dinoprost and Escherichia-coli-Infections

Uterine infections are a major reproductive problem in livestock. We conducted two experiments to investigate factors that may modulate uterine responses to infectious bacteria. In Exp. 1, ewes received intrauterine inoculations of either saline or bacteria (75 x 10(7) cfu of Actinomyces pyogenes and 35 x 10(7) cfu of Escherichia coli) on either d 0 or 7 of the estrous cycle. Vena caval samples containing uteroovarian blood were collected twice daily from 12 h before until 6 d after inoculation. Only ewes inoculated with bacteria on d 7 developed infections. Basal (4.8 vs .4 pmol), lipopolysaccharide-stimulated (14.2 vs 6.1 pmol), and concanavalin A-stimulated (65.8 vs 21.6 pmol) blastogenesis (i.e., [3H]thymidine incorporation) of vena caval lymphocytes was greater (P < or = .002) for ewes inoculated with bacteria or saline on d 0 rather than on d 7. The number (per 100 white blood cells) of lymphocytes was greater (41.3 vs 30.8, P < .001) and that of neutrophils was less (42.5 vs 51.6, P < .001) in ewes inoculated on d 0 rather than d 7. Bacteria increased (P < .05) vena caval PGF(2 alpha) but not PGE2 concentrations. In Exp. 2, two protein fractions (molecular weights of > or = 100 kDa and approximately 12.7 kDa) from chromatography of uterine flushings collected on d 0 or 7, or 18 d after ovariectomy on d 0 or 7, modulated phytohemagglutinin-stimulated blastogenesis; the heavier fraction from d 0 had a stimulatory component, but the major effects of the fractions were inhibitory. The differences in immune function and regulation between d 0 and 7 probably explain how the uterus of follicular phase ewes was able to prevent the development of an infection.

Topics: Actinomyces; Actinomycosis; Animals; Dinoprost; Dinoprostone; Eosinophils; Escherichia coli; Escherichia coli Infections; Estrogens; Estrus; Female; Follicular Phase; Luteal Phase; Lymphocyte Activation; Lymphocytes; Monocytes; Neutrophils; Progesterone; Sheep; Sheep Diseases; Time Factors; Uterine Diseases; Uterus

Chronic, subclinical intramammary infection depresses fertility. We previously found that 30% of subclinical mastitic cows exhibit delayed ovulation, low circulating estradiol levels, and delayed luteinizing hormone surge. We examined the function of preovulatory follicles of cows experiencing subclinical mastitis or a past event of acute clinical mastitis. Cows were diagnosed for mastitis by somatic cell count and bacteriological examination. All clinical infections were caused by Escherichia coli, and most subclinical infections were caused by Streptococcus dysgalactiae and coagulase-negative staphylococci. On day 6 of the cycle, cows received PGF2α; 42 h later, follicular fluids and granulosa cells or theca cells were aspirated from preovulatory follicles in vivo or following slaughter, respectively. Overall, follicular estradiol and androstenedione concentrations in the subclinical group (n = 28) were 40% lower (P < 0.05) than those in uninfected cows (n = 24) and lower than in past clinical mastitic cows (n = 9). Distribution analysis revealed a clear divergence among subclinical cows: one-third (9/28) exhibited low follicular estradiol; the other two-thirds had normal levels similar to all uninfected (P < 0.01) and most clinical cows (P < 0.08) that had normal follicular estradiol levels. Subclinical normal-estradiol cows had twofold higher (P < 0.05) circulating estradiol concentrations and sevenfold and fourfold higher (P < 0.05) follicular androstenedione levels and estradiol-to-progesterone ratio, respectively, than subclinical low-estradiol cows. Follicular progesterone level was not affected. Reduced expression (P < 0.05) of LHCGR in theca and granulosa cells, CYP11A1 (mRNA and protein) and CYP17A1 in theca cells, and CYP19A1 in granulosa cells may have contributed to the lower follicular steroid production in the subclinical low-estradiol subgroup. StAR and HSD3B1 in theca cells and FSHR in granulosa cells were not affected. Mastitis did not alter follicular growth dynamics, and no carryover effect of past clinical mastitis on follicular function was detected. These data indicate that a considerable proportion (one-third) of subclinical mastitic cows have abnormal follicular steroidogenesis, which can explain the reproductive failure associated with this disease.

Topics: Animals; Base Sequence; Cattle; Dinoprost; Escherichia coli; Escherichia coli Infections; Female; Gene Expression; Mammary Glands, Animal; Mastitis, Bovine; Membrane Proteins; Ovarian Follicle; Staphylococcal Infections; Staphylococcus; Steroid Hydroxylases; Steroids; Streptococcal Infections; Streptococcus

Escherichia coli (E. coli) is the most frequent bacterium isolated in cases of cystic endometrial hyperplasia-pyometra complex, the most frequent endometrial disorder in the bitch. Toll-like receptors (TLRs) play an essential role in the innate immune system. The aim of this study was to compare transcription of genes encoding TLR2, TLR4 and LPS ligands (CD14, MD-2, LBP), prostaglandin synthesis enzymes (COX1, COX2, PGES1 and PGFS), and to compare COX1 and COX2 protein expression and PGE(2) and PGF(2alpha) endometrial content in the endometrium of canine diestrous uteri with (n=7) or without (n=7) pyometra. All cases of pyometra were hyperplastic and E. coli was the only isolated bacteria, while diestrous normal uteri did not present signs of cystic endometrial hyperplasia and were negative for bacteriology. Except for COX1, transcription of all genes was significantly higher in pyometra than in normal endometria. COX1 protein was observed in both normal and pyometra uteri, but COX2 protein was only present in pyometra cases. Endometrial PGE(2) and PGF(2alpha) content were significantly higher in pyometra than in normal diestrous endometria. In conclusion, data obtained in this study provides evidence that pyometra-isolated E. coli induces the up-regulation of TLR2 and TLR4 genes in the canine diestrous endometrium. This up-regulation, which is probably the result of the stimulation by LPS and lipoprotein E. coli constituents, leads to the endometrial up-regulation of PG synthesis genes. This, in turn, results in a higher endometrial concentration of PGE(2) and PGF(2alpha), which may further regulate the local inflammatory response.

Topics: Acute-Phase Proteins; Animals; Carrier Proteins; Cyclooxygenase 1; Cyclooxygenase 2; Dinoprost; Dinoprostone; Dog Diseases; Dogs; Endometrial Hyperplasia; Escherichia coli; Escherichia coli Infections; Female; Gene Expression Regulation; Lipopolysaccharide Receptors; Lipopolysaccharides; Lymphocyte Antigen 96; Membrane Glycoproteins; Pyometra; Toll-Like Receptor 2; Toll-Like Receptor 4; Transcription, Genetic; Up-Regulation; Uterus

The aim of this study was to determine the prostaglandins (PGs) production and ovarian function in gilts after intrauterine infusions of 10(6) and 10(9) colony-forming units (cfu)/ml of Escherichia coli (E. coli). In Experiments 1 and 2, 30 ml of saline or 30 ml of E. coli suspension containing 10(6) or 10(9)cfu/ml, were infused once into each uterine horn in three groups of gilts on day 3 of the estrous cycle, respectively. In Experiment 1, 17 days after treatment it was revealed that inoculation of E. coli 10(9)cfu/ml induced severe acute or subacute endometritis while 10(6)cfu of E. coli evoked moderate acute endometritis or resulted in no inflammatory changes. In the gilts receiving 10(9)cfu/ml of E. coli, the concentration of 13,14-dihydro-15-keto-PGF(2)alpha in blood from the jugular vein was elevated (P<0.05-0.001) compared to concentration in the gilts inoculated with 10(6)cfu on days 8-17 after treatment. Both the E. coli-treated groups had a lower (P<0.05, P<0.01) progesterone plasma level from days 10 to 14 after administration than the control group. On day 17 of the study, infusion of E. coli 10(9)cfu/ml, in comparison to 10(6)cfu, resulted in the greater (P<0.001) content of PGE(2) in the myometrium. The content of both PGs in the endometrium as well as PGF(2alpha) in the myometrium of gilts-treated with 10(9)cfu/ml of E. coli was lower (P<0.001) than in gilts-treated with 10(6)cfu of bacteria. Newly formed corpora lutea were found in the gilts infused with 10(6), but not those infused with 10(9)cfu/ml of E. coli on day 17 after infusion. On day 8 of the study (Experiment 2), the blood from utero-ovarian vein of the gilts-treated with 10(9)cfu/ml of bacteria had a higher (P<0.05) PGF(2alpha) level and lower (P<0.001) PGE(2) level than following infusion of E. coli 10(6)cfu/ml. Also on day 8 of the study, the content of PGE(2) in the endometrium, both the PGs in the myometrium as well as cyclooxygenase-2 in the endometrium and myometrium was greater (P<0.01, P<0.001) after applying 10(9)cfu/ml than 10(6)cfu/ml of E. coli. These results indicate that intrauterine infusions of 10(6) or 10(9)cfu/ml of E. coli lead to the development of inflammatory states of different intensities which is connected with different PGF(2alpha) and PGE(2) production and function of ovaries.

Topics: Animals; Colony Count, Microbial; Dinoprost; Endometritis; Escherichia coli Infections; Female; Ovary; Random Allocation; Swine; Swine Diseases

To characterize oestrus-related factors affecting the induction of and recovery from pyometra in bitches, 60 clinically healthy beagle bitches were used for induction of pyometra by inoculation of Escherichia coli into the uterus during oestrous and metoestrous stages. The animals were classified into the following six groups according to inoculation time: Days 1-10, 11-20, 21-30, 31-40, 41-50 and 51-60 after LH surge. The incidence of pyometra during the periods Days 11-20 and 21-30 after LH surge was 90.9% and 78.9% respectively, while that during Days 1-10 and 51-60 after LH surge was less than 20%, and the patterns of the incidence of pyometra and the serum progesterone levels were similar. There was no difference in the incidence of pyometra induced in bitches less than 5 years old compared to bitches over 6 years old. Oestrus in all of the bitches with pyometra induced by E. coli returned with or without PGF 2alpha treatment, unlike in bitches with spontaneous pyometra. The duration of the oestrous cycle in the non-treated and PGF 2alpha-treated groups was 231.4+/-55.2 days and 162.1+/-40.6 days (P < 0.001), respectively, and there was no difference in the rate of return of oestrus between the two groups. The conception rate in all of the bitches in which oestrus had returned was 81.8%. The above findings indicate that the period during which severe pyometra could be induced was limited to the early stage in metoestrus.

Topics: Animals; Animals, Newborn; Dinoprost; Dog Diseases; Dogs; Escherichia coli; Escherichia coli Infections; Estrus; Female; Litter Size; Luteinizing Hormone; Male; Parasympatholytics; Pregnancy; Progesterone; Pyrrolidines; Random Allocation; Uterine Diseases

In sheep and cattle, the postpartum uterus is resistant to bacterial challenge until after corpora lutea develop. A 2 x 2 factorial arrangement of treatments was used to determine whether prostaglandins may mediate the effects of progesterone in transforming the postpartum uterus from resistant to susceptible. On d 14 postpartum, ewes (n = 6/group) were ovariectomized or sham ovariectomized, and the vena cava was catheterized for daily collection of uteroovarian-enriched blood. From d 15 to 20, ewes received twice daily intramuscular injections of progesterone in sesame oil or plain sesame oil. On d 20, each uterus received 75 x 10(7) cfu of Arcanobacterium pyogenes and 35 x 10(7) cfu of Escherichia coli. Uteri were collected on d 25 and examined for signs of infection. For each blood sample, unstimulated and mitogen-stimulated lymphocyte proliferation was measured as [3H]thymidine incorporation, smears were prepared for differential white blood cell (WBC) counts, and progesterone, prostaglandin F2alpha, (PGF2alpha), and prostaglandin E2 (PGE2) were quantified. All 12 progesterone-treated, but only two of the 12 oil-treated, ewes developed uterine infections (P < 0.001). Progesterone treatment increased (P < 0.001; 3.1 vs 1.5 ng/mL) and ovariectomy decreased (P < 0.001; 3.7 vs 0.9 ng/mL) vena caval progesterone. Progesterone treatment reduced (P < 0.01) PGF2alpha, (303.9 vs 801.3 pg/mL), and PGF2alpha was greater (P < 0.05) before than after inoculation (626.4 vs 478.8 pg/mL). The PGE2 concentration was greater in progesterone-treated, ovary-intact ewes than in ewes in the other groups (ovariectomy x progesterone treatment; P < 0.01). Ovariectomy increased (P < 0.005; 4.4 vs 2.9 pmol) and progesterone treatment decreased (P < 0.05; 3.2 vs 4.1 pmol) concanavalin A-stimulated lymphocyte proliferation. Ovariectomy increased lipopolysaccharides-stimulated proliferation (P < 0.05; 2.4 vs 1.9 pmol). For neutrophils per 100 WBC, the ovariectomy x progesterone and progesterone x period interactions were significant (P < 0.01). The ovariectomy x progesterone interaction was significant (P < 0.01) for lymphocytes per 100 WBC. Ovariectomy decreased monocytes (P < 0.001; 10 vs 13) and increased eosinophils (P < 0.001; 10 vs 5) per 100 WBC. Progesterone makes the postpartum uterus in ewes susceptible to infection, but ovariectomy allows ewes to remain resistant; uterine prostaglandins may mediate this change. This model creates opportunities to determine the mechanism

Topics: Actinomycetales Infections; Animals; Dinoprost; Dinoprostone; Disease Susceptibility; Escherichia coli Infections; Female; Ovariectomy; Postpartum Period; Progesterone; Puerperal Infection; Random Allocation; Sheep; Sheep Diseases; Uterine Diseases; Uterus

Topics: Animals; Anti-Bacterial Agents; Dinoprost; Dog Diseases; Dogs; Escherichia coli Infections; Female; Leukocyte Count; Polyuria; Suppuration; Urinalysis; Uterine Diseases

Retinols seem to be of clinical importance in ameliorating the clinical consequences of septic shock. These beneficial effects of retinols are suggested to be due to an antioxidant property. The present study was undertaken in order to confirm or rule out such an effect of retinol palmitate (RP) in experimental septic shock by measuring F2-isoprostanes and a major prostaglandin F2 alpha metabolite as indicators of oxidative injury and inflammatory response, respectively.. Fourteen anaesthetised pigs were randomly given an injection of RP (2.300 IU x kg-1) or the corresponding volume of vehicle. All pigs received a continuous infusion of E. coli endotoxin (10 micrograms x kg-1 x h-1). Blood samples were analysed for lipid peroxidation products (8-iso-PGF2 alpha), indicating free radical induced oxidative injury and 15-keto-dihydro-PGF2 alpha indicating cyclooxygenase-mediated inflammatory response).. Significantly elevated levels of 8-iso-PGF2 alpha were seen at 3, 5 and 6 hours of endotoxaemia in the vehicle + endotoxin group as compared to RP + endotoxin group. Endotoxin induced cyclooxygenase-mediated inflammatory response was not affected by RP.. This study is the first one to show that RP counteracts oxidative injury rather than inflammatory response in experimental septic shock. These results may be of importance for the understanding of some beneficial effects of RP during endotoxaemia (i.e. improved systemic haemodynamics and reduced serum levels of endotoxin). Our results may explain the therapeutic effects of nutrients rich in caroten/retinols used in some clinical studies.

Topics: Analysis of Variance; Animals; Antioxidants; Dinoprost; Disease Models, Animal; Diterpenes; Endotoxins; Escherichia coli Infections; F2-Isoprostanes; Female; Inflammation; Lipid Peroxidation; Male; Oxidative Stress; Radioimmunoassay; Random Allocation; Retinyl Esters; Shock, Septic; Swine; Vitamin A

Human septic shock can be replicated in the endotoxaemic pig. Endotoxaemia causes a multitude of events, including reduced PaO(2) and increased lipid peroxidation. This study was designed to evaluate the possible effects of a commonly used anaesthetic drug with known antioxidant properties (propofol) during porcine endotoxaemia.. Ten pigs were anaesthetised and given a 6 h E. coli endotoxin infusion. The animals received, randomly, a supplementary continuous infusion of propofol emulsion (containing 0.005% EDTA) or the corresponding volume of vehicle (controls). Pathophysiologic responses were determined. Non-enzymatic (by measuring plasma 8-iso-PGF(2 alpha) and enzymatic (by measuring plasma 15-keto-dihydro-PGF(2 alpha)) lipid peroxidations were evaluated. Plasma levels of the endogenous antioxidants alpha- and gamma-tocopherols, were also analysed.. Endotoxaemia increased plasma levels of 8-iso-PGF(2 alpha) (1st-4th h) and 15-keto-dihydro-PGF(2 alpha) (1st-4th h) significantly more in controls than in the propofol+endotoxin group. PaO(2) was significantly less affected by endotoxin in the propofol treated animals (2nd-4th h). Mean arterial pressure (4th-6th h) and systemic vascular resistance (6th h) were reduced significantly more by endotoxin among the propofol-treated animals. Vitamin E (alpha-tocopherol) increased in all animals, significantly more in the propofol+endotoxin group (1/2-6th h) than in the control group.. Propofol reduced endotoxin-induced free radical mediated and cyclooxygenase catalysed lipid peroxidation significantly. The implication is that propofol counteracts endotoxin-induced deterioration of PaO(2).

Topics: Anesthetics, Intravenous; Animals; Dinoprost; Endotoxemia; Escherichia coli Infections; F2-Isoprostanes; Inflammation; Lipid Peroxidation; Oxidative Stress; Propofol; Radioimmunoassay; Shock, Septic; Swine; Vitamin E

This study investigates the plasma levels of 8-iso-PGF2alpha, a non-enzymatic, and 15-K-DH-PGF2alpha, a cyclooxygenase catalyzed oxidation product of arachidonic acid in an experimental porcine endotoxemic shock model. A significant (P < 0.001) and rapid appearance and disappearance of PGF2alpha metabolite after endotoxin infusion was very similar in both non-survival and survival groups indicating an acute progression and recession of inflammation. When oxidative injury was assessed by measuring free 8-iso-PGF2alpha the levels in plasma increased significantly up to 2 h and remained at this level until death among the non-survivors. This was apparently different from the survivors where the 8-iso-PGF2alpha levels increased to its height at 1 h, then decreased to the basal levels after 5 h. Thus, free radical and cyclooxygenase catalyzed oxidation of arachidonic acid occurs during endotoxemia. Free radical dependent oxidative injury following endotoxin induced inflammation may be the major cause of organ failure and increased mortality.

Topics: Animals; Arachidonic Acid; Biomarkers; Dinoprost; Endotoxemia; Escherichia coli Infections; F2-Isoprostanes; Female; Inflammation; Male; Oxidative Stress; Radioimmunoassay; Shock, Septic; Survival Analysis; Swine; Time Factors

The effects of bacteria on in vitro ureteric contractility were studied, using a model which allowed selective exposure of organisms to the ureteric mucosa and smooth muscle, respectively. A cannula attached to a pressure transducer was ligated into the proximal lumen of 2.5-cm segments of canine ureter. The distal ureter was ligated to form a closed pressure monitored system, and the segment suspended in a 20-ml organ bath containing Krebs Henseleit buffer at physiological pH and temperature. Following onset of spontaneous activity, broths of Escherichia coli, Proteus mirabilis, Pseudomonas aeruginosa and Staphylococcus aureus were added to either the buffer solution or ureteric lumen in doses of > 10(6) organisms/ml. Experiments were repeated using heat-killed organisms, bacterial filtrates and E. coli endotoxin. Ureteric contractility was stimulated by organisms added to the buffer medium, but reversibly inhibited by bacteria placed in the ureteric lumen. Heat-killed organisms, endotoxin and live filtrates had no effect on normal motility when exposed to either the ureteric mucosa or muscularis respectively. These findings reflect the conflicting changes in ureteric motility seen in vivo when bacteria are administered systemically or directly into the ureteric lumen.

Topics: Animals; Bacterial Infections; Dinoprost; Dogs; Endotoxins; Escherichia coli Infections; Gentamicins; Histamine; Muscle Contraction; Organ Culture Techniques; Staphylococcal Infections; Ureter; Urinary Tract Infections

In hypermetabolic sepsis, gluconeogenesis is markedly elevated during fasting, and is manifested as an increased rate of glucose appearance (Ra). The likely causes of such a change are alterations in 1) concentration of systemic hormones, 2) concentration of glucose precursors, especially lactate, 3) activity of the key enzymes of the pathway, and 4) hormone receptors and/or transmembrane signalling mechanisms, involved in the hormonal regulation of the pathway. In this study, we investigated the importance of the latter two factors in the increase of gluconeogenesis during hypermetabolic sepsis. Rats were rendered septic by repeated subcutaneous administration of live Escherichia coli. The livers were perfused in vitro in a nonrecirculating mode to measure the rate of gluconeogenesis from saturating concentrations of lactate (5 mM) or lactate (5 mM) + pyruvate (0.5 mM), and the response of gluconeogenesis to vasopressin (VP, 0.1 and 1.0 nM), glucagon (Glc, 0.1 and 1.0 nM), and prostaglandin (PG) F2 alpha (5 microM). The rate of gluconeogenesis without precursor supply was approximately 20-30 mumoles/100 g b w/hr during the first 4-6 min of perfusion, followed by a continuous decline to very low levels. Infusion of lactate (5 mM) or lactate (5 mM) + pyruvate (0.5 mM) increased glucose output, and maintained it at approximately 100-110 and approximately 130-140 mumoles/100 g b w/hr, respectively. VP, Glc, and PGF2 alpha stimulated the rate of gluconeogenesis in a dose-dependent manner (VP and Glc). No differences were observed between control and septic rats using these stimuli.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Animals; Dinoprost; Disease Models, Animal; Escherichia coli Infections; Glucagon; Gluconeogenesis; Hormones; In Vitro Techniques; Injections, Subcutaneous; Kinetics; Liver; Male; Perfusion; Rats; Rats, Sprague-Dawley; Vasopressins

Bacterial infection has been implicated in premature labor in humans. To elucidate mechanisms and potential intervention strategies, we sought to develop a model of infection-induced pregnancy loss in rabbits. On day 21 (70% of gestation), each uterine horn was inoculated hysteroscopically with 0.2 ml containing saline solution of 10(6) cfu Escherichia coli or Bacteroides bivius or Fusobacterium necrophorum. Fetal viability was assessed. Animals were sacrificed at various times or as delivery occurred. Serum progesterone and amniotic fluid prostaglandins were measured. Cultures and histologic sections were prepared. Compared with the saline solution group, E coli and F. necrophorum-inoculated rabbits were significantly more likely to deliver (16 of 16 and six of seven with mean times of 31.9 +/- 10.7 and 28.3 +/- 11.5 hours, respectively for E. coli and F. necrophorum). Positive amniotic fluid cultures for the E. coli group were found in 11 of 12 (92%) and for the F. necrophorum group in three of three cases (100%). Histologic inflammation was seen heavily in both the E. coli and F. necrophorum groups, whereas it was absent in the saline solution group. Inoculation with B. bivius led to a much lower pregnancy loss rate (eight of 32) and less histologic inflammation despite positive uterine cultures in most animals. This model may provide an opportunity to determine mechanisms of clinical or subclinical intraamniotic infection and to test intervention strategies.

Topics: Abortion, Septic; Amniotic Fluid; Animals; Bacterial Infections; Bacteroides Infections; Dinoprost; Dinoprostone; Disease Models, Animal; Escherichia coli Infections; Female; Fetal Viability; Fusobacterium Infections; Fusobacterium necrophorum; Placenta; Pregnancy; Pregnancy Outcome; Progesterone; Rabbits

The PGE2, PGI2, PGF2 alpha and TxA2 synthesizing activities were studied in an isolated microsomal fraction of rat kidney after temporary, unilateral ureter obstruction and E. coli infection. In the early phase of regeneration the synthesis of vasodilatory PGI2 was increased, whereas that of vasoconstrictory PGF2 alpha was decreased. An increased PGE2 synthesizing activity was observed when renal obstruction was associated with infection. The role of these changes in regenerating the haemodynamics and function of postobstructive kidney is discussed.

Topics: Animals; Dinoprost; Dinoprostone; Epoprostenol; Escherichia coli Infections; Female; Kidney; Prostaglandin Endoperoxides; Prostaglandins E; Prostaglandins F; Prostaglandins G; Rats; Thromboxane A2; Ureteral Obstruction

Concentrations of prostaglandin F2 alpha (PGF2 alpha) and thromboxane B2 (TXB2) were evaluated in the milk of cows with naturally occurring (n = 3) and experimentally induced (n = 5) acute coliform mastitis. These arachidonic acid metabolites were measured by radioimmunoassay in unextracted milk. Experimental infections were induced by inoculating 600 to 1,200 colony-forming units of Escherichia coli into 1 mammary quarter per experimental cow. In the experimental cows, milk was collected before inoculation and at 12, 24, 36, 48, 60, and 72 hours after inoculation. Somatic cell concentrations, bovine serum albumin, and concentrations of PGF2 alpha and TXB2 were determined in milk collected at each sampling. Mild-to-moderate increases in milk PGF2 alpha and TXB2 concentrations were observed in cows with naturally occurring mastitis. the increases corresponded to the clinical severity and course of mastitis. In the experimental cows, increases in milk PGF2 alpha and TXB2 concentrations were observed, but the increases were not significant, using a statistical model that included factors of treatment, cows, hours after inoculation, cows-by-treatment and hours-by-treatment interactions, and random error (residual). Results of the present study indicated a large biological variability in milk arachidonic acid metabolite concentrations in cows with acute coliform mastitis, and that arachidonic acid metabolites may be important in the pathophysiologic process of acute coliform mastitis.

Topics: Acute Disease; Analysis of Variance; Animals; Arachidonic Acid; Arachidonic Acids; Cattle; Dinoprost; Escherichia coli Infections; Female; Lactation; Mastitis, Bovine; Milk; Pregnancy; Prostaglandins F; Radioimmunoassay; Thromboxane B2; Thromboxanes

The authors studied the effect of indomethacin and naproxen on the changes of renal prostaglandin E and F2 alpha concentration in experimental kidney infection, as well as the action of arginine-vasopressin in healthy rats. Naproxen proved to be an effective inhibitor of prostaglandin synthesis, as did indomethacin. In control animals an increased prostaglandin E and F2 alpha synthesis was observed caused by arginine vasopressin. It is supposed that ADH--depending on its concentration--has a metabolic modulator role in prostaglandin synthesis, which raises the possibility of a self-regulatory mechanism of water reabsorption.

Topics: Animals; Arginine Vasopressin; Deamino Arginine Vasopressin; Dinoprost; Escherichia coli Infections; Female; Indomethacin; Kidney; Naproxen; Nephritis; Prostaglandins E; Prostaglandins F; Rats; Rats, Inbred Strains