Prostaglandin E1 Groups Research Articles

Effects of Prostaglandin E1 on Mastectomy Flap Necrosis in Immediate Implant-Based Breast Reconstruction.

Necrosis of a cutaneous flap including the nipple-areola complex is a common complication in immediate implant-based breast reconstruction following nipple-sparing mastectomy (NSM)/skin-sparing mastectomy (SSM). This study aimed to evaluate the efficacy of prostaglandin E1 (PGE1) in reducing such complications. A retrospective analysis of prospectively collected data was conducted at two centers, and the cohort consisted of patients undergoing NSM/SSM followed by immediate reconstruction with a prosthesis. Patients who were randomly allocated to the treatment group were administered daily intravenous PGE1 (10 μg/2 mL) beginning intraoperatively through postoperative day 6. Skin flap complications including nipple/skin necrosis, delayed wound healing, and postoperative wound revision were recorded. Complication rates were compared between the PGE1 and control groups. A total of 276 breasts in 259 patients were included for analysis (139 breasts in the treatment group and 137 breasts in the control group). There was no difference in patient demographics between the control and treatment groups. Reconstructed breasts receiving PGE1 had significantly lower rates of overall skin complications (21.6% versus 34.3%; P = 0.022) and wound revision (2.9% versus 9.5%; P = 0.025). Among NSM cases, the PGE1 group showed a significantly lower rate of nipple necrosis (15.5% versus 29.4%; P = 0.027). In the multivariate analysis, the use of PGE1 significantly reduced the risk of overall skin flap complications (OR, 0.491; P = 0.018) and wound revision (OR, 0.213; P = 0.018) in NSM/SSM cases, and nipple necrosis (OR, 0.357; P = 0.008) in NSM cases. PGE1 can be effective in reducing risk of mastectomy flap complications in immediate implant-based breast reconstructions. Therapeutic, III.

Prevention of contrast-induced nephropathy with prostaglandin E1 in patients undergoing percutaneous coronary procedures: A meta-analysis of 24 randomized controlled trials .

Contrast-induced nephropathy (CIN) is the third most common cause of acute kidney injury in hospitalized patients. There have been many conflicting results across trials that have evaluated the prophylactic efficacy of prostaglandin E1 (PGE1) for prevention of CIN in patients undergoing percutaneous coronary procedures. PGE1 may have renal-protective effects due to its pleiotropic properties. The aim of this study was to evaluate the efficacy of PGE1 in preventing CIN. We searched PubMed, Embase, Cochrane Library, Chinese Biomedical Literature, China National Knowledge Infrastructure, VIP Information/Chinese Scientific Journals, and WANFANG databases for randomized controlled trials (RCTs) comparing the preventive effects of PGE1 versus controls (conventional hydration, no PGE1, or placebo) on CIN in patients undergoing percutaneous coronary procedures from January 1999 to June 2016. Study characteristics and outcome data were abstracted by two independent reviewers; the risk of bias was also assessed by two reviewers. 24 RCTs involving 3,915 patients were included. Compared with controls, PGE1 reduced the risk of CIN (risk ratio: 0.40, 95% confidence interval (CI): 0.33, 0.48; p < 0.01). Serum creatinine levels in the PGE1 groups were significantly lower than in the control groups at 24, 48, and 72hours after operation (mean difference (MD): -10.06, 95% CI: -16.94, -3.19; MD: -15.47, 95% CI: -21.75, -9.18; and MD: -11.15, 95% CI: -14.40, -7.91, respectively). Cystatin C was significantly lower for the PGE1 group than the control groups at 24, 48, and 72 hours after operation (MD: -0.24, 95% CI: -0.40, -0.07; MD: -0.34, 95% CI: -0.53, -0.14; and MD: -0.32, 95% CI: -0.49, -0.15, respectively). PGE1 may play an important role in reducing the incidence of CIN in patients undergoing percutaneous coronary procedures. .

PGE1 improves diabetic peripheral neuropathy in patients with type 2 diabetes

BackgroundDiabetic peripheral neuropathy (DPN) is the most common chronic complication of diabetes. We aim to investigate the efficacy of Prostaglandin E1 (PGE1) treatment in addition to intensive insulin therapy on DPN in patients with type 2 diabetes. MethodsSeventy-seven patients with DPN received daily intravenous injection of Prostaglandin E1 (PGE1) in lipid microspheres (Lipo-PGE1) for 10days as an additional therapy to standard glucose control therapy (PGE1 group). Another 42 patients with DPN receiving only standard glucose control therapy (intensive insulin therapy) acted as a control group. Michigan neuropathy screening instrument (MNSI) score, neurophysiology examination, transcutaneous oxygen sensory threshold, and ankle-brachial index (ABI) were measured to evaluate the efficacy of PGE1 treatment as compared with control group. ResultsStandard glucose control therapy decreased plasma glucose to a similar level in both PGE1 and control groups. Compare to control group, PGE1 group displayed improvement in several nerve electrophysiological indexes. MNSI score was significantly improved in patients who received PGE1 treatment compared with the control group (p<0.001) after 10days of PGE1 treatment. Similarly, nerve conduction velocity and foot sensory thresholds (p<0.05 for all) also significantly improved compared with the control group after 10days of PGE1 treatment. However, only intensive insulin therapy did not improve any neural function. ConclusionsLipo-PGE1 can effectively improve neural function of patients with DPN.

Prevention of contrast-induced nephropathy with prostaglandin E1 in high-risk patients undergoing percutaneous coronary intervention

Contrast-induced nephropathy (CIN) is an important complication in the use of iodinated contrast media. The present study aimed to assess the safety and efficacy of prostaglandin E1 (PGE1) in prevention of CIN in patients with high-risk factors undergoing percutaneous coronary intervention (PCI). The study group consisted of 163 patients who had undergone a coronary intervention procedure between January 1, 2012 and October 31, 2012. Study participants were randomly assigned to either the PGE1 group (82 patients) or the control group (81 patients). Patients in the PGE1 group received PGE1 intravenous infusion of 20 ng/kg/min for 6 h before and after the administration of contrast media. The control group received 0.9 % sodium chloride solution for routine hydration only. A nonionic, low-osmolality contrast agent was used in our laboratory at this time. Serum creatinine (Scr) values and estimated glomerular filtration rate were measured before and within 48 h of the administration of contrast agents. CIN was defined as an increase of ≥0.5 mg/dL or ≥ a 25 % increase in Scr concentrations over baseline within 48 h of angiography. The amount of contrast agent administered was similar for the PGE1 and control groups (156 ± 63 vs. 161 ± 68 mL, P > 0.05). The incidence of CIN was lower in the PGE1 group than in the control group (3.7 vs. 11.1 %, P < 0.05). No serious adverse effects were observed. In patients with high-risk factors undergoing PCI, the use of PGE1 for prevention of CIN is safe and efficacious.

In vitro viability of human cavernosal endothelial and fibroblastic cells after exposure to papaverine/phentolamine and prostaglandin E1

To investigate the influence of commercially available vasoactive drugs on human cavernosal endothelial and fibroblastic cells in vitro, as although corporal fibrosis is a well known side-effect of intracavernosal injection therapy for erectile dysfunction, the possible detrimental effect of these agents on the endothelium lining the cavernosal vascular spaces is uncertain. Cultured primary endothelial (13) and fibroblastic cells (12), obtained from potent patients undergoing penile surgery, were exposed to different physiological dilutions of prostaglandin E1 (PGE1), papaverine/phentolamine or the respective triple-mix of these agents for 30 min. Viable cells were counted and cell metabolic activity measured in these cultures 48 h after drug exposure. There was a significant dose-dependent decrease in the viable cell count after exposure to papaverine-containing formulations, probably because of the low pH of this substance. This cytotoxic effect was more pronounced in endothelial than in fibroblastic cells, and was not apparent in the PGE1 groups. The relative increase in cell metabolic activity in cultures affected by a moderate cytotoxic effect indicated a regenerative process. These comparative results in endothelial and fibroblastic cell cultures suggest that the endothelium rather than the interstitium of the corpus cavernosum is more sensitive to side-effects produced by intracavernosal injection therapy with papaverine. Thus, unfavourable consequences on the function of the endothelial layer might be as important as the risk of interstitial fibrosis. As these effects were not detected for PGE1 this drug should be preferred to papaverine in clinical practice.

Effect of prostaglandin E1 on inflammatory responses and gas exchange in patients undergoing surgery for oesophageal cancer

Oesophageal surgery causes morbidity and mortality from respiratory complications. We tested the possibility that prostaglandin E1 (PGE1) could reduce inflammatory cytokine responses and improve gas exchange after oesophagectomy. We randomized 14 patients into two groups. One group received PGE1 20 ng kg(-1) min(-1) i.v. during anaesthesia (PGE1 group) and the other group did not (control group). Anaesthesia was maintained with sevoflurane and epidural anaesthesia. During oesophagectomy, ventilation of one lung was carried out with a double-lumen bronchial tube. The patients were extubated on or after the first postoperative day. Blood samples were taken at induction of anaesthesia, at the end of thoracotomy, at the end of the operation, 2 h after surgery and on the first day after surgery. The groups were similar for ASA physical status, age, FEV1%, operation time, duration of thoracotomy, intraoperative fluid volume and blood loss. The arterial blood gas and arterial pressure during surgery were also similar in the PGE1 and control groups. However, the PaO2/FiO2 ratio on the first day after surgery was significantly greater in the PGE1 group compared with the control group. Serum concentrations of IL-6 and IL-8 increased after surgery in both groups. IL-6 was significantly less in the PGE1 group at the end of the operation and 2 h after the operation. Intraoperative PGE1 reduced IL-6 production in patients undergoing oesophagectomy and oxygenation was better in the postoperative period.

Right ventricular performance during hypotension induced by prostaglandin E1, nicardipine HCl, glycerine trinitrate, and isosorbide dinitrate

This study investigated right ventricular (RV) performance during hypotensive anesthesia and compared the effect of the vasodilators prostaglandin E1 (PGE1), nicardipine HCl (Nic), glycerin trinitrate (GTN), and isosorbide dinitrate (ISDN) on RV function. Fifty patients were allocated into four groups [PGE1 (n=20), Nic (n=10), GTN (n=10), and ISDN (n=10)] in random order. Pulmonary and RV hemodynamics were measured using a rapid-response thermodilution catheter before and during induced hypotension, when systolic arterial pressure was maintained at 80 mmHg. In the PGE1, GTN, and ISDN groups, RV end-diastolic volume (RVEDV) and pulmonary vascular resistance were reduced in a similar manner. However, RV ejection fraction increased only in the PGE1 group, and as a consequence, RV stroke volume (RVSV) was maintained. Nic did not change the RV parameters observed, but reduced only systemic vascular resistance (SVR). PGE1 enhanced RV function during induced hypotension. Nic was a useful alternative agent for hypotensive anesthesia. GTN and ISDN reduced RV preload and RVSV; however, cardiac output was maintained by increasing heart rate (HR). Therefore, such nitrates should be used under an adequate RV preload.

Prostaglandin E1 administration following orthotopic liver transplantation: a randomized prospective multicenter trial

Klein, A S; Cofer, J B; Pruett, T L; Thuluvath, P J; McGory, R; Uber, L; Stevenson, W C; Baliga, P; Burdick, J F

Prostaglandin E1 administration following orthotopic liver transplantation: A randomized prospective multicenter trial

BACKGROUND & AIMS: Prostaglandin E1 (PGE1) has been used after orthotopic liver transplantation (OLT) based on limited clinical data suggesting PGE1 infusion improves immediate hepatic allograft function. The aim of this study was to conduct a randomized double-blinded multicenter trial to evaluate the effect of PGE1 on early hepatic and renal function in patients undergoing OLT. METHODS: One hundred eighteen patients were randomized to receive either PGE1 or crystalloid placebo intravenously after allograft revascularization. Primary end points were incidence of primary allograft nonfunction (PNF) or severe renal dysfunction. RESULTS: The incidence of PNF was 6.7% (4 of 60) and 6.9% (4 of 58) in the control and PGE1 groups, respectively. PGE1 infusion was, however, associated with improved early renal function (mean peak creatinine level of 1.4 +/- 1.0 and 2.0 +/- 1.0 in patients treated with PGE1 and placebo, respectively; P < 0.001). Severe renal dysfunction occurred more frequently in the placebo group (26.7%) than in the PGE1 group (13.8%; P = 0.65). Additionally, dialysis treatments were more frequent in the placebo group (0.7 +/- 2.0 per patient) than in the PGE1 group (0.2 +/- 1.0 per patient; P = 0.10). Initial intensive care unit stay was shorter in patients treated with PGE1 (4.0 +/- 3.6 days) compared with controls (10.5 +/- 17.1 days) (P < 0.01). CONCLUSIONS: PGE1 administration after OLT resulted in improved renal function and decreased initial postoperative intensive care unit stay but did not affect the incidence of PNF. (Gastroenterology 1996 Sep;111(3):710-5)

Effect of low-dose infusion of prostaglandin E1 on vecuronium-induced neuromuscular blockade.

The effect of low-dose (20 ng·kg-1·min-1) infusion of prostaglandin E1 (PGE1) on vecuronium-induced neuromuscular blockade was studied. The study population consisted of 24 elderly patients (65-75 years old) and 24 younger adult patients (25-56 years old). They were randomly assigned to the control and PGE1 groups. The steady-state dose requirement (SSDR) of vecuronium was derived from ondemand infusion of the drug which produced a stable twitch height of 20% of its baseline reading, and recovery time after steady-state infusion was defined as the time for recovery from twitch height from 25% to 75%. The patients in the PGE1 group received an infusion of PGE1 20 ng·kg-1·min-1, while those in the control group received an infusion of normal saline. The SSDR (23.2±9.1 and 34.2±5.9 μg·kg-1. hr-1, respectively;P=0.02) was significantly less and the recovery time (35.0±9.5 and 19.9±4.2 min, respectively;P=0.01) was significantly longer in the elderly than in the younger patients. However, low-dose infusion of PGE1 significantly increased the SSDR (23.2±9.1 to 37.4±3.7 μg· kg-1·hr-1;P=0.01) and shortened the recovery time (35.0±9.5 to 23.5±4.0 min;P=0.02) in elderly patients. We concluded that low-dose infusion of PGE1 is effective in preventing the prolonged action of vecuronium in elderly patients.

Haemodynamic changes during induced hypotension — comparison of trimethaphan with prostaglandin E1 assessed using transoesophageal echocardiography

Haemodynamic changes during induced hypotension depend upon the hypotensive agent used. We investigated if, using transoesophageal echocardiography (TEE), we could identify the haemodynamic differences between trimethaphan and prostaglandin E1. Twenty-nine patients undergoing total hip replacement were selected for study. Hypotension was induced to a mean arterial pressure of 8.0-9.3 kPa with either trimethaphan (5-20 micrograms.kg-1.min-1) or prostaglandin E1 (0.5-2.0 micrograms.kg-1.min-1). The left atrial dimension, cardiac output, fractional shortening, pulmonary venous flow and mitral valve flow were evaluated using TEE. During induced hypotension, left atrial dimension decreased in both trimethaphan and prostaglandin E1 groups (P < 0.05). In the trimethaphan-treated patients systolic velocity in pulmonary venous flow decreased from 41.9 +/- 4.8 cm.sec-1 before induced hypotension to 27.8 +/- 4.2 cm.sec-1 by 30 min after stable hypotension had been established (P < 0.01). The late/early ratio of peak velocity in mitral blood flow decreased in prostaglandin E1 treated patients. Cardiac output increased from 4.2 +/- 0.5 L.min-1 to 5.3 +/- 0.4 L.min-1 during 30 min hypotension with prostaglandin E1 administration (P < 0.05), but cardiac output decreased from 5.0 +/- 0.5 to 3.5 +/- 0.4 L.min-1 with trimethaphan (P < 0.01). The differences in haemodynamic variables could be attributed to the venule dilatation effect of trimethaphan. We conclude that it was possible to detect the haemodynamic differences between trimethephan and prostaglandin E1 using TEE.

An in vitro evaluation of prostaglandin E1 and I2 on hypothermic injury to immature myocytes.

The purpose of this study was to evaluate the functional and biochemical effects of Prostaglandin E1 (PGE1) and prostaglandin I2 (PGI2) on cardiac myocytes incubated under hypothermic conditions. Cardiac myocytes were isolated from neonatal rat ventricles and cultured for 4 days with MCDB 107 medium. Following this, 12.5 x 10(5) myocytes/flask were incubated at 4 degrees C for 24 h in media with PGE1, at concentrations of 0 M (group E0), 10(-9) M (group E1), 10(-8) M (group E2), 10(-7) M (group E3), or 10(-6) M (group E4); or with PGI2 at concentrations of 0 M PGI (group I0), 10(-9) M (group I1), 10(-8) M (group 12), 10(-7) M (group I3), or 10(-6) M (group I4). After hypothermic incubation, creatine phosphokinase (CPK) and lactate dehydrogenase (LDH) were measured, and the myocytes were then cultured for 24 h at 37 degrees C to evaluate the recovery of the myocyte beating rate. Of the PGI2 groups, only group I2 recovered significantly more than the control group (group I0), at 47.9 +/- 28.5% (mean +/- SD) of the control, being the beating rate prior to hypothermic incubation, whereas it was 18.1 +/- 9.7% in group I0 (P < 0.025); however, there were no significant differences among the PGE1 groups. Moreover, the release of CPK and LDH was significantly suppressed in group 12 compared to the control, being 57.7 +/- 27.6 mIU/flask (P < 0.05) and 275.1 +/- 83.0 mIU/flask (P < 0.025), respectively, in group I2, and 96.8 +/- 38.3 mIU/flask and 439.6 +/- 147.1 mIU/flask in group I0. Again, no significant differences were observed among the PGE1 groups. In conclusion, PGI2 was found to have a direct cytoprotective effect on immature myocytes which suggests that PGI2 may promote cardiac preservation in the neonatal period.

The effect of prostaglandin E1 on colonic anastomotic healing

In an attempt to show the effect of prostaglandin E1 (PGE1) on colonic anastomotic healing the authors measured collagen synthesis and counted inflammatory cells (polymorphonuclear leukocytes "PMN," histiocytes, lymphocytes, and plasma cells) and compared the results to those of aprotinin and control groups. The authors performed colonic anastomoses on 45 male albino rats, which were divided into three groups. Measurements of collagen synthesis and counts of inflammatory cells in the first group were evaluated as control data. They administered 2000 units aprotinin daily for two days in the second group and 2 micrograms PGE1 daily for two days in the third group. Collagen content as hydroxyproline in the resected anastomotic part of the colon was measured and the inflammatory cells were counted on the first, third, fifth, and tenth days. The results showed that PGE1-administered rats had significantly higher collagen levels (5.21 +/- 1.35 micrograms hydroxyproline/mgr tissue, P less than 0.05 and 3.81 +/- 0.63 micrograms/mg, P less than 0.05) on the third and fifth days, respectively, compared with the control and aprotinin groups. The aprotinin group also had higher collagen levels (3.34 +/- 0.27 micrograms/mg, P less than 0.05 and 3.07 +/- 0.40 micrograms/mg, P less than 0.05) on the third and fifth days, respectively, compared with the control group. There were no statistically important differences in the collagen contents of the control, aprotinin, and PGE1 groups on the tenth day and there was an increase in the collagen content in all groups (P less than 0.05). The inflammatory cells, including PMNs, histiocytes, lymphocytes, and plasma cells, which play an important role in the inflammatory stage of colonic anastomotic healing, were also counted. The cells were counted on the third, fifth, and tenth days and the results were evaluated as (+) positive and more positive. The results of the control and aprotinin groups were found as ( ), ( ), and (++) on the third, fifth, and tenth days, respectively. In the PGE1-administered group the inflammatory cells were counted as (+), (++), and (++) on the third, fifth, and tenth days, respectively. In addition, there was an increase in fibroblast synthesis and new vessel formation on the tenth day. Thus, it was shown that PGE1 decreased inflammatory cells and increased collagen synthesis in the early stage of colonic anastomoses and fibroblasts in the late stage more effectively when compared with the control and aprotinin groups.(ABSTRACT TRUNCATED AT 400 WORDS)

Pulmonary blood flow distribution after lobar oleic acid injury: A PET study

We evaluated the importance of hypoxic vasoconstriction as a mechanism for pulmonary blood flow reduction during unilobar oleic acid lung injury in dogs. Pulmonary blood flow (PBF) and lung water were measured with positron emission tomography. Data from the injured left (LCL) and right (RCL) caudal lobes were compared in 23 dogs. Six dogs were used to demonstrate that endotoxin (15 micrograms/kg) prevents changes in regional PBF during selective hypoxic ventilation of the LCL. In 17 dogs, oleic acid (OA, 0.015 ml/kg) was injected into the LCL through a balloon-wedged pulmonary arterial catheter. Five dogs received OA only (control group), eight received endotoxin (15 mcg/kg) before OA was administered (endotoxin group), and four were treated with prostaglandin E1 (PGE1) after OA (PGE1 group). The base-line left-to-right PBF ratio (LCL/RCL PBF) was 1.01 +/- 0.11 (SD) for the control group and 1.07 +/- 0.16 for the PGE1 group. One minute after OA, LCL/RCL PBF feel significantly (0.32 +/- 0.15 and 0.32 +/- 0.13 for the control and PGE1 groups, respectively) before any significant increase in lung water was detected. In all 17 dogs that received OA, the LCL/RCL PBF remained severely reduced 60 min after OA compared with base-line values (0.41 +/- 0.15, 0.49 +/- 0.06, and 0.26 +/- 0.13 for the control, PGF1, and endotoxin groups, respectively) despite treatment with endotoxin or PGE1. Lung water measurements obtained 60 min after OA increased significantly (P less than 0.05) in the injured lobe (LCL) but not in the normal lobe (RCL) in all dog groups, whereas PBF to the LCL remained significantly reduced.(ABSTRACT TRUNCATED AT 250 WORDS)

Randomized Double-Blind, Multicenter Study of Prostaglandin E1 in Patients with the Adult Respiratory Distress Syndrome

Prostaglandin E1 (PGE1) was compared to placebo in a 100-patient (50 PGE1, 50 placebo) randomized, double-blind, clinical trial to determine whether PGE1 therapy enhances survival of patients with adult respiratory distress syndrome (ARDS) when infused through a central line at 30 ng/kg/min continuously for seven days. At 30 days postinfusion, 30 PGE1 and 24 placebo patients had died. Total deaths judged to be related to the syndrome were 32 and 28 in the PGE1 and placebo groups respectively at six months. We conclude that PGE1 did not enhance survival in patients with established ARDS. PGE1 augmented the hyperdynamic circulation of these patients by reducing systemic and pulmonary vascular resistance, which resulted in a reduction of blood pressures and increased stroke volume, cardiac output, and heart rate. An improvement in oxygen availability and oxygen consumption was observed with PGE1 therapy. PGE1 was associated with an increased incidence of diarrhea (six patients in the PGE1 group vs one in the placebo group, p less than 0.05). Other adverse effects included hypotension (ten patients in the PGE1 group vs seven in the placebo group), fever (six patients in the PGE1 group vs three in the placebo group), and non-fatal dysrhythmias (ten in the PGE1 group vs five in the placebo group).

Pulmonary blood flow distribution after lobar oleic acid injury: a PET study.

We evaluated the importance of hypoxic vasoconstriction as a mechanism for pulmonary blood flow reduction during unilobar oleic acid lung injury in dogs. Pulmonary blood flow (PBF) and lung water were measured with positron emission tomography. Data from the injured left (LCL) and right (RCL) caudal lobes were compared in 23 dogs. Six dogs were used to demonstrate that endotoxin (15 micrograms/kg) prevents changes in regional PBF during selective hypoxic ventilation of the LCL. In 17 dogs, oleic acid (OA, 0.015 ml/kg) was injected into the LCL through a balloon-wedged pulmonary arterial catheter. Five dogs received OA only (control group), eight received endotoxin (15 mcg/kg) before OA was administered (endotoxin group), and four were treated with prostaglandin E1 (PGE1) after OA (PGE1 group). The base-line left-to-right PBF ratio (LCL/RCL PBF) was 1.01 +/- 0.11 (SD) for the control group and 1.07 +/- 0.16 for the PGE1 group. One minute after OA, LCL/RCL PBF feel significantly (0.32 +/- 0.15 and 0.32 +/- 0.13 for the control and PGE1 groups, respectively) before any significant increase in lung water was detected. In all 17 dogs that received OA, the LCL/RCL PBF remained severely reduced 60 min after OA compared with base-line values (0.41 +/- 0.15, 0.49 +/- 0.06, and 0.26 +/- 0.13 for the control, PGF1, and endotoxin groups, respectively) despite treatment with endotoxin or PGE1. Lung water measurements obtained 60 min after OA increased significantly (P less than 0.05) in the injured lobe (LCL) but not in the normal lobe (RCL) in all dog groups, whereas PBF to the LCL remained significantly reduced.(ABSTRACT TRUNCATED AT 250 WORDS)

播種性血管内凝固症候群（ＤＩＣ）に関する実験的研究 ＩＩＩ 実験的家兎ＤＩＣにおけるプロスタグランディンＥ１の効果

We have previously reported that an experimental model of disseminated intravascular coagulation (DIC) could be induced by continuous infusion of endotoxin (ET) at a dose of 3mg/kg during 3hrs, in rabbits. Using this model, the effects of prostaglandin E1 (PGE1) against DIC were investigated. Our study was made in control rabbits and rabbits infused with PGE1. The animals were divided into 4 groups as follows;Group I (control group): physiological saline infusion d-ET (3mg/kg) infusionGroup II (PGE1 group): PGE1 (125ng/kg/min) infusion+ET (3mg/kg) infusionGroup III (PGE1 group): PGE1 (25ng/kg/min) infusion+ ET (3mg/kg) infusionGroup IV (PGE1 group): PGE1 (5ng/kg/min) infusion+ET (3mg/kg) infusionTentative diagnostic criteria for DIC were designed as DIC scoring system. The DIC score was useful to determine the degree of the DIC state (DIC score>6 points) and evaluate the effects of PGE1 infusion against DIC. The results of the present study demonstrated the following scores for each group: 7.4±0.9 in Group I, 2.3±1.2 in Group II, 2. 8±1.5 in Group III, and 3.5±1.0 in Group IV. The inhibition of development of DIC was noted in PGE1 groups. However, mortality was not reduced in Group II against Group I. These results suggested that a moderate dose of PGE1 (Group III) might be most effective for prevention of DIC.

Hemodynamic effects of prostaglandin E1 during cardiopulmonary bypass in infants and children.

Effects of prostaglandin E1 (PGE1) and phenoxybenzamine (POB) on the hemodynamics during cardiopulmonary bypass (CPB) were studied in 30 infants and children. Patients were grouped into three; PGE1 was given to ten patients, POB to another ten, and the other ten patients served as the control. Vasodilating drugs were withheld. PGE1 was infused at 0.01 to 0.02 microgram/kg/min during CPB, and POB at 1.0 mg/kg within the initial 10 minutes of bypass. There was a significant drop in arterial and venous pressure at the time of initiation of bypass in both the PGE1 and POB groups. In the PGE1 group in particular, such a stable hemodynamic condition of over 60 mm Hg in mean arterial pressure, 7.5 to 12.5 cmH2O in central venous pressure, 1300 to 1700 dynes . sec . cm -5 in systemic vascular resistance was maintained throughout CPB, as compared with the other two groups. PGE1 contributed to an adequate diuresis and the preservation of platelets. Our findings indicate that PGE1 has potential clinical advantages for application during CPB.