Biomedical subjects

Raul C Ordorica

Publications and source records attributed to Raul C Ordorica.

4 recordsLinked to original sources

PubMed2006

Sexual function after surgery for prostate or bladder cancer.

BACKGROUND: Compromised sexual function is often a side effect for patients following radical surgical procedures for bladder or prostate cancer. METHODS: The authors review the classification and physiology of sexual function and dysfunction. Moreover, they explain the possible pathophysiology directly resulting from surgery, and they discuss several approaches available to address these problems. RESULTS: Options for male sexual dysfunction, primarily erectile dysfunction resulting from radical prostatectomy or surgery for bladder cancer, range from patient education to penile prosthesis implantation. Female sexual dysfunction caused by surgical intervention for bladder cancer includes problems with libido, arousal, orgasm, and dyspareunia. Treatment options for women can include sex therapy, hormonal therapy, and preventive strategies. However, no consensus has been established on the most effective agents and time points to treat male or female sexual dysfunction following radical cystectomies or prostatectomies. The chronic intermittent treatment of erectile dysfunction following radical prostatectomy has been commonly referred to as penile rehabilitation. CONCLUSIONS: Additional research is needed to obtain further data concerning sexual dysfunction in both men and women following radical pelvic surgeries. Modification of surgical techniques, the use of various treatment modalities for sexual dysfunction, and the development of new agents will help to successfully minimize or prevent damage and restore normal sexual function after local surgical therapy for prostate or bladder cancer in the future.

Erectile Dysfunction↗

PubMed2004

Macrophage migration inhibitory factor is upregulated in an endotoxin-induced model of bladder inflammation in rats.

Macrophage migration inhibitory factor (MIF) is a proinflammatory cytokine found in epithelial cells as preformed stores, such that MIF release can activate innate immune responses. Our identification of MIF stores in the urothelium suggests that MIF may function in the bladder's initial response to infectious stimuli, such as lipopolysaccharide (LPS). To test this hypothesis, we observed changes in MIF, cyclooxygenase-2 (COX-2) and c-fos in the bladder, L6-S1 spinal cord, dorsal root ganglion (DRG), and major pelvic ganglion (MPG) and MIF changes in the prostate following intravesical LPS. Intravesical LPS induced bladder edema and leukocyte infiltration, as well as increased MIF protein and mRNA in the bladder and lumbosacral spinal cord. Expression of immediate-early gene c-fos, a transcription factor used as a marker of neuronal activation, increased in the L6-S1 spinal cord and L6-S1 DRG of rats that received LPS. We conclude that significant increases in bladder MIF expression and protein in response to intravesical LPS may represent part of this organ's initial innate immune response. In addition, MIF upregulation may represent a neural response to visceral inflammation. Finally, changes in prostate MIF content after intravesical LPS suggest that MIF may be involved in viscerovisceral interactions associated with chronic pelvic pain syndromes.

Animals↗

PubMed2003

Hydrochloric acid induced changes in macrophage migration inhibitory factor in the bladder, peripheral and central nervous system of the rat.

PURPOSE: We established the presence of the proinflammatory cytokine macrophage migration inhibitory factor (MIF) in the bladder and in nervous system structures innervating the bladder, and evaluated changes in MIF and cyclooxygenase-2 (COX-2) protein levels and expression following chemical cystitis. MATERIALS AND METHODS: Male Sprague-Dawley rats were anesthetized and a catheter was introduced into the bladder dome. Cystitis was induced by infusing 0.4 N HCl into the bladder. Control rats received a similar volume of saline. Two hours later the bladder, major pelvic ganglia (MPG), L6/S1 dorsal root ganglia (DRG) and L6/S1 spinal cord were removed and assayed for MIF and COX-2 protein, and mRNA using Western blot and quantitative reverse transcriptase-polymerase chain reaction techniques. RESULTS: Immunohistochemistry showed MIF located mainly in the urothelium of saline treated rats. Instillation of HCl into the bladder resulted in marked epithelial denudation, moderate edema and vasodilatation in the submucosa. MIF protein levels decreased but MIF mRNA expression remained unchanged in bladders treated with HCl compared with controls. However, MIF protein and mRNA levels increased in the MPG, L6/S1 DRG and L6/S1 spinal cord of HCl treated animals. COX-2 protein was not detected in the bladder, DRG or MPG of saline-treated rats. However, a small amount was present in the L6/S1 cord. On the other hand, HCl treated rats showed marked increases in COX-2 protein levels in all tissues examined. Similarly although cox-2 mRNA was constitutively expressed in all tissues examined, expression increased following HCl treatment. CONCLUSIONS: Chemical cystitis induced by intravesical HCl in rats increases the protein levels and mRNA expression of MIF and COX-2 in central and peripheral nervous system tissues that are involved in innervating the bladder. This finding suggests that MIF may be involved in bladder inflammation and may have a role in the peripheral and central nervous system pathways that regulate bladder reflexes in response to bladder inflammation.

Animals↗

PubMed2002

Central effects of clozapine in regulating micturition in anesthetized rats.

BACKGROUND: We previously showed that systemic administration of the atypical neuroleptic clozapine in the rat altered a number of urodynamic variables and inhibited the external urethral sphincter. Since clozapine acts at several receptor types both at the periphery and the central nervous system, the site of action remained uncertain. Therefore, the purpose of this study was to determine the effects of central administration of clozapine on the bladder and the external urethral sphincter during cystometry and to examine differences in spinal versus supraspinal administration. We extended our observations by delivering clozapine centrally in anesthetized rats instrumented with either an intrathecal (L6-S1 spinal segment) or an intracerebroventricular (lateral ventricle) catheter. RESULTS: Clozapine decreased micturition volume and increased residual volume possibly by acting at a supraspinal site. Expulsion time and amplitude of the high frequency oscillations were reduced by clozapine possibly by acting at a spinal site. Bladder capacity was increased after central clozapine but probably due to a peripheral effect. Clozapine acting at spinal and supraspinal sites increased pressure threshold. Contraction time and peak pressure were not affected by clozapine. The EMG from the external urethral sphincter was also reduced following clozapine centrally and suggests a spinal and a supraspinal site of action. CONCLUSIONS: The results from the present study suggest that spinal and supraspinal central sites mediate clozapine's action in inhibiting expulsion parameters and the external urethral sphincter of the rat. Therefore, the reduction in the voiding efficiency observed after clozapine appears to be mediated by spinal and supraspinal sites.

Animals↗