| Right ventricular performance during increased afterload impaired by hypercapnic acidosis in conscious dogs. | |
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MedLine Citation:
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PMID: 6129076 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Since heart failure may occur in the setting of lung dysfunction and CO2 retention with only modest increases in cardiac work load, we questioned whether myocardial function is impaired by hypercapnic acidosis. To determine the influence of hypercapnic acidosis on right ventricular function, we measured the effects of acute (2 hours) and chronic (2 weeks) hypercapnic acidosis on right ventricular performance during normal and increased right ventricular afterload in five conscious dogs. Systemic hemodynamic and right ventricular functions were unaltered during normal right ventricular afterload by acute hypercapnic acidosis (PaCO2 = 49 +/- 3 mm Hg, pH = 7.27 +/- 0.003). As right ventricular afterload was increased by progressive balloon occlusion of the right ventricular outflow tract during acute hypercapnic acidosis, the rise (slope) in right ventricular end-diastolic pressure was increased 4-fold (P less than 0.01) over that observed in normocapnic control. Maximum isovolumic right ventricular dP/dt rose (P less than 0.05) comparably with increasing right ventricular afterload during normocapnic control and acute hypercapnic acidosis. Chronic hypercapnic acidosis (PaCO2 = 55 +/- 2 mm Hg, pH = 7.28 +/- 0.01) resulted in systemic vasodilation and increased (P less than 0.05) heart rate and cardiac output during normal right ventricular afterload. As right ventricular afterload was increased during chronic hypercapnic acidosis, the rate of rise in right ventricular end-diastolic pressure was 2-fold (P less than 0.01) above normocapnic control but maximum isovolumic right ventricular dP/dt was unchanged in contrast to normocapnic control and acute hypercapnic acidosis. Moreover, cardiac output fell and stroke work was unchanged with increasing afterload during chronic hypercapnic acidosis. beta-Adrenergic blockade resulted in an increased (P less than 0.01) rate of rise in right ventricular end-diastolic pressure with afterload during normocapnic control and chronic hypercapnic acidosis. We conclude that hypercapnic acidosis results in diminished right ventricular performance during increased right ventricular afterload, evidenced by accentuated rise in right ventricular end-diastolic pressure, and may contribute to the congestive heart failure and edema observed in patients with pulmonary hypertension and CO2 retention. |
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Authors:
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C E Rose; K Van Benthuysen; J T Jackson; C E Tucker; D L Kaiser; R F Grover; J V Weil |
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Publication Detail:
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Type: Journal Article; Research Support, U.S. Gov't, P.H.S. |
Journal Detail:
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Title: Circulation research Volume: 52 ISSN: 0009-7330 ISO Abbreviation: Circ. Res. Publication Date: 1983 Jan |
Date Detail:
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Created Date: 1983-02-25 Completed Date: 1983-02-25 Revised Date: 2007-11-15 |
Medline Journal Info:
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Nlm Unique ID: 0047103 Medline TA: Circ Res Country: UNITED STATES |
Other Details:
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Languages: eng Pagination: 76-84 Citation Subset: IM |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Acidosis, Respiratory
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complications,
physiopathology* Acute Disease Adrenergic beta-Agonists / pharmacology Adrenergic beta-Antagonists / pharmacology Animals Chronic Disease Dogs Heart Failure / complications, physiopathology* Hemodynamics / drug effects Lung Diseases, Obstructive / complications, physiopathology* Myocardial Contraction* / drug effects |
| Grant Support | |
ID/Acronym/Agency:
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HL-07171/HL/NHLBI NIH HHS; HL-14985/HL/NHLBI NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Adrenergic beta-Agonists; 0/Adrenergic beta-Antagonists |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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