Effects of oral hydralazine on gas exchange in patients with cor pulmonale

Miller, Michael J.; Chappell, Timothy R.; Cook, William R.; Olazabal, Jose R. De; Rubin, Lewis J.

doi:10.1016/0002-9343(83)90872-0

Cited by 24 publications

(11 citation statements)

References 16 publications

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“…The acute beneficial effect of nifedipine on HPV disappeared 2 months after the start of nife dipine treatment [18]. As a result of the reversal of hy poxic HPV and increased perfusion of hypovcntilated lung regions, nifedipine produced a decrease in P a02, except when subjects exercised in room air [7], On the contrary, some reports have shown that a vasodilata tor can either improve (hydralazine) [19] or cause no change (verapamil) [20] in the gas exchange. The changes in Pa02 observed in COPD patients with vasodilatator administration are difficult to interpret because of the possible multiple sites of action: car diac output, ventilation, ventilation-perfusion rela tionship, oxygen uptake and increased sympathetic nerve traffic due to systemic hypotension.…”

Section: Discussionmentioning

confidence: 99%

Effects of Nifedipine on Diffusing Capacity and Pulmonary Capillary Blood Volume in Chronic Obstructive Pulmonary Disease

Dujić

Tocilj²,

Slavkovic³

1991

Respiration

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The acute dose-dependent effects of nifedipine on the pulmonary diffusing capacity for CO and other lung function indices were investigated in patients with chronic obstructive pulmonary disease (COPD) in a randomized double-blind, cross-over, placebo-controlled trial. Seventeen successive, clinically stable, moderate COPD patients with pulmonary hypertension and 15 control subjects were included in the study. The diffusing capacity of the lungs for carbon monoxide (DLCO) was measured with the single-breath method. Nifedipine (10 and 20 mg) and placebo were administered sublingually at room air. Nifedipine (10 and 20 mg) increased DLCO and DLCO/alveolar volume; however, a larger effect was observed with 10 mg. In addition, nifedipine increased the pulmonary capillary blood volume dose-dependently while arterial oxygenation was improved only with 10 mg nifedipine. Venous shunt was significantly increased with 20 mg nifedipine whereas spirometric parameters were unaffected. The percent DLCO change with 10 or 20 mg nifedipine was inversely correlated with baseline DLCO, but not with the severity of obstruction. Nifedipine did not have any effect in the control group, except for mild hypotension and a reflex increase in the heart rate. It is concluded that 10 mg nifedipine probably has an effect on the pulmonary circulation in moderate COPD patients with pulmonary hypertension

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Section: Discussionmentioning

confidence: 99%

Effects of Nifedipine on Diffusing Capacity and Pulmonary Capillary Blood Volume in Chronic Obstructive Pulmonary Disease

Dujić

Tocilj²,

Slavkovic³

1991

Respiration

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“…The stance against use of vasodilators is based on failure to improve outcome with more traditional agents such as calcium channel blockers and only limited data in support of use of the newer agents. There are a number of older reports of small series of patients treated with systemic vasodilators, usually calcium channel blockers or hydralazine (56)(57)(58)(59)(60)(61).…”

Section: Treatmentmentioning

confidence: 99%

Pulmonary Hypertension in COPD: A Review and Consideration of the Role of Arterial Vasodilators

Burger

2009

COPD: Journal of Chronic Obstructive Pulmonary Disease

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The possibility that pulmonary hypertension (PH) may develop in patients with chronic obstructive pulmonary disease (COPD) is well established, but prevalence data vary. The current World Health Organization clinical classification includes COPD in diagnostic group III: PH associated with disorders of the respiratory system or hypoxemia. The National Institute of Health defines PH as a mean pulmonary artery pressure of greater than 25 mmHg. Approximately 10% of the patients seen over the last decade in the PH Clinic at Mayo Clinic in Jacksonville, Florida, have PH due to COPD. The pathophysiology is likely complex and involves hypoxic pulmonary vasoconstriction. Ultimately, chronic hypoxia results in vascular remodeling with narrowing of the vascular lumen. The right heart is forced to generate increased driving pressures to overcome the increased vascular resistance. As the disease progresses, cor pulmonale may develop. The mortality in this setting is increased with five-year survival of 20% to 36% and seems to correlate with worsening PH and age. Fortunately, the PH in most cases is mild and occurs primarily in those with severe hypoxemia. Only 1% to 4% of patients have PH seemingly out of proportion to the severity of the COPD. This disproportionate subgroup may represent an important phenotype that requires a different therapeutic approach. Although supplemental oxygen remains the primary treatment for all PH in association with chronic hypoxia, pulmonary arterial vasodilators may have a therapeutic role in this subgroup. Vasodilators may worsen gas exchange, however, and to date, have no proven benefit. Rigorous future study will be required to determine whether there is a role for using pulmonary arterial vasodilators in this setting.

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“…It has been demonstrated that hydralazine improves arterial oxygenation when it is used to treat pulmonary hypertension (Rubin et al 1982;Miller et al 1983;Keller et al 1984;Corriveau et al 1987Corriveau et al , 1988. The improvement in arterial oxygenation following hydralazine may have resulted from an increase in minute ventilation in patients with cor pulmonale (Miller et al 1983) and patients with chronic obstructive pulmonary disease (COPD; Corriveau et al 1988).…”

Section: The Effect Of Hydralazine On Ventilationmentioning

confidence: 99%

“…The improvement in arterial oxygenation following hydralazine may have resulted from an increase in minute ventilation in patients with cor pulmonale (Miller et al 1983) and patients with chronic obstructive pulmonary disease (COPD; Corriveau et al 1988). It also may have resulted from…”

Section: The Effect Of Hydralazine On Ventilationmentioning

confidence: 99%

“…One possible explanation for these differences is that they simply relate to heterogeneity within the disease states studied, for example underlying differences in ventilation-perfusion matching. Despite the uncertaintly surrounding the effects of hydralazine on the pulmonary circulation, there is nevertheless agreement that hydralazine improves oxygenation through its effect as a respiratory stimulant (Rubin et al 1982;Miller et al 1983;Keller et al 1984;Corriveau et al 1987;Corriveau et al 1988). However, this effect of hydralazine complicates the interpretation of its effects on the pulmonary circulation still further, because, in those studies where a reduction in pulmonary vascular resistance was detected, it cannot be determined whether it arose from a direct effect of hydralazine on the vasculature or from an indirect effect through the increase in oxygenation.…”

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confidence: 99%

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Effects of hydralazine on the pulmonary vasculature and respiratory control in humans

Liu

Balanos

Fatemian

et al. 2007

Experimental Physiology

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This study sought: (1) to clarify the effects of hydralazine on both the pulmonary vasculature and respiratory control in euoxia and hypoxia in healthy humans; and (2) to determine whether hydralazine alters the expression of genes regulated by hypoxia-inducible factor 1 (HIF-1). Ten volunteers participated in two 2 day protocols. Hydralazine (25 mg) or placebo was administered at 1 pm and 11 pm on the first day, and at 1 pm on the second day. In the mornings and afternoons of both days, we measured plasma vascular endothelial growth factor (VEGF) and erythropoietin (EPO) concentrations (both HIF-1-regulated gene products), systemic arterial blood pressure, and changes in heart rate, cardiac output, maximal systolic pressure difference across the tricuspid valve (ΔP max ) and ventilation in response to 20 min of isocapnic hypoxia. Recent hydralazine: (1) decreased diastolic blood pressure; (2) increased heart rate and cardiac output in euoxia and hypoxia whilst having no effect on ΔP max ; and (3) increased the ventilatory sensitivity to hypoxia. Hydralazine had no effect on plasma EPO or VEGF concentration. We conclude that hydralazine increases the sensitivity of the ventilatory response to hypoxia, but lacks any effect on the pulmonary vasculature at the dose studied. It did not affect the expression of HIF-1-regulated genes. Hydralazine is a vasodilator (Stunkard et al. 1954) whose mode of action remains uncertain. It has been employed in the treatment of pulmonary hypertension, where some authors have found that it reduces pulmonary vascular resistance (Packer et al. 1982;Keller et al. 1984;Groves et al. 1985), but others have found that it has no such effect (Lupi-Herrera et al. 1984). One possible explanation for these differences is that they simply relate to heterogeneity within the disease states studied, for example underlying differences in ventilation-perfusion matching. Despite the uncertaintly surrounding the effects of hydralazine on the pulmonary circulation, there is nevertheless agreement that hydralazine improves oxygenation through its effect as a respiratory stimulant (Rubin et al. 1982;Miller et al. 1983;Keller et al. 1984;Corriveau et al. 1987;Corriveau et al. 1988). However, this effect of hydralazine complicates the interpretation of its effects on the pulmonary circulation still further, because, in those studies where a reduction in pulmonary vascular resistance was detected, it cannot be determined whether it arose from a direct effect of hydralazine on the vasculature or from an indirect effect through the increase in oxygenation.The first purpose of this study was to clarify the effects of hydralazine on both the pulmonary vasculature and respiratory control in humans. The study sought to do this in normal, healthy volunteers so that the complicating effects of heterogeneous disease states would be removed. Furthermore, it sought to do this under tightly regulated conditions for partial pressures of O 2 (P O 2 ) and CO 2 (P CO 2 ) so that any secondary effects of hydralazine on the...

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Effects of oral hydralazine on gas exchange in patients with cor pulmonale

Cited by 24 publications

References 16 publications

Effects of Nifedipine on Diffusing Capacity and Pulmonary Capillary Blood Volume in Chronic Obstructive Pulmonary Disease

Effects of Nifedipine on Diffusing Capacity and Pulmonary Capillary Blood Volume in Chronic Obstructive Pulmonary Disease

Pulmonary Hypertension in COPD: A Review and Consideration of the Role of Arterial Vasodilators

Effects of hydralazine on the pulmonary vasculature and respiratory control in humans

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