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Biomedical subjects

K Bjøro

Publications and source records attributed to K Bjøro.

At least 73 records · Page 4Linked to original sources

Mutagenicity testing of amniotic fluid from diabetic women, with special reference to their smoking habits.

Amniotic fluid from 16 diabetic and 78 healthy women at term was tested for capacity to cause mutations in Salmonella typhimurium bacterial tester strain TA98 (Ames test). Diabetes as well as heavy smoking increased the mutagenic activity of amniotic fluid. The difference between groups of diabetics and controls was significant in both nonsmokers and women who had smoked more than 5 cigarettes the last 48 h before delivery. It seems plausible that metabolic disturbances, perhaps enhanced by a lowered oxygenation, in some instances could produce mutagenic compounds. Mutagenic activity in amniotic fluid may be one of the factors underlying the increased incidence of congenital malformations in the offspring of diabetic women. Early mutations could cause such developmental errors in the embryos, and possibly also in future generations by damage to germ cells. Heavy smoking alone also caused an increase in mutagenic activity in term amniotic fluid. Our findings reflected an enhancing effect of smoking in diabetes. A pregnant diabetic woman who smoked would thus further endanger her already jeopardized pregnancy.

Amniotic Fluid↗

Breech delivery. An obstetrical analysis.

Fivehundred and eighty consecutive breech births during the period 1972-79 were analvsed for factors associated with neonatal mortality. The overall neonatal mortality in breech deliveries in this series of cases was 4.1%. Multivariate analyses (logistic regression) selected only 4 of 56 variables tested as significant (p less than 0.05) risk factors for neonatal death. The overall most important risk factor was low birth weight (p less than 0.0001). In addition, diabetes in the mother, malformations, and Apgar score 5 min less than 7 increased the risk of neonatal death. Cesarean section was carried out in 8.1% during the period 1972-75, but increased to 32.6% from 1976-79 without any reduction in neonatal mortality. Neonatal mortality figures were not significantly improved for infant delivered by cesarean section compared with those born vaginally.

Adult↗

Altered prostanoid formation in human umbilical vasculature in response to variations in oxygen tension.

Prostanoid formation in human umbilical vessels perfused in vitro was assessed at different oxygen tensions. At an atmosphere of 5% oxygen the production rate of prostacyclin (measured as 6-keto-PGF1 alpha) was higher, while those of thromboxane A2 (measured as TXB2), PGE2 and PGF2 alpha were lower than with 20%, 50% and 95% oxygen. The stimulatory effect of angiotensin II on prostanoid production was found to be independent on the prevailing oxygen tension. Vascular formation of prostanoids thus seems to be at least partially affected by the ambient oxygen tension. Though altered oxygen tension does not seem to affect angiotensin induced prostanoid formation, the action of other vasoactive agents influencing vascular formation of prostanoids may respond differently to hypoxia or hyperoxia.

Female↗

Formation of prostanoids in human umbilical vessels perfused in vitro.

Four major prostanoids (6-keto-PGF1 alpha, PGE2, PGF2 alpha and TXB2) were measured by specific radioimmunoassays in the outputs from human umbilical vessels perfused in vitro. As evaluated by scanning electron microscopy (SEM) only few blood platelets were attached to the vessel wall. After an initial flush with decreasing concentrations of all four prostanoids, a stable stage was reached, lasting for 4-5 hours. During this stage the production could be inhibited by indomethacin and only slightly stimulated with arachidonic acid. The TXA2 synthetase inhibitor UK 38485 depressed the TXB2 production, while only slightly affecting the other three prostanoids at very high concentrations. The arteries produced relatively more 6-keto-PGF1 alpha than did the vein.

6-Ketoprostaglandin F1 alpha↗

Prostacyclin and thromboxane formation in human umbilical arteries following stimulation with vasoactive autacoids.

The formation of prostacyclin (PGI2) and thromboxane A2 (TXA2) (measured as the stable metabolites 6-keto-PGF1 alpha and TXB2) during stimulation with vasoactive autacoids was registered in human umbilical arteries perfused in vitro. Responses were registered within 3-4 minutes after addition of the substances. Both angiotensin I and II were found to increase the formation of PGI2 while depressing that of TXA2. Serotonin increased the formation of TXA2 but not that of PGI2. Both PGE2 and PGF2 alpha stimulated the PGI2 formation. The TXA2 mimetic U46619, increased PGI2 production, whereas PGI2 slightly increased the formation of TXA2. All responses were found to be completely inhibited by indomethacin.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗

Pseudomonas aeruginosa virulence factors: modifications by sub-inhibitory concentrations of carbenicillin or gentamicin.

A virulent strain of Pseudomonas aeruginosa was assayed for adhesion to HEp-2 cells, production of toxin A, and production of elastase, in the presence of sub-inhibitory concentrations of carbenicillin and gentamicin. Both antibiotics, assayed in a concentration of 1:12 of their minimum bactericidal concentration (MBC), inhibited the production of toxin A. Gentamicin at this concentration totally abolished the production of elastase, whereas carbenicillin had little or no effect on this factor. Both antibiotics inhibited the bacterial adhesion, but in different ways. While gentamicin had a strong activity of slow onset, carbenicillin had a transitory activity of rapid onset, with return towards normal values after 90 min incubation.

Adhesiveness↗

Effects of vasoactive autacoids on different segments of human umbilicoplacental vessels.

Effects of serotonin, prostaglandin E2, prostaglandin F2 alpha, U 46619 (a thromboxane A2 mimetic) and angiotensin I and II on the perfusion pressure were studied on vessel segments from human umbilical arteries, placental arteries and the umbilical vein during in vitro perfusions. All drugs were found to induce vasoconstriction. Serotonin displayed strong vasoconstrictor potencies in all vessel segments, whereas the responsiveness to the other autacoids differed greatly in the various segments. In the umbilical artery prostanoids were most potent in the juxtafetal segment, whereas angiotensin I and II displayed greatest effects in the juxtaplacental segment. The results lend additional support to the concept that angiotensins and prostanoids are of importance in the regulation of fetal extracorporeal blood flow.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗

In vitro perfusion studies on human umbilical arteries. I. Vasoactive effects of serotonin, PGF2 alpha and PGE2.

A method was developed for the assessment of in vitro perfusion of the umbilical cord arteries. A perfusion pressure of 60-80 mmHg gave flow rates ranging from 30 to 40 ml/min per artery. Serotonin, PGF2 alpha and PGE2 were added to the perfusate and tested for vasoactivity. All substances induced a dose-dependent vasoconstriction. Serotonin proved to be the most potent vasoconstrictor. The minimum dose required to induce visible pressure responses was 10(-9) - 10(-8) M of serotonin and 10(-7) M of PGF2 alpha and PGE2. When adding methysergide to the perfusate, the serotonin response was abolished, while the effects of the prostanoids remained unaltered.

Dinoprost↗

In vitro perfusion studies on human umbilical arteries. II. Effects of prostacyclin and a thromboxane A2 mimetic.

Vascular effects of a thromboxane A2 mimetic, U46619, and prostacyclin on human umbilical arteries have been investigated by in vitro perfusions. Administration of U46619 invariably induced vasoconstrictory responses which were found to be dose-dependent and consistently stronger than those observed with other prostaglandins (e.g. PGF2 alpha and PGE2). Infusion of prostacyclin alone did not lead to significant alterations in the arterial perfusion pressure. However, when prostacyclin was introduced after a constriction with U46619 had been established, a transient pressure decrease was observed. When both drugs were introduced simultaneously, the U46619 response was suppressed. This suppression was partial and dependent on the PGI2 concentration.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗

Characterization of the responses to serotonin and prostanoids in human umbilical arteries perfused in vitro.

In order to characterize the action of some vasoactive autacoids on the umbilical artery, pressure responses of serotonin, PGE2, PGF2 alpha and U46619 (a thromboxane A2 mimetic) have been investigated during in vitro perfusion. Serotonin, PGE2 and PGF2 alpha caused biphasic responses in which both the dilator and the constrictor phases were found to be dose-dependent. Indomethacin or SQ 29.548 (a thromboxane A2 receptor antagonist) did not affect the response to serotonin, whereas indomethacin reduced or abolished the vasodilator and vasoconstrictor action of PGE2 and PGF2 alpha. U46619 induced monophasic pressor responses which were abolished by SQ 29.548. The results indicate that PGE2 and PGF2 alpha, but not serotonin, interfere with the local production of vasoactive prostanoids. The altered synthetic activity modify the responses to PGE2 and PGF2 alpha in the umbilical artery.

Bridged Bicyclo Compounds, Heterocyclic↗

Altered angiotensin-prostanoid interactions in umbilical arteries in pregnancy-induced hypertension.

The production rate of four prostanoids (PGE2, PGF2 alpha, 6-keto-PGF1 alpha and TXB2) in human umbilical cords from normal pregnancies (control) and cases with pregnancy-induced hypertension (PIH) were compared. The cords in the PIH-group produced significantly less 6-keto-PGF1 alpha and more TXB2 than did those in the control-group. Production rates of PGE2 and PGF2 alpha were almost equal in the two groups. After stimulation with angiotensin II the PIH-cords displayed a far smaller increase in 6-keto-PGF1 alpha production compared to the control cords. The responses in PGE2 and PGF2 alpha production were again equal in the two groups. The present results indicate that the angiotensin-prostanoid interactions are disturbed in fetal as well as in maternal vessels. Such a disturbance may explain the observed relative hypersensitivity to angiotensin II observed in gravidae prone to develop pregnancy-induced hypertension.

6-Ketoprostaglandin F1 alpha↗

Effects of angiotensin I and II and their interactions with some prostanoids in perfused human umbilical arteries.

In perfused human umbilical arteries both angiotensin I and II induced vasoconstriction with a monophasic response. Angiotensin I and II induced vasoconstrictions at doses greater than or equal to 10(-8) M and 10(-9) M respectively. Captopril inhibited the angiotensin I response while the angiotensin II receptor blocker Sar1-Ala8 AII inhibited the effect of both angiotensins. PGI2 attenuated the angiotensin II response in a dose dependent pattern. PGE2 and PGF2 alpha in concentrations below the critical levels for creating pressure responses per se, also attenuated the angiotensin II response. The cyclooxygenase inhibitor indomethacin potentiated the angiotensin II response indicating that endogenous production of prostanoids is of importance in the modulation of angiotensin effects.

Angiotensin I↗

Pressure- and temperature-dependent adhesion of Pseudomonas aeruginosa to HEp-2 cells.

Pseudomonas aeruginosa bacteria adhere to human epitheloid (HEp-2) cells in culture. Under normal atmospheric conditions (1 ATA), this adhesion increased significantly when the temperature rose from 22 to 37 degrees C. Under hyperbaric atmosphere (= air, 7 ATA) conditions, a similar, significant enhancement of bacterial adhesion to the cells was noted when the temperature rose. If the temperature was kept stable at 22 or 37 degrees C and the pressure was increased from 1 to 7 ATA, a pressure-induced enhancement was observed. This was statistically significant, at both temperature levels. Temperature-induced or -stimulated adhesion may help to explain some outbreaks of P. aeruginosa infections, for instance in whirlpools. The enhancement of this phenomenon under hyperbaric atmosphere conditions could have some relevance to recurrent P. aeruginosa otitis externa, a most common nuisance among professional divers.

Adhesiveness↗

Correlation between adhesion of Pseudomonas aeruginosa bacteria to cell surfaces and the presence of some factors related to virulence.

Recent isolates of Pseudomonas aeruginosa strains and 12-month-old subcultivated variants of the same strains have been assayed for adhesiveness to HEp-2 cells. P. aeruginosa adhesion factors were located both to the bacterial surface and extracellularly. Generally, loss of adhesiveness upon subcultivation could be restituted by adding extracellular factor from the recent isolate. While the extracellular adhesins were neutralized by non-specific serum factors, the surface-bound adhesins of a recent isolate were blocked by antibodies only.

Adhesiveness↗

The role of chronic non-specific inflammatory lesions of the placenta in intra-uterine growth retardation.

Placentae from 108 cases of intra-uterine growth retardation (IUGR) were examined microscopically with special emphasis on the occurrence of chronic non-specific inflammatory lesions. Sixteen cases (14.8%) showed severe villitis (SV) while 15 (13.8%) showed moderate villitis (MV). The SV-cases seemed to be more severely growth retarded, while no differences in the growth patterns appeared. A greater part of the SV-cases than of those with moderate or no villitis were cases without maternal or fetal causes for the growth retardation. The placental weight and placental index were higher in the cases with severe villitis. A mixture of lymphocytes and histiocytes was the most common finding among the placentae with villitis. Six cases of umbilical cord thrombangitis were registered, the majority of these being associated with villitis. The present findings suggest an association between intrauterine growth retardation and villitis of unknown etiology.

Birth Weight↗