6-ketoprostaglandin-f1-alpha and Flushing

This study aimed to reveal the appropriate timing for the intravenous administration of flurbiprofen axetil for preventing mesenteric traction syndrome (MTS), caused by prostacyclin release.. In this prospective, randomized, clinical study, forty-five patients who were undergoing elective surgery for colorectal cancer via laparotomy were enrolled. Patients were randomly divided into 3 groups: a preoperative group (n = 16) receiving flurbiprofen axetil directly before surgery; a post-MTS group (n = 14) receiving following MTS onset; and a control group (n = 15) who were not administered flurbiprofen axetil. 6-keto-PGF1α, a stable metabolite of prostacyclin, levels were measured and mean blood pressures were recorded.. In the preoperative group, 6-keto-PGF1α levels did not increase, blood pressure levels did not decrease, and no facial flushing was observed. In both the post-MTS and control groups, 6-keto-PGF1α levels increased markedly after mesenteric traction and blood pressure decreased significantly. The post-MTS group exhibited a faster decreasing trend in 6-keto-PGF1α levels and quick restore of the mean blood pressure, and the use of vasopressors and phenylephrine were lower than that in the control group.. Even therapeutic administration of flurbiprofen axetil after the onset of MTS has also effects on MTS by suppressing prostacyclin production.. Clinical trial number: UMIN000009111 . (Registered 14 October 2012).

Topics: 6-Ketoprostaglandin F1 alpha; Aged; Anti-Inflammatory Agents, Non-Steroidal; Blood Pressure; Colorectal Neoplasms; Epoprostenol; Female; Flurbiprofen; Flushing; Hemodynamics; Humans; Hypotension; Infusions, Intravenous; Intraoperative Complications; Laparotomy; Male; Middle Aged; Prospective Studies; Syndrome; Tachycardia

The use of remifentanil is often associated with the observation of mesenteric traction syndrome (MTS) soon after manipulation of the intestine during abdominal surgery. MTS symptoms include facial flushing, hypotension, and tachycardia. In the study reported here, we prospectively investigated the effects of remifentanil on the incidence of MTS in abdominal surgery.. One hundred patients scheduled for abdominal surgery were randomly assigned to two groups. In one group (n = 50), fentanyl alone was used as intravenous analgesic (control, group C); in the second group (n = 50), both fentanyl and remifentanil were used (remifentanil group, group R). In all patients, anesthesia was induced with propofol and rocuronium and then maintained with sevoflurane inhalation. Remifentanil was continuously infused for patients in group R as an analgesic. Plasma concentration of 6-keto-PGF(1α) was measured before surgery and 20 min after the skin incision was made in six patients of group R and seven patients of group C.. MTS occurred in 20 cases in group R (40.0%), but in only five cases in group C (10.0%). In both groups, the incidence of MTS was higher in laparotomy than in laparoscopic surgery. The plasma concentration of 6-keto-PGF(1α) was low in both groups before surgery and was elevated 20 min after skin incision in both groups in patients in whom MTS appeared.. The results of this study suggest that the use of remifentanil in laparotomy facilitates MTS.

Topics: 6-Ketoprostaglandin F1 alpha; Abdomen; Aged; Anesthesia Recovery Period; Anesthesia, General; Anesthetics, Intravenous; Flushing; Hemodynamics; Humans; Hypotension; Intraoperative Complications; Laparotomy; Mesentery; Middle Aged; Piperidines; Prospective Studies; Remifentanil; Splanchnic Circulation; Syndrome; Tachycardia

Our study aimed to determine the role of cyclooxygenase-2 in the release of prostaglandin-(PG)-I2 following mesenteric traction during abdominal surgery. In a prospective double-blind, randomized, placebo-controlled study, 40 patients electively scheduled for non-laparoscopic abdominal surgery, were pretreated with the cyclooxygenase-2 inhibitor parecoxib (n=20) or placebo (n=20). Heart rate, arterial blood pressure, oxygenation ratio and plasma concentrations of the stable PGI2-metabolite 6-keto-PGF1alpha were compared between groups before injection of parecoxib (-40 min), immediately before mesenteric traction (0 min), and 5, 10, and 30 min thereafter. In addition, plasma concentrations of valdecoxib, the active metabolite of the prodrug parecoxib, were determined. Plasma concentrations of 6-keto-PGF1alpha and heart rate increased in both groups after mesenteric traction. There were no significant differences between groups at individual times in heart rate, arterial blood pressure and plasma concentrations of 6-keto-PGF1alpha. Oxygenation ratio decreased after 10 and 30 min following mesenteric traction in the parecoxib group with a significant difference between treatment groups at 10 and 30 min. Plasma concentrations of valdecoxib revealed therapeutic values. Our data indicate that PGI2 release following mesenteric traction is mediated by cyclooxygenase-1.

Topics: 6-Ketoprostaglandin F1 alpha; Abdomen; Blood Pressure; Cyclooxygenase 1; Cyclooxygenase 2 Inhibitors; Double-Blind Method; Epoprostenol; Female; Flushing; Heart Rate; Humans; Hypotension; Intraoperative Complications; Isoxazoles; Laparoscopy; Male; Middle Aged; Oxygen; Prospective Studies; Sulfonamides; Surgical Procedures, Operative; Tachycardia; Time Factors; Treatment Outcome

Mesenteric traction during aortic surgery produces facial flushing, reduced mean arterial pressure (MAP), and systemic vascular resistance (SVR) with increased heart rate (HR) and cardiac index (CI). Elevated 6-keto-prostaglandin-F1 alpha (6-keto-PGF1 alpha) suggests prostacyclin is the mediator. To test this hypothesis, the cyclooxygenase inhibitor, ibuprofen (n = 14), or placebo (n = 13) was administered to patients electively scheduled for aortic reconstruction. The hemodynamic measurements and plasma concentrations of prostanoids between groups were compared immediately before (0), and 5, 10, 15, 30, and 45 min following mesenteric traction. Following mesenteric traction significant differences (P less than 0.05) were observed between the ibuprofen pretreatment and placebo group over time in SVR, MAP, HR, CI, 6-keto-PGF1 alpha, and thromboxane B2 (TXB2). Significant differences between groups at individual times were found in SVR, HR, CI, 6-keto-PGF1 alpha, and TXB2. In the placebo group flushing was accompanied by reduced SVR and MAP and increased HR and CI. The greatest effect was seen at 10 min and resolved over 30 min. Plasma concentration of 6-keto-PGF1 alpha increased from 159 +/- 103 (mean +/- SEM) pg/ml to a peak value of 3,765 +/- 803 at 10 min. A late increase in TXB2 occurred with a peak value of 1,970 +/- 891 (mean +/- SEM) pg/ml at 30 min. In the ibuprofen pretreated group no significant changes occurred in hemodynamic measurements or concentrations of prostanoids. The inhibition of 6-keto-PGF1 alpha and its associated hemodynamic changes in the treatment group, but not in the placebo group, confirms the hypothesis that prostacyclin is the mediator of the mesenteric traction response in abdominal aortic surgery.

Topics: 6-Ketoprostaglandin F1 alpha; Abdomen; Adult; Aged; Aorta; Double-Blind Method; Epoprostenol; Female; Flushing; Hemodynamics; Humans; Ibuprofen; Male; Middle Aged; Premedication; Prospective Studies; Randomized Controlled Trials as Topic; Thromboxane B2

Levels of immunoreactive 6-oxo-prostaglandin F1 alpha (6-oxo-PGF1 alpha) and thromboxane B2 (TXB2) were measured in peripheral venous plasma in a group of volunteers and non-insulin dependent diabetic patients (NIDDS). Levels of these eicosanoids were close to the limit of sensitivity of the radioimmunoassays and consequently data are reported as maximal values. Basal plasma levels of 6-oxo-PGF1 alpha did not exceed 5 pg/ml in either group and maximal levels of immunoreactive TXB2 were 125 +/- 14 and 128 +/- 8 pg/ml for volunteers and NIDDS respectively. Attempts to elicit peripheral vascular prostacyclin biosynthesis in volunteers by using forearm ischaemia produced no increase in plasma 6-oxo-PGF1 alpha levels. Measurement of the combined plasma levels of 6-oxo-PGF1 alpha, 13,14-dihydro-6-oxo-PGF1 alpha, 13,14-dihydro-6,15-dioxo-PGF1 alpha and 6-oxo-PGE1 indicated that these were also low (less than 5 pg/ml) and that failure to demonstrate increased 6-oxo-PGF1 alpha levels was unlikely to have arisen from metabolism of prostacyclin to one or more of these metabolites. Measurement of 6-oxo-PGF1 alpha and TXB2 in peripheral venous plasma before and during chloropropamide alcohol flushing (CPAF) did not provide evidence for a role for these eicosanoids in the etiology of this phenomenon. These findings point to the need for a reappraisal of studies that have described altered plasma levels of 6-oxo-PGF1 alpha and TXB2 in CPAF and other pathophysiological conditions in man.

Topics: 6-Ketoprostaglandin F1 alpha; Adult; Chlorpropamide; Diabetes Mellitus, Type 2; Ethanol; Female; Flushing; Forearm; Humans; Indomethacin; Ischemia; Male; Middle Aged; Radioimmunoassay; Thromboxane B2; Thromboxanes

Topics: 6-Ketoprostaglandin F1 alpha; Adolescent; Adult; Aged; Anesthesia; Arteries; Digestive System Surgical Procedures; Epoprostenol; Face; Female; Flushing; Gastrointestinal Neoplasms; Gastrointestinal Tract; Hemodynamics; Humans; Lasers; Liver; Male; Middle Aged; Monitoring, Intraoperative; Pancreas; Postoperative Complications; Skin; Stomach; Syndrome; Vascular Resistance; Vasodilation; Young Adult

Mesenteric traction syndrome consists of sudden tachycardia, hypotension, and cutaneous hyperemia, and frequently occurs during mesenteric traction in patients undergoing abdominal aortic aneurysm (AAA) reconstructive surgery. The etiology and clinical impact of this phenomenon are unknown, but the symptoms suggest a release of vasoactive materials from the mesenteric vascular bed. Thirty-one patients who underwent AAA surgery were studied. Mesenteric traction was accompanied by a decrease in systolic (p = 0.005) and diastolic (p less than 0.05) blood pressures, and in systemic vascular resistance (p less than 0.005), and was accompanied by an increase in heart rate (HR) (p less than 0.005), and cardiac output (p = 0.01). These hemodynamic changes coincided with an increase (p less than 0.001) in plasma concentrations of 6-keto-prostaglandin F1 (6-K-PGF1). No apparent change was found in prostaglandin E2, thromboxane B2, and histamine concentrations. The concentration of 6-K-PGF1 was correlated with diastolic blood pressure (r = -0.52, p less than 0.005) and HR (r = 0.65, p less than 0.001). Cutaneous hyperemia was observed in 58% of the patients. In an additional six patients, who had taken aspirin daily before AAA surgery, no significant changes were observed in the hemodynamic measurements or 6-K-PGF1 concentrations. These data suggest that mesenteric traction syndrome may be mediated at least in part by a selective release of prostacyclin.

Topics: 6-Ketoprostaglandin F1 alpha; Aged; Aged, 80 and over; Anesthesia, General; Aortic Aneurysm; Epoprostenol; Female; Flushing; Humans; Hypotension; Intraoperative Complications; Male; Mesenteric Arteries; Mesenteric Veins; Middle Aged; Syndrome; Tachycardia; Thromboxane B2

The relation of plasma levels of prostaglandins to the occurrence of flushing induced by niceritrol was investigated. Niceritrol increased plasma levels of PGE2 (p less than 0.01) and 6 keto-PGF1 alpha (p less than 0.05) in 10 male subjects and aspirin reduced the level of PGE2 (p less than 0.01). Five of 10 subjects had flushing, and aspirin reduced flushing in 4 subjects. On the basis of the above study, we treated 35 hyperlipidemic patients with niceritrol in combination with aspirin, investigating the effect of the treatment of serum lipids and postheparin lipolytic activity. None of the 12 cases given aspirin from the start of the treatment experienced flushing, whereas 9 of the 23 cases not given aspirin experienced flushing, which was suppressed by adding aspirin in prescription in all cases except one. Niceritrol decreased serum cholesterol, triglyceride and atherogenic index. It also increased HDL2 cholesterol and decreased HDL3 cholesterol. The LPL activity in postheparin plasma increased in all cases after niceritrol treatment. In conclusion, aspirin increased compliance of niceritrol by reducing the occurrence of flushing probably due to the decreased levels of prostaglandins, yielding favorable results for the long-term treatment of hyperlipidemia with a sufficient doses of niceritrol.

Topics: 6-Ketoprostaglandin F1 alpha; Adult; Aged; Aspirin; Cholesterol; Dinoprostone; Flushing; Humans; Hyperlipidemias; Lipids; Male; Middle Aged; Niceritrol; Nicotinic Acids; Patient Compliance; Prostaglandins; Prostaglandins E