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Abstract Purpose To evaluate the safety and effectiveness of endovascular treatment for massive haemoptysis caused by pulmonary pseudoaneurysm (PAP). Methods The clinical data, imaging data, and endovascular treatment protocol of 23 patients with massive haemoptysis caused by continuous PAP were retrospectively analysed. The success, complications, postoperative recurrence rate, and influence of the treatment on pulmonary artery pressure were also evaluated. Results Nineteen patients with a bronchial artery-pulmonary artery (BA-PA) and/or nonbronchial systemic artery-pulmonary artery (NBSA-PA) fistula underwent bronchial artery embolization (BAE) and/or nonbronchial systemic artery embolization (NBSAE) + pulmonary artery embolization (PAE). The pulmonary artery (PA) pressures before and after embolization were 52.11 ± 2.12 (35–69 cmH2O) and 33.58 ± 1.63 (22–44 cmH2O), respectively (P = 0.001). Four patients did not have a BA-PA and/or NBSA-PA fistula. Embolization was performed in two patients with a distal PAP of the pulmonalis lobar arteria. Bare stent-assisted microcoils embolization was performed in the other two patients with a PAP of the main pulmonary lobar arteries. The PA pressures of the four patients before and after treatment were 24.50 ± 1.32 (22–28 cmH2O) and 24.75 ± 1.70 (22–29 cmH2O), respectively (P = 0.850). The technique had a 100% success rate with no serious complications and a postoperative recurrence rate of 30%. Conclusion Endovascular treatment is safe and effective for massive haemoptysis caused by PAP. BAE and/or NBSAE can effectively reduce pulmonary hypertension in patients with a BA-PA and/or NBSA-PA fistula.

Regular exercise or physical activity benefits the cardiovascular system, lowers mortality and morbidity, and is a particularly important factor for maintaining the health of blood vessels by improving the function of endothelial cells. Shear stress and increased metabolic rate caused by exercise induce vasodilation by generating endothelium-derived relaxing factors (EDRF) such as nitric oxide. In addition, some studies suggest that vasodilation is also induced by endothelium-derived hyperpolarizing factors (EDHF) and substances such as H2O2. Thus, we undertook this study to show that reactive oxygen species such as H2O2 that have not previously been investigated in the field of exercise science may induce vasodilation and an increase in blood pressure, and to provide information for application in the field of exercise science. In this review, we discuss reports on H2O2 published in the fields of basic science and exercise science while focusing on vasodilation induced by H2O2. H2O2 induces vasodilation by simultaneously increasing endothelial NOS (eNOS) and directly activating the Ca2 - activated K channels of vascular smooth muscle cells. A novel study should be conducted in the field of H2O2 as a factor of vasodilation via increased metabolic rate during exercise.