Hydrogen sulphide vasodilates human pulmonary arteries: a possible role in pulmonary hypertension?

Acute rises in pulmonary artery pressures are associated with a significant mortality and morbidity due to the significant strain on the right ventricle. Although hydrogen sulphide (H2S) has been studied for its potential role in the systemic circulation, little is known of its effects on the pulmonary circulation in humans. We studied the effect of H2S at both the human isolated pulmonary arterial level as well as the human isolated perfused lung level.

Human lobar pulmonary artery rings (n=12) and lobes (n=3) were obtained from resections for patients with bronchial carcinoma. Pre-constricted fresh rings were mounted in organ baths containing normoxic Krebs solution and subsequently exposed to hydrogen sulphide whilst tension was recorded. Isolated perfused human lung models consisted of lobes ventilated via a bronchial cannula and perfused with Krebs via a pulmonary artery cannula; hydrogen sulphide was added to the perfusate and the resulting pulmonary artery and bronchial pressures were recorded.

We found that 500μM H2S caused a mean dilation of 42.3% (±5.4) from the pre-constricted tension (p<0.005) in isolated arterial rings. In addition, 500μM H2S caused a 17.73% (3.52) reduction in pulmonary artery pressures (p<0.05). Furthermore, we found that 500μM H2S caused a 14.9% (6.01) reduction in bronchial airway pressures (p<0.05).

We have shown that H2S is a potent vasodilator of human pulmonary arteries and is a significant anti-hypertensive for pulmonary artery pressures. Our results indicate that this therapeutic potential should be further evaluated in clinical trials.