The Influence of Hydrogen Ion Concentration and Hypoxia on the Pulmonary Circulation*

Enson, Yale; Giuntini, C.; Ml, Lewis; Tq, Morris; Mi, Ferrer; Rm, Harvey

doi:10.1172/jci104999

Cited by 232 publications

(16 citation statements)

References 30 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…* P < 0.05, with reference to control meaPatients with COLD usually develop pulmonary hypertension as a consequence of chronic hypoxic vasoconstriction (29). The degree of pulmonary hypertension thus usually parallels the severity of hypoxemia in this disease (30), as also observed in the present study. To investigate the potential effects of ANF on the human pulmonary circulation, we studied the responses to ANF administration at incremental infusion rates in a subgroup of seven patients with severe COLD and pulmonary hypertension.…”

Section: Discussionsupporting

confidence: 90%

“…The degree of hypercapnic acidosis appeared as another important physiological stimulus for ANF secretion in patients with COLD. Respiratory acidosis may influence ANF secretion through several potential mechanisms: (a) respiratory acidosis has been shown to potentiate the pulmonary pressor response to hypoxia (30), which may account for the positive correlation between Paco2 and pulmonary artery pressure found in our patients and in other studies (30). Respiratory acidosis could thus increase ANF secretion partly by increasing vasoconstriction in the pulmonary circulation; (b) hypercapnia may also negatively influence sodium excretion in patients with COLD, either directly, via a renal tubular effect (48), or indirectly, via a decreased renal blood flow mediated by alpha adrenergic stimuli (43).…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Atrial natriuretic factor in chronic obstructive lung disease with pulmonary hypertension. Physiological correlates and response to peptide infusion.

Adnot

Andrivet²,

Chabrier³

et al. 1989

J. Clin. Invest.

View full text Add to dashboard Cite

To investigate the physiological role of atrial natriuretic factor (ANF) in patients with hypoxic pulmonary hypertension secondary to chronic obstructive lung disease (COLD), we infused synthetic a-human ANF in seven such patients, and investigated the physiological correlates to circulating peptide levels in 24 patients with COLD.ANF infusion, at incremental rates of 0.01, 0.03, and 0.1 Mg/kg . min, increased basal plasma immunoreactive (ir) ANF (136±38 pg/ml) by 3-, 10-, and 26-fold, respectively, and reduced pulmonary artery pressure (from 33±3 to 25±2 mmHg, P < 0.001) and systemic arterial pressure (from 88±4 to 79±4 mmHg, P < 0.001) in a dose-related fashion. Cardiac index increased by 13.5% (P < 0.01) while heart rate was unchanged. Cardiac filling pressures decreased at 0.1 Mg/kg min ANF. Pulmonary and systemic vascular resistance fell by 37% (P < 0.001) and 19% (P < 0.001), respectively. Arterial oxygenation was impaired during ANF infusion, suggesting partial reversal of hypoxic pulmonary vasoconstriction. Plasma renin activity remained unchanged but aldosterone fell by 44% (P < 0.01).The levels of plasma irANF in 24 patients correlated directly with the degree of hemoconcentration (r = 0.67, P < 0.001), respiratory acidosis (r = -0.65, P < 0.001), and pulmonary hypertension (r = 0.52, P < 0.01). The results suggest that ANF may serve as a potent pulmonary vasodilator involved in the circulatory homeostasis of patients with COLD.

show abstract

Section: Discussionsupporting

confidence: 90%

Section: Discussionmentioning

confidence: 99%

Atrial natriuretic factor in chronic obstructive lung disease with pulmonary hypertension. Physiological correlates and response to peptide infusion.

Adnot

Andrivet²,

Chabrier³

et al. 1989

J. Clin. Invest.

View full text Add to dashboard Cite

show abstract

“…The mixed alveolar PO, measured at the end of the breath holding period was low enough to cause vasoconstriction in animals (Hauge & Staub 1969). Hypercapnia will augment the vasoconstrictor response to acute alveolar hypoxia (Enson et al 1964 --…”

Section: Discussionmentioning

confidence: 99%

Cardiovascular responses to face immersion and apnea during steady state muscle exercise: A heart catheterization study on humans

Bjertnæs

Hauge

Kjekshus

et al. 1984

Acta Physiologica Scandinavica

View full text Add to dashboard Cite

The cardiovascular adjustments to face immersion and apnea (FIA) in human beings during steady-state muscle exercise (163 and 98 watt) have been investigated. Using a triple lumen flow directed catheter inserted into the pulmonary artery we were able to measure cardiac output (CO) by thermodilution technique, pulmonary arterial pressure (PPA) right atrial pressure (PRA) and left ventricular filling pressure (PAD). Phasic arterial blood pressure (BP) was measured via a cannula in the radial artery. A 12 lead ECG was recorded continuously. FIA caused an immediate rise in BP (median 61%), the highest level being 25.33 kPa. CO during the last half of FIA was reduced by 49% (range 46-59, n = 7) systemic vascular resistance increased by median 200% (range 111-280). Myocardial oxygen demand determined by the heart rate pressure double product fell from median 33.6 to 16.8 (163 W) and 28.5 to 19.1 (98 W) given as beats/min X kPa X 10(2). Mean reduction was by 42%. PPA and PRA immediately increased and remained constant until a further pronounced increase was seen towards the end of FIA when pulmonary vascular resistance (PVR) went up. PACO2 and PAO2 at the end of 30 sec FIA (163 W) was 10.0 and 5.6 kPa, respectively, values which expectedly would cause pulmonary vasoconstriction. Our findings demonstrate that humans are able to make principally the same cardiovascular adjustments to diving as aquatic mammals, although the response patterns are slower and less efficient.(ABSTRACT TRUNCATED AT 250 WORDS)

show abstract

“…The mechanisms of hypoxic pulmonary vasoconstriction are reviewed elsewhere 31 , and involve alterations in potassium and calcium flux in smooth muscle cells, resulting in contraction and increased vascular tone. Pulmonary vasoconstriction can be further exacerbated by hypercapnia and acidemia in COPD 32 or by increased sympathetic activity in OSA 14 . Supplemental oxygen administration does not fully reverse the increased PA pressure observed in COPD patients 33 , however, and correlations between PA pressure and systemic oxygenation have not been robust 34 .…”

Section: Pathophysiologymentioning

confidence: 99%

Right Ventricular Dysfunction in Chronic Lung Disease

Kolb

Hassoun

2012

Cardiology Clinics

View full text Add to dashboard Cite

Right ventricular dysfunction arises in chronic lung disease when chronic hypoxemia and disruption of pulmonary vascular beds contribute to increase ventricular afterload, and is generally defined by hypertrophy with preserved myocardial contractility and cardiac output. Although the exact prevalence is unknown, right ventricular hypertrophy appears to be a common complication of chronic lung disease, and more frequently complicates advanced lung disease. Right ventricular failure is rare, except during acute exacerbations of chronic lung disease or when multiple co-morbidities are present. Treatment is targeted at correcting hypoxia and improving pulmonary gas exchange and mechanics. There are presently no convincing data to support the use of pulmonary hypertension-specific therapies in patients with right ventricular dysfunction secondary to chronic lung disease.

show abstract

The Influence of Hydrogen Ion Concentration and Hypoxia on the Pulmonary Circulation*

Cited by 232 publications

References 30 publications

Atrial natriuretic factor in chronic obstructive lung disease with pulmonary hypertension. Physiological correlates and response to peptide infusion.

Atrial natriuretic factor in chronic obstructive lung disease with pulmonary hypertension. Physiological correlates and response to peptide infusion.

Cardiovascular responses to face immersion and apnea during steady state muscle exercise: A heart catheterization study on humans

Right Ventricular Dysfunction in Chronic Lung Disease

Contact Info

Product

Resources

About