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In the Matter of the Compensation of SANDRA D. OBIE, Claimant WCB Case No. 03-06460 ORDER ON REVIEW Daniel Snyder, Claimant Attorneys Reinisch et al, Defense Attorneys Reviewing Panel: Members Biehl, Langer and Bock. Member Langer dissents. The self-insured employer requests review of Administrative Law Judge ALJ ; Somers' order that set aside its denial of claimant's occupational disease claim for a mental disorder. On review, the issue is compensability. We adopt and affirm the ALJ's order with the following changes and supplementation. On page 6, we delete the first two full paragraphs, including footnotes 2 and 3. In the fourth full paragraph on page 6, we delete the first sentence. On page 7, we delete the first full paragraph. On page 9, we change the third full paragraph to read: "Two physicians rendered opinions regarding the cause of claimant's mental disorder: Drs. Turco and Klein." Also on page 9, we delete the last two paragraphs. On page 10, we delete the first two paragraphs and begin with the ALJ's discussion of Dr. Turco's opinion.1 Claimant filed a claim for a mental disorder related to her work activities on July 7, 2003. Claimant, a corrections officer, was sent by her employer to perform a welfare check at the home of another officer who had failed to appear for work. While claimant was at that home, she learned that her coworker had committed suicide. We supplement the ALJ's order to address the employer's argument that the record establishes that claimant's work incident combined with contributory preexisting conditions. The ALJ reasoned that the medical evidence did not establish that claimant had a preexisting condition that "contributes to disability or need for treatment, " pursuant to ORS 656.005 24 ; b ; . For the following reasons, we agree with the ALJ. Dr. Turco, psychiatrist, examined claimant on behalf of the employer and performed psychological tests. He was aware of claimant's previous treatment for. Aging-related CVOD, no functional and histological determinations have been demonstrated concurrently in the same groups of animals. In other models of fibrosis e.g. in the penile tunica albuginea, where the fibrosis is characterized by an increase in collagen over the intracellular compartment, the fibrosis is associated with the production of pro-fibrotic factors such as transforming growth factor beta1 TGFB1 ; , plasminogen activator inhibitor 1, and reactive oxygen species ROS ; during oxidative stress 22-29 ; . This is accompanied by the induction of the inducible nitric oxide synthase NOS2A ; that acts as an endogenous antifibrotic mechanism in response to the pro-fibrotic processes, by producing nitric oxide which quenches ROS in a reaction originating peroxynitrite, and by a direct reduction of collagen synthesis by both nitric oxide and its down-stream product, cGMP 24-27, 29-32 ; . The expression of NOS2A accompanying fibrosis and oxidative stress has also been seen in the above mentioned rat models for aging of the arterial vessels, cavernosal nerve damage, and types 1 and 2 diabetes, as well as in chronic smoking 16, 17, 20, ; . This agrees with studies in the NOS2A knock out mouse where NOS2A depletion intensifies experimental fibrosis of the kidney and liver, suggesting that the antifibrotic role of NOS2A is not restricted to the urogenital and vascular systems 33, 34 ; . Long-term over-expression of NOS2A and nitric oxide production via intratunical Nos2a cDNA gene transfer, or long-term oral administration of the PDE5A inhibitors sildenafil and vardenafil, that elevate cGMP, or long-term treatment with the PDE4A inhibitor pentoxifylline, that increases cAMP, reduces penile fibrosis in either the rat models of Peyronie's disease and or cavernosal nerve damage, and in the latter case, also prevents CVOD 17, 26, 32 ; . In addition, it is conceivable that long-term treatment with PDE5A inhibitors could up-regulate NOS2A expression via cGMP modulation and thus contributes to SMC protection 35-41 ; . Indeed, in the clinical setting there have been occasional reports in men that long-term continuous oral administration of pentoxifylline or sildenafil may ameliorate erectile dysfunction 42-44 ; . More recently, chronic treatment with tadalafil improved endothelial function and.

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