Intracavernosal self injection therapy is now being widely used to treat patients with erectile dysfunction. However, there is a large number of patients who gives up the self injection program due to the fear of needle or injection. Therefore, the less invasive route of drug administration is highly recommended. We investigated the efficacy of intraurethral instillation of PGE1 solution in comparison with the trimix intracavernosal injection. A total of 24 patients have been observed with either injection of trimix (11 patients), or intraurethral instillation of PGE1 (13 patients). All patients were evaluated with the penile doppler ultrasonography before 5,15,30 and 45 minutes after the drug administration. Penile length and circumference were measured before and after intraurethral administration of PGE1. Ten out of 11 patients (91%) showed positive response in trimix group and nine of 13 patients (69.2%) in PGE1 group. Mean length and circumference of penile shaft before and after the pharmacologic erection test showed significant difference in PGE1 group. The mean peak systolic velocity at 30 minutes was 28.5% 10.53 cm/sec in Trimix group and 28.2 t8.47 cm/sec in PGE, group (p=0.4773). The mean end diastolic velocity at 30 minutes was 8.4 5.23 cm/sec in Trimix group and 8.2=4.21 cm/sec in PGE1 group (p=0.4689). With the intraurethral administration of PGE1, urethral pain and irritation were the noticeable complications but systemic side effect was not noticed In conclusion, PGE1 intraurethral instillation can be satisfactorily used for the patients with erectile dysfunction of psychogenic, less prominent organic and neurogenic origin, although the effect of intraurethral instillation of PGE1 is obviously less than that of Trimix intracavernosal injection.
Alprostadil* ; Erectile Dysfunction* ; Humans ; Male ; Needles ; Prostaglandins E ; Ultrasonography, Doppler

Inflammation of the prostate gland results in accessory sexual gland secretory dysfunction. The prostate gland and seminal vesicle provide specific factors to the seminal plasma which are essential to the male fertility such as prostaglandins. To evaluate the affection of prostatitis on the concentrations of prostaglandins in semen and its relation to the male fertility, prostaglandin(PG)E and PGF2 degrees C alpha were measured by radioimmunoassay method in semen samples from 20 normal men, 32 prostatitis patients with normal sperm quality, 16 prostatitis patients with abnormal sperm quality and 17 infertile patients with abnormal sperm quality. The results were as follows. 1. Inflammation of prostate caused significant decrease in the PGE/PGE2 degrees C alpha ratio in semen. 2. The PGE/PGF2 degrees C alpha ratio in semen from prostatitis patients was decreased significantly when the number of white blood cells increased. 3. The PGE/PGF2 degrees C alpha ratio in semen from infertile patients was lower than that from normal man. 4. The PGE/PGF2 degrees C alpha ratio in semen from prostatitis patients with abnormal sperm quality was more decreased significantly than that from infertile patients. 5. The change of concentration of PGE2 degrees C alpha in semen affected more than that of PGE on the change of the PGE/PGF2 degrees C alpha ratio. In view of our findings it seems that prostatitis causes subfertility by decreasing the PGE/ PGF2 degrees C alpha ratio in semen and these results suggest that the seminal PGE/PGF2 degrees C alpha ratio is important to the male fertility potential in that their levels are significantly interdependent with white blood cells in expressed prostatic secretion.
Dinoprost ; Dinoprostone ; Fertility ; Humans ; Infertility ; Inflammation ; Leukocytes ; Male ; Prostaglandins E ; Prostaglandins* ; Prostate ; Prostatitis* ; Radioimmunoassay ; Semen* ; Seminal Vesicles ; Spermatozoa

PURPOSE: T lymphocytes from patients with renal cell carcinoma(RCC) show reduced immune function and impaired activation of the transcription factor, NFkB. Recent work from this laboratory shows that supernatant fluid from RCC explants can inhibit activation of NFkB. Because PGE2 can suppress T cell function and is present in supernatant fluid from RCC explants, we determined if PGE2 could suppress the activation of NFkB. MATERIALS AND METHODS: Peripheral blood T cells from normal volunteers and RCC patients were stimulated with crosslinked antiCD3 antibody and IL-2(1000u/ml) or PMA(20ng/m1) and lonomycin(0.75rg/m1) for various lengths of time. The effect that PGE, and RCC-5(supernatant fluid from RCC) had on NFkB was assessed by adding PGE2 or RCC-S to normal T cells using western blotting and electrophoretic mobility shift assay(EMSA). RESULTS: T cell activation results in the nuclear expression of two KB binding complexes(C 1 and C2) as determined by EMSA. However, PGE2 suppressed the nuclear expression of KB binding activity with 10-5M PGE2 having the most effect. PGE2 and RCC-S suppressed the expression of Cl which is composed of NFkB1, ReIA and c-Rel whereas it had minimal erect on C2 which is composed only of NFkB1. Western blotting verified that PGE2 and RCC-S significantly reduced the nuclear but not the cytoplasmic levels of ReIA, NFkBl and c-Rel. Furthermore, the results obtained with PGE2 and RCC-S are similar to those obtained with T cells from RCC patients CONCLUSIONS: These results demonstrate that PGE2 can suppress NFkB activation in T cells through inhibiting the nuclear translocation of ReIA, NFkBl and c-Rel. PGE2 may contribute to the inhibition of NFkB that is mediated by RCC supernatant.
Blotting, Western ; Carcinoma, Renal Cell* ; Cytoplasm ; Dinoprostone* ; Healthy Volunteers ; Humans ; Prostaglandins E ; T-Lymphocytes* ; Transcription Factors

In this investigation, the bladder of guinea pig was longitudinally mounted in the muscle chamber and contracted by electrical field stimulation(EFS). It was purposed to elucidate the physiological significance of prostaglandin(PG) on the neurotransmitter release from nerve ending. 1. The inhibitory response of 5 x 0.0000001 g/ml atropine was significant only by high frequency (p<0.05) However. the curve of frequency-response were shifted to left upward by 5 x 0.00000001 g/ml phentolamine, it were not significant. Because the contraction was completely abolished by 0.00000001 and 0.0000001g/ml tetrodotoxin, it was evident that the responses to electrical stimulation are entirely due to nerve mediated excitation. 2. The curve of frequency-response were significantly shifted to left upward by 5x 0.00000001 and 5x0.0000001 g/ml arachidonic acid(p<0.05). Though the contraction were inhibited by 5x0.0000001g/ml atropine it was not significant. 3. The curves of frequency-response showed dose-response relation by 5x 0.00000001, 5 x0.000000001 and 5x 0.0000000001g/ml PGE2. The contraction was significant only by high frequency in 5x0.0000000001g/ml PGE. and the frequency-response curves were significant in varying frequencies in 5x0.000000001and 5x0.00000001g/ml PGE2(p<0.05). 4. Although the contraction was found by 5x0.0001g/ml aspirin, the curves of frequency-response were not significant. The contraction by 5x 0.0001g/ml aspirin and 5x0.000001/ml arachidonic acid was not significant too.
Animals ; Arachidonic Acid ; Aspirin ; Atropine ; Dinoprostone ; Electric Stimulation ; Guinea Pigs ; Nerve Endings ; Neurotransmitter Agents ; Phentolamine ; Prostaglandins E ; Tetrodotoxin ; Urinary Bladder

PURPOSE: Interleukin 6 (IL-6) and IL-8 participate in the pathogenesis of chronic rhinosinusitis with nasal polyps, and their levels are increased by prostaglandin E2 (PGE2) in different cell types. The purposes of this study were to determine whether PGE2 has any effect on the increase in the levels of IL-6 and IL-8 in nasal polyp-derived fibroblasts (NPDFs) and subsequently investigate the possible mechanism of this effect. METHODS: Different concentrations of PGE2 were used to stimulate NPDFs at different time intervals. NPDFs were treated with agonists and antagonists of E prostanoid (EP) receptors. To determine the signaling pathway for the expression of PGE2-induced IL-6 and IL-8, PGE2 was treated with Akt and NF-kappaB inhibitors in NPDFs. Reverse transcription-polymerase chain reaction for IL-6 and IL-8 mRNAs was performed. IL-6 and IL-8 levels were measured byenzyme-linked immunosorbent assay (ELISA). The activation of Akt and NF-kappaB was evaluated by western blot analysis. RESULTS: PGE2 significantly increased the mRNA and protein expression levels of IL-6 and IL-8 in NPDFs. The EP2 and EP4 agonists and antagonists induced and inhibited IL-6 expression. However, the EP4 agonist and antagonist were only observed to induce and inhibit IL-8 expression level. The Akt and NF-kappaB inhibitors significantly blocked PGE2-induced expression of IL-6 and IL-8. CONCLUSIONS: PGE2 increases IL-6 expression via EP2 and EP4 receptors, and IL-8 expression via the EP4 receptor in NPDFs. It also activates the Akt and NF-kappaB signal pathways for the production of IL-6 and IL-8 in NPDFs. These results suggest that signaling pathway for IL-6 and IL-8 expression induced by PGE2 might be a useful therapeutic target for the treatment of nasal polyposis.
Blotting, Western ; Dinoprostone* ; Fibroblasts* ; Interleukin-6* ; Interleukin-8* ; Nasal Polyps ; NF-kappa B ; Prostaglandins E ; RNA, Messenger ; Signal Transduction

BACKGROUND: Interrupted aortic arch is a rare congenital heart anomaly which still shows high surgical mortality. In this study, we investigated the causes of and the risk factors for mortality to improve the surgical outcomes for this difficult disease entity. MATERIAL AND METHOD: From 1984 to 2004, 42 patients diagnosed as IAA were reviewed retrospectively. Age, body weight at operation, preoperative diagnosis, preoperative PGE 1 requirement, type of interrupted aortic arch, degree of left ventricular outflow stenosis, CPB time, and ACC time were the possible risk factors for mortality. RESULT: There were 14 hospital deaths. Preoperative use of PGE1, need for circulartory assist and aortic cross clamp time proved to be positive risk factors for mortality on univariate analysis. Preoperative left ventricular outflow stenosis was considered a risk factor for mortality but it did not show statistical significance (p-value=0.61). Causes of death included hypoxia due to pulmonary banding, left ventricular outtract stenosis, infection, mitral valve regurgitation, long cardiopulmonary bypass time and failure of coronary transfer failure in TGA patients. CONCLUSION: In this study, we demonstrated that surgical mortality is still high due to the risk factors including preoperative status and long operative time. However preoperative subaortic dimension was not related statistically to operative death statistically. Adequate preoperative management and short operation time are mandatory for better survival outcome.
Alprostadil ; Anoxia ; Aorta, Thoracic* ; Body Weight ; Cardiopulmonary Bypass ; Cause of Death ; Constriction, Pathologic ; Diagnosis ; Heart ; Humans ; Mitral Valve Insufficiency ; Mortality* ; Operative Time ; Prostaglandins E ; Retrospective Studies ; Risk Factors*

The interruption of hepatic blood flow has been adopted as a method of bleeding control in hepatectomy and liver transplantation. But this occlusion of hepatic inflow may result in significant hepatic injury by various kinds of oxygen radicals produced as a result of hepatic ischemia and following reperfusion. Arterial ketone body ratio(AKBR) is adequatc and convenient parameter by which both acute and prolonged changes of the hepatic function can be estimated. Pharmacological modulation of hepatic injury during warm ischemia and early reperfusion has shown some benefical effects. The authors conducted an experiment to evaluate the inhibitory effect of glutathione and prostaglandin E on hepatic injury due to acute hepatic ischemia and reperfusion. Thirty rabbits were divided into three groups, such as control(n=10), GSH(n=10) and PGE(n=10) groups. Acute hepatic ischemia was induced through the application of portal triad cross-clamping for 30 minutes, and thereafter hepatic reperfusion was induced with the removal of cross-clamping. A single bolus of 200 mg glutathione was injected 10 min before clamp in GSH group, and 200 ng/kg/min of PGE continuously from 10 min before clamp to 30 min after declamp in PGE group. AKBR and hepatic histological findings hefore clamp, 30 min after clamp, 5 min and 30 min after declamp, respectively were compared among 3 groups AKBR was markedly decreased during the clamping period in all groups (P<0.05). In control and PGE groups AKRR was significantly increased after reperfusion than before clamp (P<0.05), but was significantly lower than before clamp. Thirty minutes after reperfusion in GSH group AKBR returned to normal level and was significantly higher than in control group (P<0.05). On light tnicroscopic examination of liver biopsy, mild swollen hepatocytes in the centrilobular zone were seen at ischemia and reperfusion in control and GSH groups, but nearly normal hepatic architectures in PGE group. These results suggest that glutathione has some benefical effect on protection of hepatic dysfunction, and PGE1 on protection of hepatocellular injury during hepatic ischemia and reperfusion.
Alprostadil* ; Biopsy ; Constriction ; Glutathione* ; Hemorrhage ; Hepatectomy ; Hepatocytes ; Ischemia* ; Liver ; Liver Transplantation ; Prostaglandins E ; Rabbits* ; Reactive Oxygen Species ; Reperfusion Injury ; Reperfusion* ; Warm Ischemia

One of the primary functions for which bones have evolved is to act as a structural support. To achieve this, bones remodel throughout life so that their structure remains optimal for the prevailing mechanical environment. Bone remodeling consists of an initial phase of osteoclastic bone resorption followed by a bone formation period. Prostaglandins are potent regulators of bone formation and bone resorption that can have both stimulatory and inhibitory effects. Elevation of intracellular cAMP is an important intracellular signaling mechanism involved in the regulation of the expression of many proteins. In this study we examine whether PGE or DBcAMP affects osteoblastic activation or osteoclastic differentiation in mouse bone marrow cells and osteosarcoma ROS 17/2.8 cells. The effect of PGE and DBcAMP on the cell proliferation was measured by the incorporation of [3H]- thymidine into DNA. As a result, PGE2 (0.5-1 ug/ml) and DBcAMP (0.1-0.5 mM) inhibited the [3H]-thymidine incorporation into DNA in a dose dependent manner. The effect of PGE2 and DBcAMP on the induction of alkaline phosphatase (ALP) was investigated in ROS 17/2.8 cells cultured in medium containing 0.4% fetal bovine serum. PGE and DBcAMP stimulated ALP activity in the cells in a dose- dependent manner. PGE2 also increased the intracellular cAMP content in a dose- dependent fashion with a maximal effect at 0.5 ug/ml. ROS 17/2.8 cells release nitric oxide upon stimulation of PGE2 or DBcAMP with interferon-r. PGE2 and DBcAMP increase the phosphorylation level of CREB (cAMP response element binding protein) without any change on the amount of CREB protein. Also, PGE (10-6 M) and DBcAMP (10-4 M) significantly increase the generation of osteoclasts in mouse bone marrow cell culture system. In conclusion, the results of this study suggested that cAMP appears to be an important regulatory molecule in the processes of bone formation and resorption.
Alkaline Phosphatase ; Animals ; Bone Marrow Cells ; Bone Remodeling ; Bone Resorption ; Bucladesine* ; Cell Proliferation ; Cyclic AMP Response Element-Binding Protein ; Dinoprostone* ; DNA ; Metabolism* ; Mice ; Nitric Oxide ; Osteoblasts ; Osteoclasts ; Osteogenesis ; Osteosarcoma ; Phosphorylation ; Prostaglandins ; Prostaglandins E ; Response Elements ; Thymidine

PURPOSE: Concentrations of prostaglandin(PG) in the central nervous system is very low in physiologic conditions and are known to increase in response to febrile convulsions. And, intracerebroventricular injection of prostaglandin E-2(PGE) in unanesthetized cats is accompanied by a rise in body temperature, a decrease in convulsions, and a modulation of the convulsive thresholds, but the possible physiological role of different PGs in induction, termination, and recurrences of seizure activity is not clear. We observed the change of PGE according to temperatures in first febrile convulsions, and the relationship between the recurrence of febrile convulsions and PGE. METHOD: In the present study, the body temperatures of patients with initial febrile convulsions were measured. Spinal taps were performed. All CSF samples were stored in a deep freezer at 30degrees C until the time of analysis and tested by Prostaglandin E2 [125I] assay system, Biotra Assays, Amersham Inc. Most children were treated with antipyretics immediately and tepid water massage. 105 patients with febrile convulsions could be studied for 36 months and the times of recurrence after first febrile convulsion during those period were measured. During febrile convulsions, no anticonvulsants were used. Based on 105 children with febrile convulsions, we analyzed the results. RESULTS: The results were as follows : The levels of PGE at temperature 38.4 degrees C, 38.5 degrees C temperature 39.4 degrees C, and temperature 39.5 degrees C were 27.7+/-21.0 pg/mL, 83.6+/-38.3 pg/mL, and 205.6+/-40.0 pg/mL. The levels of PGE during 3 months recurrence group were 79.1+/-15.8 pg/mL, those during 4-6 months recurrence group were 134.9+/-74.6 pg/mL, those during 7-9 months recurrence group were 118.9+/-39.9 pg/mL, those during 10-12 months recurrence group were 133.5+/-69.2 pg/mL, those during 13-18 months recurrence group were 106.5+/-106.4 pg/mL, those during 19-24 months recurrence group were 123.7+/-100.6 pg/mL, and those during 25-36 months recurrence group were 142.1+/-172.5 pg/mL. CONCLUSION: Significantly elevated concentrations of PGE in febrile convulsions were found and related to increased body temperature. In the recurrent groups of febrile convulsions, there was no relationship between PGE levels and recurrences time of febrile convulsions. It is not clear that increased PGE levels are, at least in part, to be related to recurrences of febrile convulsions. We think that more comprehensive research is needed to clarify the role of increased PGE in first febrile convulsion and the relationship to recurrences of febrile convulsions.
Animals ; Anticonvulsants ; Antipyretics ; Body Temperature ; Cats ; Central Nervous System ; Child ; Dinoprostone ; Humans ; Massage ; Prostaglandins E ; Recurrence* ; Seizures ; Seizures, Febrile* ; Spinal Puncture ; Water

Primary irritant dermatitis is one of the most common skin disease caused by various hazardous chemicals produced from the environment. For the detection of skin irritant potency, in vivo models such as human and animal patch test have been used, Keratinocyte culture method which has been set up very recently is another alternative in vivo method of detecting skin irritarlcy. LVe have investigated the effects of three skin irritants, phenol, benzoyl peroxide (BP), and sodium lauryl sulfate(SLS) on the keratinocyte culture system. Prostaglandin E(PGE) measurement, cell count and electron microscopic observation were performed after adding three irritants of different concentrations to the cultured keranocyte cells. The main results of this study were as follows : 1. There were statistically significant decreased cell number in concentration of 10 M phenol, 10 4M BP and SLS. The order of cytotoxic potency was SLS>BP >phenol. 2. In case of PGE production, decreased PGE production was observed 6 hours after addition of the irritants, except 10 M phenol and 10M BP groups. Decrea sing tendency sustained until 24 hours, however all were statistically nonsignificant comparing with control group. 3. Electron microscopic finding showed that dilatation of endoplasmic reticulums in 10 M phenol group, condensation and dilatation of mitochondrias in 10 4M BP group, and most of the cells were swollen in 10 4M SLS group. These results suggest that cell count is a useful model for performing cytotoxi city test in keratinocyte culture decreased PGE production represents cytotoxic effect in high concentration of primary irritants and ultrastructural changes may reflect the different pathomechanisms in cytotoxicity.
Animals ; Benzoyl Peroxide ; Cell Count ; Dermatitis, Irritant ; Dilatation ; Dinoprostone ; Endoplasmic Reticulum ; Hazardous Substances ; Humans* ; Irritants* ; Keratinocytes* ; Mitochondria ; Patch Tests ; Phenol ; Prostaglandins E ; Skin ; Skin Diseases ; Sodium