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Excessive Sitting

Sitting could either cause or make the pain worse

"In my opinion, there are definitely jobs which are high-risk for chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS). There have been no reports in the literature but 1/3 of my patients have computer-support or computer-related jobs."
(Comment from a leading prostatitis researcher)

Cycling, prolonged erection and prolonged sitting all involve significant perineal compression forces which starve the urethra, bladder and prostate of blood. Sitting puts pressure on the prostate, and pressure is a mast cell degranulation trigger. Sitting also compresses the pudendal nerve, possibly leading to Pudendal Nerve Entrapment (PNE). We have a page on PNE.

Blood starvation is known as "ischemia". When the blood returns to the area it is known as "reperfusion". As a result of this, one can suffer an "ischemia-reperfusion injury", which has long been known to result in inflammation in the area affected. An IR injury may also lead to inflammation through nerve damage. That's the whole concept in a nutshell. It's a well known and much-studied concept in medicine, where transplanted organs may become inflamed after blood deprivation, for instance. To make matters worse, the prostate is a poorly blood-perfused gland anyway, so the ischemia caused by excessive sitting may make a gland with a marginal blood supply even more susceptible to this kind of injury.

Interestingly, Quercetin reduces ischemia-reperfusion injury and its inflammatory sequelae [Transplantation. 66:147, 1998].

A special cushion is usually recommended for people with sitting jobs.

J Urol 2001;165:2086-2090

Urethra Is More Sensitive To Ischemia Than Bladder: Evidence From An In Vitro Rat Study

Gennady Bratslavsky, Barry Kogan, Robert Levin
Albany College of Medicine, Albany College of Pharmacy and Stratton Veterans Affairs Medical Center, Albany, New York

Purpose: Experimental studies have demonstrated that ischemia may induce significant bladder dysfunction. Because multiple causes leading to bladder ischemia also decrease urethral perfusion, we assessed the effect of in vitro ischemia on the contractile responses of the rat bladder and urethra. We evaluated the hypothesis that neurogenic dysfunction in urethral ischemic injury occurs before myogenic dysfunction is present. We also compared contractile responses of the rat bladder and urethra to in vitro ischemia followed by reoxygenation.

Materials and Methods: Isolated strips of rat bladder detrusor muscle and prostatic urethra were incubated in normal physiological medium and stimulated electrically and chemically. In vitro ischemia was produced by incubating tissue in ischemic medium for 30 or 60 minutes. The maximal tension and maximal rate of tension generated were analyzed digitally before ischemia and after ischemia followed by reoxygenation.

Results: We demonstrated that after 30 minutes of ischemia followed by reperfusion the maximal rate of tension generated decreased significantly only in the urethra and only in response to field stimulation. After 60 minutes of ischemia the decrease in urethral contractile responses was greater than the decrease in bladder contractile responses. Ischemia 60 minutes in duration caused a significant decrease in the maximal rate of tension generated as well as maximal tension in the urethra and bladder but only in response to field stimulation.

Conclusions: This experiment demonstrates that the urethra is more sensitive to ischemic injury than the bladder. Our finding may explain the development and symptoms of urinary incontinence secondary to sphincteric damage before bladder dysfunction is present. We also demonstrated that in the bladder and urethra the response to field (neurogenic) stimulation is the most sensitive form of stimulation to ischemia.

J Urol 2001;165:1019-1026

Chronic Ischemia Alters Prostate Structure And Reactivity In Rabbits

Robert Kozlowski, Richard T Kershen, Mike B Siroky, Robert J Krane, Kazem M Azadzoi

From the Departments of Urology and Pathology, Boston University School of Medicine and Department of Urology, Boston Veterans Affairs Medical Center, Boston, Massachusetts

Purpose: Autopsy studies performed in men older than 80 years old have demonstrated that 90% have histological evidence of benign prostatic hyperplasia. Despite this fact pressure flow studies in men of this age who are referred for the evaluation of lower urinary tract symptoms have shown that only 40% have evidence of bladder outlet obstruction. To our knowledge the specific features of benign prostatic hyperplasia responsible for bladder outlet obstruction are not known. To investigate the possible etiological factors responsible for bladder outlet obstruction we determined whether chronic ischemia alters the structural and functional properties of the prostate.

Materials and Methods: Male New Zealand White rabbits weighing 3.5 to 4 kg. were divided into a chronic prostate ischemia (12), hypercholesterolemia (8) and age matched control (8) group. The chronic prostate ischemia group underwent balloon endothelial injury of the iliac arteries and received a 0.5% cholesterol diet, the hypercholesterolemia group received a 0.5% cholesterol diet only and controls received a regular diet. After 12 weeks using anesthesia iliac artery and prostatic blood flow was measured by an ultrasonic and laser Doppler flowmeter, respectively. The animals were then sacrificed and the prostate was processed for histological evaluation, immunohistochemical staining for vascular endothelial growth factor expression and organ bath studies.

Results: Iliac artery and prostatic blood flow was significantly decreased in the chronic prostate ischemia compared with the hypercholesterolemia and control groups. Histological findings included thickening and fibrosis of the prostatic stroma and cystic atrophy of the epithelium in the chronic prostate ischemia group as well as minor thickening of the stroma in the hypercholesterolemia group. These structural changes correlated with decreased vascular endothelial growth factor expression. Organ bath studies showed that chronic ischemia and to a lesser extent hypercholesterolemia impaired electrical field stimulation induced neurogenic relaxation of the prostatic tissue. Neurogenic relaxation of the prostatic tissue was improved by combined treatment with indomethacin and L-arginine in the hypercholesterolemia but not in the chronic prostate ischemia group. Nitric oxide donor sodium nitroprusside produced comparable relaxation in all 3 groups.

Conclusions: Chronic ischemia causes marked changes in prostatic structure and contractility. Ischemia induced glandular atrophy was consistently associated with decreased vascular endothelial growth factor expression. Decreased relaxation of the ischemic tissue to electrical field stimulation appears to involve the nitric oxide pathway. The nitric oxide precursor L-arginine reversed hypercholesterolemia induced impairment of prostatic tissue relaxation. Our study suggests that chronic ischemia results in thickening and fibrosis of the prostate, changing its mechanical properties. Chronic ischemia also impairs neurogenic relaxation in the prostate. We discuss the possible relationship of these changes to clinical bladder outlet obstruction.

J Urol 1999 Oct;162(4):1490-5 Related Articles, Books, LinkOut

Direct detection of nitric oxide in rat urinary bladder during ischemia-reperfusion.

Saito M, Miyagawa I
Department of Urology, Tottori University Faculty of Medicine, Yonago, Japan.

PURPOSE: We attempted to investigate the role of nitric oxide (NO) in ischemia-reperfusion injury in the rat bladder.

MATERIALS AND METHODS: Rat abdominal aorta were clamped with a small clip to induce ischemia-reperfusion injury in the rat bladder dome. To investigate the role of NO in ischemia-reperfusion injury, N(G)-nitro-L-arginine methylester (L-NAME, 30 mg./kg.) was injected intraperitoneally to measure carbachol-induced contractions of 60 minutes ischemia-30 minutes reperfusion in the rat bladder dome. In vivo real-time blood flow and NO release were measured in the rat bladder with a laser Doppler flowmeter and an NO-selective electrode, respectively. Moreover, participation of NO synthase subtypes was investigated by immunohistochemical staining of bladder sections with anti-endothelial I and anti-inducible NO synthase subtype antibodies.

RESULT: Treatment with L-NAME (30 mg./kg., i.p.) partially prevented the reduction of bladder strips in contraction induced by the ischemia-reperfusion. Clamping of the aorta decreased blood flow to 10% of the basal level measured before the clamping. Administration of L-NAME reduced the blood flow to the bladder by 65% compared to the control level during ischemia-reperfusion. Real-time monitoring of NO in the bladder revealed that ischemia increased NO release, which, in turn, reached a plateau 30-40 minutes after the induction of ischemia. Immediately after the reperfusion, NO release returned to the basal level. In the control rat bladder, the endothelial subtype (eNOS) was observed in the mucosa. After the ischemia-reperfusion, iNOS was detected in the infiltrated neutrophils in the muscular and submucosal regions.

CONCLUSION: Our data indicate that NO from leukocytes may participate in cell/tissue injury during ischemia-reperfusion of the rat bladder and that the damage may be preventable by treatment with L-NAME.

Effect of the bioflavonoids quercetin and curcumin on ischemic renal injury: a new class of renoprotective agents.

Transplantation 1998; 66(2): 147-52.

Shoskes DA.

BACKGROUND: Nonimmune renal injury plays an important role in acute and chronic rejection by triggering an injury response through cytokine and chemokine release. Bioflavonoids are agents with potential immunosuppressive and renoprotective properties. We studied the effects of quercetin and curcumin, two bioflavonoids, on ischemia-reperfusion in the rat.

METHODS: Rats underwent 30 min of left renal pedicle occlusion with simultaneous right nephrectomy and were pretreated with quercetin or curcumin. Serial serum creatinine was measured, and renal expression of the chemokines regulated upon activation, normal T-cell expressed and secreted (RANTES), monocyte chemoattractant protein-1 (MCP-1), and allograft inflammatory factor (AIF) was quantified by polymerase chain reaction.

RESULTS: Pretreatment with quercetin or curcumin resulted in preservation of histological integrity, with a decrease in tubular damage and interstitial inflammation. On day 2 after ischemia-reperfusion, quercetin pretreatment decreased the mean serum creatinine level from 6.5+/-1.4 to 3.3+/-0.5 mg/dl (P=0.06). On day 7, the creatinine level for control animals was 7.5+/-1.5 mg/dl, which was significantly decreased by pretreatment with quercetin, curcumin, or both together (creatinine levels: 1.6+/-1.3, 1.8+/-0.2, and 2.0+/-0.4 mg/dl, respectively; all P<0.05 vs. untreated). By semiquantitative polymerase chain reaction, RANTES, MCP-1, and AIF were detected at high levels in kidneys on day 2 but not in normal kidneys. Pretreatment with quercetin or curcumin strongly attenuated this expression.

CONCLUSION: Quercetin and curcumin reduce ischemia- reperfusion injury and its inflammatory sequelae. The bioflavonoids hold promise as agents that can reduce immune and nonimmune renal injury, the key risk factors in chronic graft los