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Query: UMLS:C0016382 (flushing)
 6,387 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Flush is a common side effect of nicotinic acid therapy in patients. The effect is present as long as the level of nicotinic acid increases in the plasma. The mechanism of flush after nicotinic acid has been studied in the ears of guinea-pigs in vivo. The threshold dose of nicotinic acid (1-3 mg/kg) to raise the skin temperature of the ears and to increase the cyclic AMP level of this tissue was similar. Indomethacin and acetylsalicylic acid which inhibit the synthesis of prostaglandins markedly reduce the duration and intensity of the flush. In isolated slices from guinea-pig ears, nicotinic acid increased the level of cyclic AMP; this effect was inhibited by indomethacin. The stimulating action of prostaglandin E1 on the cyclic AMP level of the ear slices was not inhibited by indomethacin. Since administration to man of both cyclic AMP and prostaglandin E1 produces flush it is suggested that nicotinic acid may induce flush by the formation of some prostaglandin which then increases the formation of cyclic AMP.
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PMID:Studies on the mechanism of flush induced by nicotinic acid. 19 86

We examined the hypothesis that the degree of inflation of the lungs at the time of harvest may have an important role in postpreservation function. Lungs of donor dogs randomly assigned to groups 1 (n = 5) and 2 (n = 5) were ventilated with large tidal volumes (tidal volume, 25 ml/kg; positive end-expiratory pressure, 5 cm H2O; respiratory rate, 12 breaths/min, inspired oxygen fraction 1.0) and were inflated to 30 cm H2O for 15 seconds before pulmonary artery flush and again immediately before tracheal crossclamping. In group 3 (n = 5) donor lungs were normally ventilated (tidal volume, 12.5 ml/kg, positive end-expiratory pressure 0 cm H2O; respiratory rate 12 breaths/min, inspired oxygen fraction, 1.0) and were not hyperinflated before pulmonary artery flushing; the trachea was crossclamped at end-inspiration. In groups 1 and 3 a large bolus (25 micrograms/kg) of prostaglandin E1 was injected into the pulmonary artery before flushing and was also added to the pulmonary artery flush solution (500 micrograms/L). A rapid (approximately 50 seconds), high-volume mm Hg), hypothermic (4 degrees C) pulmonary artery flush was performed in all hypothermic (4 degrees C) pulmonary artery flush was performed in all groups with modified Euro-Collins solution. Heart-lung blocks were stored at 4 degrees C for approximately 29 hours before left single lung allografting. An inflatable cuff was placed around the recipient right pulmonary artery, allowing independent study of the transplanted lung. Hyperinflated lungs harvested with or without prostaglandin E1 provided equivalently excellent early posttransplant function (arterial oxygen tension [mean +/- standard deviation]: group 1; 503 +/- 45, vs group 2; 529 +/- 150 mm Hg; inspired oxygen fraction 1.0). Mean arterial oxygen tension was significantly lower in group 3 (116 +/- 78 mm Hg) than in either groups 1 or 2 (p < 0.0002 for either comparison). Copious reperfusion pulmonary edema was a constant feature in group 3 but was not seen in groups 1 and 2. All 10 recipients in groups 1 and 2 survived the 3-day assessment period without difficulty; two of the five recipients in group 3 died during initial unilateral perfusion of the transplanted lung. Donor hyperventilation and inflation to 30 cm H2O before hypothermic storage can help provide excellent posttransplantation lung function after 30-hour preservation, with or without prostaglandin E1 pretreatment. We speculate that this improvement may be due to effects of increased lung volume on pulmonary vascular tone and/or surfactant metabolism.
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PMID:Reliable thirty-hour lung preservation by donor lung hyperinflation. 140 66

The study aimed to compare the intraoperative hemodynamic changes during orthotopic liver transplantation (OLT) with those during heterotopic liver transplantation (HLT) after different durations of cold storage of the graft. The effect of prostaglandin E1 (PGE1) on these parameters was also studied. Sixty-nine female Yorkshire pigs underwent either OLT (n = 32) or HLT (n = 37) with a graft stored for 2 hr (n = 31), 24 hr (n = 16), 48 hr (n = 7), or 72 hr (n = 15). In 16 transplantations in the various groups, PGE1 was given intravenously to both donor and recipient animals and it was added to the preservation and flushing solutions. Univariate nonparametric tests (Mann-Whitney and Wilcoxon rank-sum) were used for analysis of cardiac output (CO), mean arterial pressure (MAP), left and right ventricular minute work (LVMW, RVMW), pulmonary capillary wedge pressure (PCWP), and systemic and pulmonary vascular resistance (SVR, PVR), at different intervals during the operative procedure. For the three main variables--i.e., the type of transplantation, the use of PGE1, and the preservation time, multiple regression analysis was performed. During HLT, portal vein clamping lowered MAP and CO, while during the anhepatic phase in OLT, SVR increased and CO dropped. After recirculation of the graft, an increase in PVR and a decrease in SVR were found in both OLT and HLT. At different stages of the surgical procedure, longer graft storage time diminished CO and MAP (P less than 0.001), especially in OLT. PGE1 appeared to reduce the cardiovascular reserves needed to compensate the changes after recirculation of the graft. The observed differences in intraoperative hemodynamics between OLT and HLT can partly be attributed to differences in operative techniques. Extension of the graft preservation period resulted in poor cardiac performance, more so in OLT than HLT. The native liver in HLT might be able to metabolize the presumed myocardial depressant factors, released by the graft upon reperfusion. Prostaglandin E1 did not protect against the reperfusion syndrome.
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PMID:The effects of long-term graft preservation and prostaglandin E1 on intraoperative hemodynamic changes in liver transplantation. A comparison between orthotopic and heterotopic transplantation in the pig. 141 21

The role of prostaglandin E1 (PgE1) and prostacyclin in enhancing the ischemic tolerance of single-lung grafts was investigated. Fifteen donor dogs underwent pulmonary artery flushing with 60 mL/kg of 4 degrees C modified Euro-Collins solution; 5 dogs each received a 15-minute infusion of PgE1, prostacyclin, or saline solution before flushing. After 12 hours of storage at 4 degrees C, left lung transplantation was performed in 15 recipient dogs. Measurements were performed after 10 minutes of right pulmonary artery snaring before transplantation, after transplantation, and after 2, 4, and 6 hours of reperfusion. At 6 hours, the oxygen tensions (on 100% O2) were 478 +/- 64, 296 +/- 75, 79 +/- 12, and 71 +/- 23 mm Hg in control (nontransplanted), prostacyclin-, PgE1-, and saline-treated dogs, respectively (p less than 0.05, prostacyclin or control versus saline and PgE1 dogs). Mean pulmonary artery pressures increased within each group during reperfusion, but were not significantly different among groups. Similarly, peak inspiratory pressures and wet weight to dry weight ratios were not significantly different among groups after 6 hours of reperfusion. We conclude that donor pretreatment with prostacyclin is associated with superior oxygen transfer in canine lung allografts after 12 hours of cold storage, transplantation, and 6 hours of reperfusion. In this model, donor pretreatment with PgE1 conferred no benefit to prolonged lung allograft preservation.
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PMID:Prolonged preservation of canine lung allografts: the role of prostaglandins. 202 3

The present study was performed in order to explore the influence of ova present within rat oviducts on: a) tubal spontaneous motility and b) oviduct prostaglandin production. It was found that the isometric developed tension (IDT) of tubes isolated from proestrous rats (preovulatory oviducts) was significantly higher (P less than 0.01) than the IDT of tubes from rats at estrus and at metestrus (postovulatory oviducts). After flushing the oviducts with KRB solution (i.e., after removing existing ova) the IDT of the oviducts obtained from estrous rats increased significantly (P less than 0.01), whereas the IDT of tubes isolated from proestrous rats (i.e., preparations without ova) was not modified. On the other hand, isolated tubes containing their corresponding ova released into the suspending solution significantly more PGE1 than PGE2 or PGF2 alpha (P less than 0.005). It was particularly interesting to find that after flushing the oviducts, tissue production of PGE1, PGE2 and PGF2 alpha was similar. Finally, when dose response curves for PGE1 and for PGE2 on the spontaneous contractions of oviducts isolated from rats at proestrus, estrus and metestrus were constructed, both PGs evoked an inhibitory inotropic action. The ED50 for PGE1 in tubes from estrous rats was significantly smaller (P less than 0.01) than that for metestrous animals but significantly greater (P less than 0.01) than that observed in oviducts from proestrous rats. The ED50 for PGE2 did not change in the different tested periods of the sex cycle. Results reported herein suggest the possibility that the ova present within rat oviducts, may influence their own transport along the tubes by modifying the amount of prostaglandins produced by the oviducts or via their own prostaglandin synthesis.
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PMID:Influence of ova within rat oviducts on spontaneous motility and on prostaglandin production. 225 Dec 92

Using cardiopulmonary bypass to cool the graft and flushing the lungs with cold crystalloid solution are the most popular methods for clinical cardiopulmonary preservation. Heart-lung transplantation was carried out in 11 cynomolgus monkeys. Donor cardiac preservation was achieved with cold crystalloid cardioplegic solution (10 ml per kilogram of body weight) in all animals. Lung preservation was achieved with a rollerhead pump and by cooling (12 degrees C) the donor in one group of 4 animals (deep hypothermia group) and infusing cold (4 degrees C) modified Euro-Collins solution (15 ml/kg X 4 minutes) into the main pulmonary artery of 7 donors pretreated with prostaglandin E1 (PGE1) (PGE1 group). PGE1 was given intravenously (0.5 to 4.0 micrograms/kg/min) beginning 15 minutes prior to aortic cross-clamping and was continued during administration of the pulmonary cooling solution. In the deep hypothermia group, no pharmacotherapy was used. Grafts were stored at 4 degrees C for about 6 hours. After heart-lung transplantation, arterial blood gases were measured on 40% inspired oxygen and 2 to 3 cm of positive end-expiratory pressure, and were significantly higher in the PGE1 group than the deep hypothermia group after 8 hours of reperfusion (p = 0.04). The partial pressure of arterial oxygen decreased significantly during the 8 hours of reperfusion in the deep hypothermia group (153 to 108 mm Hg; p = 0.01) and increased in the PGE1 group (189 to 218 mm Hg;p = 0.0002). Eighty-six percent of the animals in the PGE1 group survived more than 24 hours (p = 0.03). There were no survivors in the deep hypothermia group.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Donor deep hypothermia or donor pretreatment with prostaglandin E1 and single pulmonary artery flush for heart-lung graft preservation: an experimental primate study. 314 74

The in vivo rabbit ileum was used to study the relationship of cholera enterotoxin-induced water and electrolyte secretion and mucus secretion and to determine whether the enterotoxin influenced the intestinal mucus blanket. In experiments in which luminal fluid viscosity was used to assess mucus secretion, it was found that while cholera enterotoxin induced a sustained secretion of water and electrolytes, the toxin-induced mucus hypersecretion was short lived (3 to 5 h) and subsequent exposure of the mucosa to cholera enterotoxin or prostaglandin E1 did not stimulate mucus secretion further. Dibutyryl cyclic AMP and theophylline caused a modest mucus secretion in ileal loops which differed from that of cholera enterotoxin in both magnitude and in the fact that the mucus secretion occurred 2 to 3 h after the onset of water and electrolyte secretion. An oral replacement solution was used in the ileum to reduce the enterotoxin-induced loss of water and electrolytes into the lumen. While such a solution slowed the appearance of acidic glycoprotein in the intestinal lumen, it did not change the amount of glycoprotein secreted over a 7-h period, suggesting that toxin-induced mucus secretion was not simply due to a flushing action of the experimentally caused diarrhea. To assess mucus blanket thickness, neutral glycoprotein was recovered from the blanket of rabbit ileal loops 7 h after exposure to cholera enterotoxin and the thickness of the mucus blanket was measured directly 4 and 18 h after toxin exposure. Both methods indicated that even though cholera enterotoxin-induced mucus hypersecretion had subsided and there was histological evidence of goblet cell mucin depletion, there was a sustained increase in mucus blanket thickness that was detectable for at least 18 h after mucosal enterotoxin exposure.
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PMID:Cholera enterotoxin-induced mucus secretion and increase in the mucus blanket of the rabbit ileum in vivo. 316 91

Platelet concentration was measured in samples from the various components of a bloodflow circuit, including the reservoir, the tube (with i.d. between 50 and 210 micron), and the discharge. The tube sample was collected by halting the flow and then flushing out a length of tube; thus, this sample collected equally from all radial locations. As the discharge sample was well mixed, it reflected the velocity field in the tube. Each reservoir sample was a traditional bulk collection. To ensure that the results represented the physical effects of flow on regional platelet concentration and could be interpreted with simple mass balance relationships, strong anticoagulation (sodium citrate and heparin) and platelet inhibition (prostaglandin E1) were used. Results for all tube diameters and for reservoir hematocrits from 5.5 to 77% and wall shear rates from 80 to 8000 sec-1 show that tubular platelet concentration is greater than reservoir or discharge platelet concentrations, which are equal. For platelet-rich plasma the tubular platelet concentration is decreased compared to the reservoir or discharge values. Mass balances show that the elevated tubular platelet concentration is due to an excess of platelets in radial locations with below average speeds; coupled with the need for red cells, this suggests that excess platelets have a near-wall location. Nonparametric statistical tests show that wall shear rate is a significant variable at a 0.05 confidence level; inner diameter is not found to be a significant variable, probably because of the limited diameter range studied and the experimental errors involved in determining platelet concentrations.
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PMID:Regional platelet concentration in blood flow through capillary tubes. 376 31

Available published material of adverse reactions to prostaglandins (PGs) at various dosages routes and levels is reviewed. Animal studies are of 2 kinds: studies of pharmacological effects and studies of toxicological reactions (i.e., acute dose levels). The pharmacology of PGs show the drugs have 3 areas of action: 1) smooth muscle effects, either contraction or relaxation (cardiovascular effects and reproductive tract; relaxation of vascular smooth muscles by some PGs and contraction by others); 2) nervous system effects; and 3) lipid and carbohydrate metabolism. In humans, PGE1 was administered intravenously and it was found that adverse effects were related to rate of administration rather than to total dose; side effects included flushing, headache, visual disturbances, and restlessness, factors which might suggest a correlation with central nervous system effects (as found in animal studies). PGE1 administered at acute doses orally, by inhalation, and intradermally show effects attributable to gastrointestinal disturbances, respiratory problems, and erythematous responses. In general, studies in humans of other PGs have found similar adverse reactions, all of which are explained by known mechanisms of action of PGs. Dose levels constituting acutity are dependent on route (i.e., oral doses are much higher than intravenous doses), with rapid intravenous infusion causing the most adverse reactions.
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PMID:Toxicology of the prostaglandins. 421 9

In a study of 32 patients, there were 29 cases of intra-uterine fetal death and 3 cases of hydatidiform mole. The intravenous administration of either prostaglandin E1, E2 or F2 successfully induced labor in 29 out of the 32 cases. 2 patients delivered following additional intravenous oxytocin and there was 1 failure due to the development of upper limb cyanosis. Side-effects included vomitng, phlebitis, facial flushing, rigors, pyrexia and uterine hypertonus. The method confirms the high success rates reported previously but the incidence of side-effects was disturbing. It is emphasized that prostaglandin E1 was used during this original research trial when prostaglandins were 1st investigated clinically. Prostaglandin E1 has not been made available commerically.
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PMID:Induction of labour and abortion by intravenous prostaglandins in pregnancies complicated by intra-uterine foetal death and hydatidiform mole. 444


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