Abstract
IntroductionCardiovascular agents are pivotal in the therapy of heart failure. Apart from their action on ventricular contractility and systemic afterload, they affect pulmonary arteries and veins. Although these effects are crucial in heart failure with coexisting pulmonary hypertension or lung oedema, they are poorly defined, especially in pulmonary veins. Therefore, we investigated the pulmonary vascular effects of adrenoceptor agonists, vasopressin and angiotensin II in the model of precision-cut lung slices that allows simultaneous studies of pulmonary arteries and veins.Materials and MethodsPrecision-cut lung slices were prepared from guinea pigs and imaged by videomicroscopy. Concentration-response curves of cardiovascular drugs were analysed in pulmonary arteries and veins.ResultsPulmonary veins responded stronger than arteries to α1-agonists (contraction) and β2-agonists (relaxation). Notably, inhibition of β2-adrenoceptors unmasked the α1-mimetic effect of norepinephrine and epinephrine in pulmonary veins. Vasopressin and angiotensin II contracted pulmonary veins via V1a and AT1 receptors, respectively, without affecting pulmonary arteries.DiscussionVasopressin and (nor)epinephrine in combination with β2-inhibition caused pulmonary venoconstriction. If applicable in humans, these treatments would enhance capillary hydrostatic pressures and lung oedema, suggesting their cautious use in left heart failure. Vice versa, the prevention of pulmonary venoconstriction by AT1 receptor antagonists might contribute to their beneficial effects seen in left heart failure. Further, α1-mimetic agents might exacerbate pulmonary hypertension and right ventricular failure by contracting pulmonary arteries, whereas vasopressin might not.
Highlights
Cardiovascular agents are pivotal in the therapy of heart failure
Inhibition of b2-adrenoceptors unmasked the a1-mimetic effect of norepinephrine and epinephrine in pulmonary veins
The prevention of pulmonary venoconstriction by AT1 receptor antagonists might contribute to their beneficial effects seen in left heart failure
Summary
Cardiovascular agents are pivotal in the therapy of heart failure Apart from their action on ventricular contractility and systemic afterload, they affect pulmonary arteries and veins. These effects are crucial in heart failure with coexisting pulmonary hypertension or lung oedema, they are poorly defined, especially in pulmonary veins. Contraction of pulmonary veins (PVs) increases pulmonary capillary pressure and causes hydrostatic pulmonary oedema and deterioration of gas exchange. It is clinically important how PAs and PVs respond to cardiovascular agents. Pulmonary vessels differ from systemic vessels in their response to hypoxia, hypercapnia and acidosis [8], results from systemic vessels may not be applicable to the low pressure pulmonary vascular bed
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