced increase in Ppa was blunted by increased Pla at all levels of Q studied. We conclude that in anesthetized piglets at fixed Pla hypoxia increases the slope of Ppa-Q plots without affecting Pi and an increase in Pla inhibits hypoxic pulmonary vasoconstriction. The results suggest that no closing pressure higher than normal Pla contributes to hyperoxic or hypoxic Ppa in the intact porcine pulmonary circulation.
    Type of Medium: Online Resource
    ISSN: 8750-7587 , 1522-1601
    URL: Article
    DOI: 10.1152/jappl.1994.76.4.1502
    RVK:
    WA 15000
    RVK:
    XA 52094
    Language: English
    Publisher: American Physiological Society
    Publication Date: 1994
    detail.hit.zdb_id: 219139-8
    detail.hit.zdb_id: 1404365-8
    SSG: 12
    SSG: 31
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  • 5
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    Stimulus-response curve of hypoxic pulmonary vasoconstriction in intact dogs: effects of ASA
    American Physiological Society ; 1994
    In:  Journal of Applied Physiology Vol. 77, No. 1 ( 1994-07-01), p. 476-480
    Details
    In: Journal of Applied Physiology, American Physiological Society, Vol. 77, No. 1 ( 1994-07-01), p. 476-480
    Abstract: Hypoxic pulmonary vasoconstriction (HPV) has been reported to decrease during severe hypoxia in isolated lungs, but it remains unknown whether this decrease occurs in the intact animal and how it is affected by cyclooxygenase inhibition. We investigated the HPV stimulus-response relationship in eight pentobarbital sodium-anesthetized intact dogs with a naturally occurring response to hypoxia (“responders”). The pulmonary arterial minus wedge pressure difference (Ppa-Ppw) was measured at 11 inspired O2 fraction (FIO2) values between 0.40 and 0.04 while ventilation, cardiac output, and acid-base status were kept constant. Ppa-Ppw increased by 8 +/- 1 mmHg between FIO2 of 0.40 and 0.10 (alveolar PO2 of approximately 40 Torr) and decreased by 3 +/- 1 mmHg between FIO2 of 0.10 and 0.04. To assess the effects of cyclooxygenase inhibition, similar stimulus-response curves were obtained after administration of 20 mg/kg of acetylsalicylic acid (ASA) in 16 more dogs selected as either nonresponders or responders to hypoxia. ASA restored HPV in nonresponders and enhanced HPV in responders, with the difference between Ppa-Ppw at FIO2 of 0.10 and 0.40 increasing from 1 +/- 1 to 8 +/- 1 mmHg (P 〈 0.001) and from 7 +/- 1 to 10 +/- 1 mmHg (P 〈 0.05), respectively. In both groups, the shape of the stimulus-response curve after ASA was comparable to that of spontaneous HPV, with a maximum at FIO2 of 0.10 and a significant decrease at lower FIO2. We conclude that severe hypoxia attenuates HPV in the intact animal and that ASA restores or enhances HPV by affecting the magnitude of the hypoxic response and not the sensitivity to hypoxia.
    Type of Medium: Online Resource
    ISSN: 8750-7587 , 1522-1601
    URL: Article
    DOI: 10.1152/jappl.1994.77.1.476
    RVK:
    WA 15000
    RVK:
    XA 52094
    Language: English
    Publisher: American Physiological Society
    Publication Date: 1994
    detail.hit.zdb_id: 219139-8
    detail.hit.zdb_id: 1404365-8
    SSG: 12
    SSG: 31
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  • 6
    Online Resource
    Online Resource
    Effects of increased pulmonary vascular tone on gas exchange in canine oleic acid pulmonary edema
    American Physiological Society ; 1988
    In:  Journal of Applied Physiology Vol. 65, No. 2 ( 1988-08-01), p. 662-668
    Details
    In: Journal of Applied Physiology, American Physiological Society, Vol. 65, No. 2 ( 1988-08-01), p. 662-668
    Abstract: Pulmonary gas exchange was investigated before and after an increase in pulmonary vascular tone induced by administration of acetylsalicylic acid (ASA), indomethacin, or almitrine in 32 pentobarbital-anesthetized and ventilated (fraction of inspired O2 0.4) dogs with oleic acid lung injury. Pulmonary vascular tone was evaluated by five-point pulmonary arterial pressure (PAP)/cardiac index (Q) plots and intrapulmonary shunt was measured using a SF6 infusion. PAP/Q plots were rectilinear in all experimental conditions. In control dogs (n = 8), oleic acid (0.09 ml/kg iv) increased PAP over the range of Q studied (1-5 l.min-1.m-2). At the same Q, arterial PO2 fell from 186 +/- 11 to 65 +/- 8 (SE) Torr and intrapulmonary shunt rose from 5 +/- 1 to 50 +/- 6% 90 min after oleic acid injection. These changes remained stable during the generation of two consecutive PAP/Q plots. ASA (1 g iv, n = 8), indomethacin (2 mg/kg iv, n = 8), and almitrine (8 micrograms.kg-1.min-1 iv, n = 8) produced a further increase in PAP at each level of Q. ASA and indomethacin, respectively, increased arterial PO2 from 61 +/- 4 to 70 +/- 3 Torr (P less than 0.05) and from 70 +/- 6 to 86 +/- 6 Torr (P less than 0.05) and decreased intrapulmonary shunt from 61 +/- 5 to 44 +/- 4% (P less than 0.05) and from 44 +/- 5 to 29 +/- 4% (P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
    Type of Medium: Online Resource
    ISSN: 8750-7587 , 1522-1601
    URL: Article
    DOI: 10.1152/jappl.1988.65.2.662
    RVK:
    WA 15000
    RVK:
    XA 52094
    Language: English
    Publisher: American Physiological Society
    Publication Date: 1988
    detail.hit.zdb_id: 219139-8
    detail.hit.zdb_id: 1404365-8
    SSG: 12
    SSG: 31
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  • 7
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    Online Resource
    Acid-base status affects gas exchange in canine oleic acid pulmonary edema
    American Physiological Society ; 1991
    In:  American Journal of Physiology-Heart and Circulatory Physiology Vol. 260, No. 4 ( 1991-04-01), p. H1080-H1086
    Details
    In: American Journal of Physiology-Heart and Circulatory Physiology, American Physiological Society, Vol. 260, No. 4 ( 1991-04-01), p. H1080-H1086
    Abstract: The effects of acidosis and alkalosis on pulmonary gas exchange were studied in 32 pentobarbital sodium-anesthetized intact dogs after induction of oleic acid (0.06 ml/kg) pulmonary edema. Gas exchange was assessed at constant ventilation and constant cardiac output, by venous admixture calculations and by intrapulmonary shunt measurements using the sulfur hexafluoride (SF6) method. Metabolic acidosis (pH 7.20) and alkalosis (pH 7.60) were induced with HCl and Carbicarb (isosmolar Na2CO3 and NaHCO3), respectively. Hypercapnia was induced by adding inspiratory CO2, whereas pH was allowed to change (respiratory acidosis, pH 7.20) or maintained constant (isolated hypercapnia). Mean intrapulmonary shunt and pulmonary arterial minus wedge pressure difference, respectively, changed from 44 to 33% (P less than 0.05) and from 9 to 10 mmHg (P greater than 0.05) in metabolic acidosis, from 44 to 62% (P less than 0.001) and from 12 to 8 mmHg (P less than 0.01) in metabolic alkalosis, from 40 to 42% (P greater than 0.05) and from 13 to 16 mmHg (P less than 0.05) in respiratory acidosis, from 42 to 52% (P less than 0.05) and from 8 to 12 mmHg (P less than 0.01) in isolated hypercapnia. These results indicate that acidosis, alkalosis, and hypercapnia markedly influence pulmonary gas exchange and/or pulmonary hemodynamics in dogs with oleic acid pulmonary edema.
    Type of Medium: Online Resource
    ISSN: 0363-6135 , 1522-1539
    URL: Article
    DOI: 10.1152/ajpheart.1991.260.4.H1080
    RVK:
    WA 15000
    Language: English
    Publisher: American Physiological Society
    Publication Date: 1991
    detail.hit.zdb_id: 603838-4
    detail.hit.zdb_id: 1477308-9
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  • 8
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    Sinoaortic deafferentation reduces intrapulmonary shunt in dogs with oleic acid lung injury
    American Physiological Society ; 1989
    In:  Journal of Applied Physiology Vol. 67, No. 2 ( 1989-08-01), p. 833-838
    Details
    In: Journal of Applied Physiology, American Physiological Society, Vol. 67, No. 2 ( 1989-08-01), p. 833-838
    Abstract: Hypoxic stimulation of the peripheral chemoreceptors has been reported to inhibit hypoxic pulmonary vasoconstriction. To evaluate the pathophysiological importance of this observation, we investigated the effects of surgical peripheral chemoreceptor denervation on pulmonary vascular tone and gas exchange in 17 pentobarbital-anesthetized dogs with oleic acid pulmonary edema. Pulmonary arterial pressure-cardiac index (Ppa/Q) plots, blood gases, and intrapulmonary shunt measured by the SF6 method were obtained at base line, after peripheral chemodenervation (n = 9) or after sham operation (n = 8), and again after 0.09 ml.kg-1 intravenous oleic acid. Over the range of Q studied (2–5 l.min-1.m-2), Ppa/Q plots were best fitted as first-order polynomials in most dogs in all experimental conditions. Chemoreceptor denervation increased Ppa at the lowest Q, while sham operation did not affect the Ppa/Q plots. Oleic acid increased Ppa over the entire range of Q and increased intrapulmonary shunt. This latter was measured at identical Q during the construction of the Ppa/Q plots. Chemoreceptor-denervated dogs, compared with sham-operated dogs, had the same pulmonary hypertension but lower intrapulmonary shunt (36 +/- 4 vs. 48 +/- 5%, means +/- SE, P less than 0.04) and venous admixture (43 +/- 4 vs. 54 +/- 3%, P less than 0.02). We conclude that in intact dogs chemoreceptor denervation attenuates the rise in intrapulmonary shunt after oleic acid lung injury. Whether this improvement in gas exchange is related to an enhanced hypoxic pulmonary vasoconstriction is uncertain.
    Type of Medium: Online Resource
    ISSN: 8750-7587 , 1522-1601
    URL: Article
    DOI: 10.1152/jappl.1989.67.2.833
    RVK:
    WA 15000
    RVK:
    XA 52094
    Language: English
    Publisher: American Physiological Society
    Publication Date: 1989
    detail.hit.zdb_id: 219139-8
    detail.hit.zdb_id: 1404365-8
    SSG: 12
    SSG: 31
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  • 9
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    TNF-α causes reversible in vivo systemic vascular barrier dysfunction via NO-dependent and -independent mechanisms
    American Physiological Society ; 1997
    In:  American Journal of Physiology-Heart and Circulatory Physiology Vol. 273, No. 6 ( 1997-12-01), p. H2565-H2574
    Details
    In: American Journal of Physiology-Heart and Circulatory Physiology, American Physiological Society, Vol. 273, No. 6 ( 1997-12-01), p. H2565-H2574
    Abstract: Tumor necrosis factor (TNF-α) and nitric oxide (NO) are important vasoactive mediators of septic shock. This study used a well-characterized quantitative permeation method to examine the effect of TNF-α and NO on systemic vascular barrier function in vivo, without confounding endotoxemia, hypotension, or organ damage. Our results showed 1) TNF-α reversibly increased albumin permeation in the systemic vasculature (e.g., lung, liver, brain, etc.); 2) TNF-α did not affect hemodynamics or blood flow or cause significant tissue injury; 3) pulmonary vascular barrier dysfunction was associated with increased lung water content and impaired oxygenation; 4) TNF-α caused inducible nitric oxide synthase (iNOS) mRNA expression in the lung and increased in vivo NO production; 5) selective inhibition of iNOS with aminoguanidine prevented TNF-α-induced lung and liver vascular barrier dysfunction; 6) aminoguanidine prevented increased tissue water content in TNF-α-treated lungs and improved oxygenation; and 7) nonselective inhibition of NOS with N G -monomethly-l-arginine increased vascular permeation in control lungs and caused severe lung injury in TNF-α-treated animals. We conclude that 1) TNF-α reversibly impairs vascular barrier integrity through NO-dependent and -independent mechanisms; 2) nonselective NOS inhibition increased vascular barrier dysfunction and caused severe lung injury, whereas selective inhibition of iNOS prevented impaired endothelial barrier integrity and pulmonary dysfunction; and 3) selective inhibition of iNOS may be beneficial in treating increased vascular permeability that complicates endotoxemia and cytokine immunotherapy.
    Type of Medium: Online Resource
    ISSN: 0363-6135 , 1522-1539
    URL: Article
    DOI: 10.1152/ajpheart.1997.273.6.H2565
    RVK:
    WA 15000
    Language: English
    Publisher: American Physiological Society
    Publication Date: 1997
    detail.hit.zdb_id: 603838-4
    detail.hit.zdb_id: 1477308-9
    SSG: 12
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  • 10
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    Pulmonary arterial pressure-flow plots in dogs: effects of isoflurane and nitroprusside
    American Physiological Society ; 1987
    In:  Journal of Applied Physiology Vol. 63, No. 3 ( 1987-09-01), p. 969-977
    Details
    In: Journal of Applied Physiology, American Physiological Society, Vol. 63, No. 3 ( 1987-09-01), p. 969-977
    Abstract: We investigated the effects of nitroprusside and isoflurane on multipoint pulmonary arterial pressure (PAP)/cardiac index (Q) plots in pentobarbital sodium-anesthetized dogs ventilated alternatively in hyperoxia (fraction of inspired O2, FIO2, 0.4) and hypoxia (FIO2 0.1). Over the entire range of Q studied, 2–5 l.min-1.m-2, hypoxia increased PAP in 16 dogs (“responders”) and did not affect PAP in 16 other dogs (“nonresponders”). A hypoxic pulmonary vasoconstriction (HPV) was restored in the nonresponders by intravenous administration of 1 g of acetylsalicylic acid (ASA). Nitroprusside (5 micrograms.kg-1.min-1) inhibited HPV in responders (n = 8) and nonresponders treated with ASA (n = 8). End-tidal 1.41% isoflurane (a minimal alveolar concentration equal to one for dogs) did not affect HPV in responders (n = 8) and nonresponders treated with ASA (n = 8). In the latter group isoflurane increased PAP at the highest Q studied (3–5 l.min-1.m-2) in hyperoxia and hypoxia. In a final group of eight dogs with Q kept constant, PAP remained unchanged during two consecutive sequences of alternated 30-min periods (maximum time to generate a PAP/Q plot) successively at FIO2 0.4 and 0.1, and the hypoxia-induced increase in PAP was reproducible. Thus the present experimental model appeared suitable for the study of the effects of hypoxia and drugs on pulmonary vascular tone of intact dogs. At the given doses HPV was inhibited by nitroprusside and not affected by isoflurane. Products of arachidonic acid metabolism possibly could be implicated in the pulmonary vascular effects of isoflurane.
    Type of Medium: Online Resource
    ISSN: 8750-7587 , 1522-1601
    URL: Article
    DOI: 10.1152/jappl.1987.63.3.969
    RVK:
    WA 15000
    RVK:
    XA 52094
    Language: English
    Publisher: American Physiological Society
    Publication Date: 1987
    detail.hit.zdb_id: 219139-8
    detail.hit.zdb_id: 1404365-8
    SSG: 12
    SSG: 31
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