No abstract available.
Humans ; Male* ; Nervous System*

Although platelet have been implicated in the pathogenesis of the thrombotic disease, the platelet aggregability was not well studied in Korea. Author measured platelet aggregability in 103 clinical cases including 30 healthy volunteers to evaluate the platelet function and the effect of Aspirin and Dipyridamole on aggregability in Korean. 24 patients with cerebral thrombosis, 24 patients with ischemic heart disease and 25 patients with hypercholesterolemia were included for this study. Aggregation tests were performed at three final concentrations of epinephrine(10microM/L) and ADP(4 microM/L, 10 microM/L) with platelet aggregometer which was made by Chrono-Log Corp. in all cases. Platelet aggregations were measured in patients who were treated with Aspirin, Dipyridamole and combined treatment of Aspirin and Dipyridamole respectively. The following results were obtained. 1) The mean maximal platelet aggregability in the normal subjects induced by 10 microM/L epinephrine was 59.3+/-24.26%, 66.6+/-14.00% in Bm and 62.5+/-19.30% in B5 in induction by 4 microM/L ADP, and 77.2+/-8.99% in Bm and 76.6+/-9.83% in B5 in induction by 10microM/L ADP. 2) The mean maximal platelet aggregability in patients with cerebral thrombosis induced by 10 microM/L epinephrine was 89.2+/-7.33%, 78.8+/-9.41% in Bm and 78.5+/-9.93% in B5 in induction by 4 microM/L ADP, and 86.4+/-7.69% in Bm and B5 in induction by 10 microM/L ADP. The results showed significantly elevated platelet aggergability than that of normal subjects(p<0.01). 3) The mean maximal platelet aggregability in patients with ischemic heart disease induced by 10 microM/L epinephrine was 88.1+/-11.99%, 78.2+/-12.50% in Bm and B5 in induction by 10 microM/L ADP. The results showed significantly elevated platelet aggregability than that of normal subjects(P<0.01). 4) The mean maximal platelet aggregability in patients with hypercholesterolemia induced by 10 microM/L epinephrine was 86.8+/-15.99%, 82.7+/-11.19% in Bm and 82.0+/-12.87% in B5 in induction by 4 microM/L ADP, and 88.5+/-11.47% in Bm and B5 in induction by 10 microM/L ADP. The results showed signifcantly elevated platelet aggregability than that of normal subjects(P<0.01). 5) The mean maximal platelet aggregability in patients with thrombotic disease was studied by Dipyridamole administration. The platelet aggregability induced by epinephrine before administration was 90.9+/- 8.52% and after administration it was 78.9+/-15.68%, and the results showed that Dipyidamole lowered aggregability significantly. The platelet aggregability induced by 4 microM/L ADP before administration was 84.0+/-11.90% in Bm and B5 and after administration it was 78.0+/-11.44% in Bm and B5, and the results showed that Dipyridamole lowered aggregability but not significant. The platelet aggregability induced by 10 microM/L ADP before administration was 89.2+/-10.39% in Bm and B5 and after administration it was 80.5+/-8.44% in Bm and B5, and the results showed that Dipyridamole lowered aggregability significantly. 6) The mean maximal platelet aggregability in patients with thrombotic disease was studied by Aspirin administration. The platelet aggregability induced by epinephrine before administration was 91.0+/-4.79% and after administration it was 47.6+/-17.72%. The platelet aggregability induced by 4 microM/L ADP before administration was 84.6+/-10.37% in Bm and B5 and after administration it was 72.6+/-11.85% in Bm and 65.3+/-15.97% in B5. The platelet aggregability induced by 10 microM/L ADP before administration was 84.9+/-6.30% in Bm and B5 and after adminstration it was 77.7+/-8.60% in Bm and 75.0+/-8.89%. The results showed that Aspirin lowered aggregability markedly. 7) The mean maximal platelet aggregability in patients with thrombotic disease was studied by combined administration of Aspirin and Dipyridamole. The platelet aggregability induced by epinephrine before administration was 86.7+/-13.77% and after administration it was 36.7+/-14.01%. The platelet aggregability induced by 4 microM/L ADP before administration was 81.5+/-12.93% in Bm and 80.6+/-14.15% in B5 amd after administration it was 54.7+/-17.27% in Bm and 44.6+/-21.17% in B5. The platelet aggregability induced by 10 microM/L ADP before administration was 87.8+/-10.11% in Bm and B5 and after administration it was 65.7+/-13.59% in Bm and 62.0+/-16.42% in B5. The results showed that combined administration of Aspirin and Dipyridamole lowered aggregability significantly and the results were lower than that of normal subjects. 8) The effects of combined treatment of Aspirin and Dipyridamole showed marked reduction of platelet aggregability than that of single treatment of Aspirin or Dipyridamole in thrombotic disease.
Adenosine Diphosphate ; Aspirin* ; Blood Platelets* ; Dipyridamole* ; Epinephrine ; Healthy Volunteers ; Humans ; Hypercholesterolemia* ; Intracranial Thrombosis ; Korea ; Myocardial Ischemia

No abstract available.

No abstract available.
Erectile Dysfunction* ; Male

To investigate role of autonomic nerves on penile erection and to further characterize the laboratory rat as animal model of penile erection, this experiment was performed by means of monitoring intracavernosal pressure following nerve stimulation in 46 rats. The results obtained were summarized as follows: Increased intracavernosal pressure as well as erection was observed following electrical stimulation( 1-10 volt, 0.5-5 Hz) on each autonomic nerve, although the hypogastric nerve required higher intensity of electrical stimuli than the parasympathetic nerve (pelvic or cavervnous nerve) to induce erectile response. Combined stimulation of the pelvic nerve and the hypogastric nerve resulted in synergistic increase of intracavernosal pressure. These results indicate the hypogastric nerve may have a potential role in mediation of penile tumescence as the parasympathetic(pelvic or cavernous) nerve and that this rat model would contribute to the further study of penile erection.
Animals ; Autonomic Nervous System ; Autonomic Pathways* ; Male ; Models, Animal ; Negotiating ; Penile Erection* ; Rats*

No abstract available.
Animals ; Male ; Penile Erection* ; Rats* ; Saponins*

No abstract available.

Nitric oxide(NO) is known to act as an important neural mediator of penile erection. Nitric oxide synthase(NOS), which produces NO, has been recently identified in autonomic neurons supplying genitourinary organs including penis. The present study was undertaken to investigate the role played by NO in erectile physiology by correlating its action with the existence and activity of NOS. Initial experiments were performed to elucidate NOS expression in the human and rat penis. Western blotting analysis identified a protein of 155KDa molecular weight identical to neural form of NOS. The NOS blot density in the human and rat penis was similar each other, which was lower than that in the cerebellum. Additional studies of NOS using assay of NADPH diaphorase activity and nitrite measurement were performed in various organs of the rat. NOS activity regionally predominated in the cerebellum, urethra, penis, and urinary bladder in the order Subsequent investigations focused on the physiologic role of NO, which was determined using an in vivo electroerection model in the rat. ntracavernous injections of NOS inhibitor (L-NOARG or L-NAME from 0.000001M to 0.001M) were found to suppress the nerve-induced erection in concentration dependent manner. Subsequent intracavernous injection of L-arginine(0.01M) partially restored penile erection suppressed by L-NOARG or L-NAME(0.001M). These results indicate that the neural form of constitutive NOS in the corpora cavernosa of the penis synthesizes NO by its catalytic action, which mediates penile erection. Furthermore, determination of cavernosal NOS expression and/or activity may allow to characterize certain pathological conditions which cause neurogenic impotence.
Animals ; Blotting, Western ; Cerebellum ; Erectile Dysfunction ; Humans ; Male ; Molecular Weight ; NADPH Dehydrogenase ; Neurons ; NG-Nitroarginine Methyl Ester ; Nitric Oxide Synthase* ; Nitric Oxide* ; Penile Erection* ; Penis ; Physiology ; Rats ; Urethra ; Urinary Bladder

Peyronie's disease(PD) is an inflammatory condition characterized by the formation of fibrous, noncompliant nodules in the tunica albuginea leading to penile deformity and bending. Repetitive microtrauma of the penis during sexual intercourse is thought to incite a local autoimmune reaction in genetically susceptible individuals. The fibrotic plaques are most likely produced by tunical fibroblasts in response to cytokine stimulation, such as by transforming growth factor-beta1. In the acute inflammatory phase, pain during erection and penile deviation are the main symptom. In later stages, PD is often associated with erectile dysfunction(ED), distal flaccidity, or both. The causes of ED include psychological factors (performance anxiety), penile pain and deformity, flail penis, and vascular disease. Conservative treatment is useful during the early inflammatory stage. Despite myriad proposed medical therapies, including numerous oral agents and local injection regimens, there have been limited advances. Surgery is typically reserved for patients who fail to respond to conservative treatment and have had no disease progression for at least several months. Penile lengthening procedures with different grafting materials have, to a great extent, replaced conventional procedures with penile plication or its modifications. Prosthesis insertion is reserved for patients with severe ED that does not respond to medical management. As the molecular mechanism of inflammation and wound healing is elucidated, new approaches for medical intervention, such as modification of fibroblast function, growth factor activity, and cytokine action, will no doubt be available for therapy of PD.
Coitus ; Congenital Abnormalities ; Disease Progression ; Fibroblasts ; Humans ; Inflammation ; Male ; Penile Induration* ; Penis ; Prostheses and Implants ; Psychology ; Transplants ; Vascular Diseases ; Wound Healing

Intravesical outlet obstruction in human is one of the most commonly observed conditions in the urologic field and often related to voiding difficulty with unstable bladder. The pathophysiological background for voiding difficulty is unknown and also difficult to investigate in human. We, herein, performed animal study to investigate whether and how short-term infravesical outlet obstruction does affect the function of rat bladder, and to establish the animal model with infravesical outlet obstruction for further studies. Infravesical outlet obstruction was created by placing a silicon sleeve around the bladder neck and proximal urethra of mature female rats. At one week after operation. cystometrical evaluation and isolated detrusor strip study was performed in each rat. The whole bladder weight of obstructed group significantly increased to four times that of control group. In cystometrical investigations, obstructed group showed unstable bladder. Furthermore, the obstructed group showed increased bladder capacity and residual urine volume, compared to those or control group. In isolated detrusor muscle strip study, contractile responses of detrusor muscle to field stimulation. bethanechol and ATP were less prominent in obstructed group than in control group. However. tetrodotoxin could not completely abolish EFS induced detrusor contraction in obstructed group, compared to that in control group. These results indicate that short-term obstructed bladder showed a significant decrease in detrusor contractility as well as abnormal detrusor contraction, which may be resulted from the degeneration of detrusor muscle, although neurogenic cause remains to be further investigated.
Adenosine Triphosphate ; Animals ; Bethanechol ; Female ; Humans ; Models, Animal ; Neck ; Rats* ; Silicones ; Tetrodotoxin ; Urethra ; Urinary Bladder Neck Obstruction ; Urinary Bladder*