Cardiovascular responses to hemorrhage during acute and chronic hypoxia

Resta, Thomas C.; Russ, R. D.; Doyle, Michael P.; Martinez, J.; Walker, Benjimen R.

doi:10.1152/ajpregu.1994.267.3.r619

Cited by 7 publications

(5 citation statements)

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“…Consistent with these changes in PCO 2 , arterial pH remained unchanged in E-IH animals during hypoxia, whereas H-IH animals became alkalotic during IH and pH remained elevated compared with E-IH during normoxic re-exposure. Although we did not measure blood gases in 2-wk CH rats, our laboratory has previously shown that 4-wk CH results in a greater PO 2 and reduced pH and PCO 2 under both normoxic and hypoxic conditions com-pared with control animals, reflecting hyperventilation and acid-base adjustments to CH (36). Whether similar acclimation occurs with long-term IH exposure remains to be determined.…”

Section: Discussionmentioning

confidence: 89%

Differential effects of chronic hypoxia and intermittent hypocapnic and eucapnic hypoxia on pulmonary vasoreactivity

Snow

Kitzis²,

Norton³

et al. 2008

Journal of Applied Physiology

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Intermittent hypoxia (IH) resulting from sleep apnea can lead to pulmonary hypertension (PH) and right heart failure, similar to chronic sustained hypoxia (CH). Supplemental CO(2), however, attenuates hypoxic PH. We therefore hypothesized that, similar to CH, IH elicits PH and associated increases in arterial endothelial nitric oxide synthase (eNOS) expression, ionomycin-dependent vasodilation, and receptor-mediated pulmonary vasoconstriction. We further hypothesized that supplemental CO(2) inhibits these responses to IH. To test these hypotheses, we measured eNOS expression by Western blot in intrapulmonary arteries from CH (2 wk, 0.5 atm), hypocapnic IH (H-IH) (3 min cycles of 5% O(2)/air flush, 7 h/day, 2 wk), and eucapnic IH (E-IH) (3 min cycles of 5% O(2), 5% CO(2)/air flush, 7 h/day, 2 wk) rats and their respective controls. Furthermore, vasodilatory responses to the calcium ionophore ionomycin and vasoconstrictor responses to the thromboxane mimetic U-46619 were measured in isolated saline-perfused lungs from each group. Hematocrit, arterial wall thickness, and right ventricle-to-total ventricle weight ratios were additionally assessed as indexes of polycythemia, arterial remodeling, and PH, respectively. Consistent with our hypotheses, E-IH resulted in attenuated polycythemia, arterial remodeling, RV hypertrophy, and eNOS upregulation compared with H-IH. However, in contrast to CH, neither H-IH nor E-IH increased ionomycin-dependent vasodilation. Furthermore, H-IH and E-IH similarly augmented U-46619-induced pulmonary vasoconstriction but to a lesser degree than CH. We conclude that maintenance of eucapnia decreases IH-induced PH and upregulation of arterial eNOS. In contrast, increases in pulmonary vasoconstrictor reactivity following H-IH are unaltered by exposure to supplemental CO(2).

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Section: Discussionmentioning

confidence: 89%

Differential effects of chronic hypoxia and intermittent hypocapnic and eucapnic hypoxia on pulmonary vasoreactivity

Snow

Kitzis²,

Norton³

et al. 2008

Journal of Applied Physiology

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“…Hypobaric and nitrogen dilution hypoxia have been used to generate pulmonary hypertension in rats. A continuous 3-week exposure of rats to a low F102 (10-12%, in nitrogen) with normobaria or to a simulated altitude of 16,000 ft (hypobaric chambers, PBar = -250 mmHg) results in progressive lung vascular muscularization and pulmonary hypertension (36,223,(234)(235)(236)(237)(238). Unlike the monocrotaline model, little if any pulmonary edema and inflammation are present in the established model (36,239,240).…”

Section: Hypoxia-induced Pulmonarymentioning

confidence: 99%

“…Acute hypoxia induces pulmonary hypertension through an increase in pulmonary arteriolar constriction, which causes resistance to blood flow through the lung. Erythropoietinmediated polycythemia follows with an increase of atrial natriuretic peptide (a cardiac hormone) in the blood (236,241). The hypoxia also stimulates production of vascular endothelial growth factor and expression of its receptor (223) as well as expression of fibronectin and laminin (220), interleukin-la (242), nitric oxide synthase (240), interleukin-6 (243), and endothelin (222), all of which are linked to vascular remodeling.…”

Section: Hypoxia-induced Pulmonarymentioning

confidence: 99%

Rodent models of cardiopulmonary disease: their potential applicability in studies of air pollutant susceptibility.

Kodavanti

Costa

Bromberg

1998

Environ Health Perspect

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The mechanisms by which increased mortality and morbidity occur in individuals with preexistent cardiopulmonary disease following acute episodes of air pollution are unknown. Studies involving air pollution effects on animal models of human cardiopulmonary diseases are both infrequent and difficult to interpret. Such models are, however, extensively used in studies of disease pathogenesis. Primarily they comprise those developed by genetic, pharmacologic, or surgical manipulations of the cardiopulmonary system. This review attempts a comprehensive description of rodent cardiopulmonary disease models in the context of their potential application to susceptibility studies of air pollutants regardless of whether the models have been previously used for such studies. The pulmonary disease models include bronchitis, emphysema, asthma/allergy, chronic obstructive pulmonary disease, interstitial fibrosis, and infection. The models of systemic hypertension and congestive heart failure include: those derived by genetics (spontaneously hypertensive, Dahl S. renin transgenic, and other rodent models); congestive heart failure models derived by surgical manipulations; viral myocarditis; and cardiomyopathy induced by adriamycin. The characteristic pathogenic features critical to understanding the susceptibility to inhaled toxicants are described. It is anticipated that this review will provide a ready reference for the selection of appropriate rodent models of cardiopulmonary diseases and identify not only their pathobiologic similarities and/or differences to humans but also their potential usefulness in susceptibility studies.ImagesFigure 2

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“…Acute hypoxia induces pulmonary hypertension through an increase in pulmonary arteriolar constriction, which causes resistance to blood flow through the lung. Erythropoietinmediated polycythemia follows with an increase of atrial natriuretic peptide (a cardiac hormone) in the blood (236,241 Although the pathogenesis of the lesions is significantly different between the monocrotaline and hyopxia models, the lesions in each model result in functional pulmonary hypertension and vascular remodeling reminiscent of the idiopathic human disorder (36,37). Chronic hypoxia typically yields a largely reversible pulmonary hypertensive condition, whereas monocrotaline results in a progressive, irreversible, and frequently fatal disorder.…”

Section: Cardiopulmonary Vascular Diseasesmentioning

confidence: 99%

Rodent Models of Cardiopulmonary Disease: Their Potential Applicability in Studies of Air Pollutant Susceptibility

Kodavanti¹,

Costa²,

Bromberg³

1998

Environmental Health Perspectives

View full text Add to dashboard Cite

The mechanisms by which increased mortality and morbidity occur in individuals with preexistent cardiopulmonary disease following acute episodes of air pollution are unknown. Studies involving air pollution effects on animal models of human cardiopulmonary diseases are both infrequent and difficult to interpret. Such models are, however, extensively used in studies of disease pathogenesis. Primarily they comprise those developed by genetic, pharmacologic, or surgical manipulations of the cardiopulmonary system. This review attempts a comprehensive description of rodent cardiopulmonary disease models in the context of their potential application to susceptibility studies of air pollutants regardless of whether the models have been previously used for such studies. The pulmonary disease models include bronchitis, emphysema, asthma/allergy, chronic obstructive pulmonary disease, interstitial fibrosis, and infection. The models of systemic hypertension and congestive heart failure include: those derived by genetics (spontaneously hypertensive, Dahl S, renin transgenic, and other rodent models); congestive heart failure models derived by surgical manipulations; viral myocarditis; and cardiomyopathy induced by adriamycin. The characteristic pathogenic features critical to understanding the susceptibility to inhaled toxicants are described. It is anticipated that this review will provide a ready reference for the selection of appropriate rodent models of cardiopulmonary diseases and identify not only their pathobiologic similarities and/or differences to humans but also their potential usefulness in susceptibility studies.

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Cardiovascular responses to hemorrhage during acute and chronic hypoxia

Cited by 7 publications

References 0 publications

Differential effects of chronic hypoxia and intermittent hypocapnic and eucapnic hypoxia on pulmonary vasoreactivity

Differential effects of chronic hypoxia and intermittent hypocapnic and eucapnic hypoxia on pulmonary vasoreactivity

Rodent models of cardiopulmonary disease: their potential applicability in studies of air pollutant susceptibility.

Rodent Models of Cardiopulmonary Disease: Their Potential Applicability in Studies of Air Pollutant Susceptibility

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