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J Thorac Cardiovasc Surg 2007;134:267-268
© 2007 The American Association for Thoracic Surgery

Letter to the Editor

Reply to the Editor

Jae Kwang Shim, MD, Yong Seon Choi, MD, Young Lan Kwak, MD

Department of Anesthesiology and Pain Medicine, Anesthesia and Pain Research, Seoul, South Korea

We appreciate the constructive comments by Dr Augoustides regarding our study.1Go He raised the issue of whether hyperoxia, which is a potent pulmonary vasodilator, was adequately controlled between the control and sildenafil groups in our study. The arterial oxygen tension (PaO2) levels were 271 ± 89 mm Hg versus 254 ± 108 mm Hg (P = .602) before the first hemodynamic measurement and 276 ± 48 mm Hg versus 235 ± 55 mm Hg (P = .03) immediately after the last measurement with 60% oxygen in the control and sildenafil groups, respectively. There were no significant changes in the PaO2 values within each group.

Hypoxic pulmonary vasoconstriction has been well studied for decades, with the stimulus identified as both mixed venous and alveolar oxygen tension in small arteries and systemic PaO2 in large pulmonary vessels.2Go However, no comprehensive data exist regarding graded response of the pulmonary vasculature to changes in PaO2 above 120 mm Hg (hyperoxia), especially in patients with long-standing valvular heart disease with concomitant pulmonary hypertension, as in our study. In an animal study, Rudolph and Yuan3Go studied the relationship between PaO2 and pulmonary vascular resistance and demonstrated that there is no further decrease in pulmonary vascular resistance above the PaO2 of 50 to 60 mm Hg. Therefore, although the PaO2 was lower in the sildenafil group after the last measurement, this should not have any further clinically significant effects on the pulmonary vascular resistance.

We agree with Augoustides that proper control of PaO2 between the groups should be mentioned to clarify any confounding factors.

We also agree that further studies with an intravenous form of sildenafil, which is currently not available in our country, should be performed, especially with regard to the period of weaning from cardiopulmonary bypass, and we hope that our study will draw much attention and further clinical research in this area.

References

  1. Shim JK, Choi YS, Oh YJ, Kim DH, Hong YW, Kwak YL. Effect of oral sildenafil citrate on intraoperative hemodynamics in patients with pulmonary hypertension undergoing valvular heart surgery. J Thorac Cardiovasc Surg 2006;132:1420-1425.[Abstract/Free Full Text]
  2. Marshall BE, Marshall C, Frasch F, Hanson CW. Role of hypoxic pulmonary vasoconstriction in pulmonary gas exchange and blood flow distribution. Intensive Care Med 1994;20:291-297.[Medline]
  3. Rudolph AM, Yuan S. Response of the pulmonary vasculature to hypoxia and H+ ion concentration changes. J Clin Invest 1966;45:399-411.[Medline]

Related Article

Intraoperative oral sildenafil for management of pulmonary hypertension: A stepping stone to the future
John G.T. Augoustides
J. Thorac. Cardiovasc. Surg. 2007 134: 267. [Extract] [Full Text] [PDF]




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