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Biomedical subjects

P Bor

Publications and source records attributed to P Bor.

At least 19 recordsLinked to original sources
PubMed1999

Serum fructosamine and fructosamine-albumin ratio as screening tests for gestational diabetes mellitus.

To evaluate the role of fructosamine/albumin ratio as an alternative screening parameter for gestational diabetes mellitus (GDM), serum fructosamine, albumin, protein, fructosamine/albumin ratio, and oral glucose tolerance were measured in 56 non-pregnant control healthy subjects, and in 96 pregnant women who screened positive after a 50 g glucose challenge-test. Oral glucose tolerance test (OGTT) identified 12 of 96 pregnant women as having GDM. Fructosamine concentration of 1.98 +/- 0.32 mmol/L (mean +/- SD) and fructosamine/albumin ratio of 47 +/- 10 mumol/g (mean +/- SD) has been obtained in nonpregnant control subjects. During the second trimester a lower fructosamine level (1.84 +/- 0.29 mmol/L, p < 0.05) and a higher fructosamine/albumin ratio (62 +/- 15 mumol/g, p < 0.001) occurs in pregnant women, when compared to non-pregnant healthy control subjects, most likely due to the low serum albumin concentration (30 +/- 6 g/L). The serum fructosamine levels and fructosamine/albumin ratio were only slightly higher in the pregnant women with GDM than in normal pregnant women (2.05 +/- 0.47 mmol/L versus 1.84 +/- 0.29 mmol/L, 67 +/- 16 mumol/g versus 62 +/- 15 mumol/g, respectively) but the differences were not statistically significant. The fructosamine and fructosamine/albumin ratio values for normal and GDM groups overlapped considerably. Sensitivity, specificity, positive predictive and negative predictive values for fructosamine were 41.7%, 85.7%, 29.4% and 91%, and for fructosamine/albumin ratio 25%, 79.8%, 15% and 88% respectively. This suggests that both fructosamine and fructosamine/albumin ratio have low sensitivity as predictors of GDM and can therefore not be used as screening tests.

Adult↗
PubMed1994

Loss of preconditioning in rabbits with vascular tolerance to nitroglycerin.

A preceding right ventricular overdrive pacing (VOP) of 500 b.p.m. for 5 min, markedly reduced the severity of global myocardial ischaemia produced by a subsequent 5-min VOP in conscious rabbits. This VOP-induced preconditioning developed in parallel with an increase in cardiac cyclic guanosine 3':5'-monophosphate (cyclic GMP) content. VOP-induced preconditioning was abolished when the animals had been made tolerant to the vasodilator effect of nitroglycerin (NG). In the heart of the NG-tolerant rabbits, neither VOP nor preconditioning increased cyclic GMP content. This suggests that changes by NG tolerance of cyclic GMP metabolism may account for the loss of VOP-induced preconditioning.

Animals↗
PubMed1994

Ventricular overdrive pacing-induced anti-ischemic effect: a conscious rabbit model of preconditioning.

To study whether ventricular overdrive pacing (VOP) induces preconditioning, rabbits were equipped with right ventricular electrode catheters for pacing and intracavital recording and polyethylene cannulas in the left ventricle and right carotid artery to measure intraventricular pressure and blood pressure. One week after surgery in conscious animals, VOP at 500 beats/min over 2, 5, or 10 min resulted in an intracavital S-T segment elevation, shortening of ventricular effective refractory period, decrease in maximum rate of pressure development and blood pressure, and increase in left ventricular end-diastolic pressure proportional to the duration of stimulation. A 5-min preconditioning VOP applied 5 or 30 min before a 10-min VOP markedly attenuated ischemic changes, whereas a 2-min VOP had no effect. In anesthetized rabbits, a 5-min VOP slightly increased guanosine 3',5'-cyclic monophosphate (cGMP) and profoundly elevated adenosine 3',5'-cyclic monophosphate (cAMP) content in left ventricular samples. When this VOP was preceded (5 or 30 min) by a preconditioning VOP, the cAMP increase was significantly attenuated, whereas the cGMP increase was amplified. We conclude that a single 5-min VOP induces preconditioning in association with alterations in cardiac cyclic nucleotide contents.

Animals↗
PubMed1993

Cicletanine attenuates overdrive pacing-induced global myocardial ischemia in rabbits: possible role of cardiac cyclic nucleotides.

BACKGROUND: This study examined whether cicletanine, an antihypertensive drug with cGMP phosphodiesterase inhibitory effect, could alleviate ventricular overdrive pacing-induced myocardial ischemia in chronically instrumented rabbits. METHODS: An electrode-catheter implanted into the right ventricle was used for pacing (500 bpm over 5 min) and for measuring intracavital ST-segment elevation and ventricular effective refractory period (VERP). PQ and QT intervals were measured in the chest-lead ECG, and dP/dtmax as well as left ventricular end-diastolic pressure (LVEDP) were recorded through a left intraventricular catheter. In separate groups, mean arterial blood pressure (MABP) was monitored from the right carotid artery. Experiments were performed on conscious rabbits after a week of convalescence. In anesthetized, open-chest rabbits, samples were taken from the left ventricle before and after drug treatment and/or overdrive pacing for determination of cGMP and cAMP contents by radioimmunoassay. RESULTS: Intravenous cicletanine, 30 mg/kg body weight, did not change resting MABP, dP/dtmax, and LVEDP, but it did reduce heart rate and prolonged PQ and QT intervals and VERP. Overdrive pacing produced intracavital ST-segment elevation, increased LVEDP, and decreased dP/dtmax and MABP. Cicletanine administered 15 minutes before pacing significantly attenuated ST-segment elevation, increased LVEDP, and decreased dP/dtmax and MABP. In anesthetized animals, cicletanine itself slightly increased cardiac cGMP and cAMP contents. Overdrive pacing moderately increased cGMP and profoundly elevated cAMP, and in overpaced rabbits, cicletanine further increased cGMO and markedly attenuated cAMP content increased by overdrive pacing. CONCLUSIONS: These results suggest that in correlation with alterations of cardiac cycle nucleotide contents, cicletanine protects the heart against pacing-induced myocardial ischemia.

Animals↗
PubMed1986

Membrane phospholipid and fatty acid changes in the mitochondrial and sarcolemmal fractions of the heart in adjuvant arthritic rats.

Adjuvant arthritis was found to induce changes in phospholipid and fatty acid composition as well as in membrane fluidity of mitochondrial and sarcolemmal fractions in the rat heart. In the sarcolemmal fraction, phosphatidylcholine content was decreased, while phosphatidylserine, phosphatidylinositol and the lysocompounds of phospholipids were increased. Mitochondria isolated from the heart of rats with adjuvant disease contained less linoleic acid than control samples. Docosatetraenoic acid and docosahexaenoic acid levels were shown to be increased in both mitochondrial and sarcolemmal fractions of the heart in treated animals. Electron spin resonance studies indicated that the break points of the curves obtained by plotting the order parameters against temperature changes were slightly shifted to lower temperature region in both subcellular fractions of arthritic rat hearts. As compared to the control values, membrane fluidity was increased both in mitochondrial and sarcolemmal fractions. The relationship of these alterations to our previous findings that adjuvant arthritis protected the rats against fatal post-infarctions arrhythmias needs further elucidation.

Animals↗
PubMed1984

Synergistic actions of prostacyclin and an isoquinoline derivative (CH-102) on ADP-induced aggregation of dog platelets in vitro.

The effect of an isoquinoline derivative, CH-102, and of prostacyclin-Na alone and their combinations on ADP-induced aggregation of dog platelets in vitro was studied. CH-102 and prostacyclin inhibited platelet aggregation in a dose-related manner with IC50 values of 3.2 X 10(-5) mol/l and of 4.8 X 10(-9) mol/l, respectively. CH-102 enhanced the platelet aggregation inhibitory effect of prostacyclin in a concentration range of 10(-6) to 2.3 X 10(-5) mol/l. The mode of interaction of the two agents characterized by the isobolic curve is a potentiated synergism.

Adenosine Diphosphate↗
PubMed1982

[Echocardiography in the diagnosis of diseases of the pericardium (author's transl)].

Echocardiography is a reliable, non-invasive and inexpensive tool for initial diagnosis and for evaluating the course of various cardiopathies. It was first used in diagnosis of pericardial effusion which is still one of it's best indications. Demonstration of an echo-free area behind the posterior wall of the left ventricle, bordered by dense echoes from the pericardium and remaining visible when the transducer is lowered, lead to the diagnosis of pericardial effusion and to quantification of the amount of fluid. The secondary effects can be assessed by analysis of parietal and valvular motion.

Diagnosis, Differential↗
PubMed1982

[Serum-ferritin assay in patients over seventy. A study on fifty-eight non anemic subjects and thirty-five anemic patients (author's transl)].

An immuno-enzymatic assay of serum ferritin was performed in subjects over 70 years of age. Wide variations in serum ferritin levels were demonstrated in the non-anemic group (17-510 ng/ml). This makes interpretation of results very difficult. In anemic patients a negative correlation was found between serum ferritin levels and TIBC (Total Iron Binding Capacity). When TIBC is under 42 mumol/l or above 63 mumol/l the two values are so closely correlated that serum ferritin assay does not provide any additional information for the diagnosis of anemia. On the contrary when TIBC is between 42 and 63 mumol/l serum ferritin can allow an estimation of tissue iron storage particularly in absolute iron deficiencies.

Aged↗
PubMed1982

Potentiation of insulin and tolbutamide of the effect of indomethacin on carrageenan paw edema in the rat.

The influence of insulin, tolbutamide and buformin on the effect of indomethacin as measured in the carrageenan paw edema assay in Sprague-Dawley rats has been studied. Small doses of these agents, having no influence on edema formation when given by themselves, were tested in combination with indomethacin. Insulin and tolbutamide potentiated the effect of indomethacin in the early phase of carrageenan paw swelling (2 hr), while they did not significantly alter the late phase (5 hr). Buformin was ineffective at any time. Insulin and tolbutamide in the doses applied moderately lowered blood sugar level, whereas buformin did not, thus tolbutamide-induced potentiation may be due to insulin release. No change in blood pressure of rats was observed under treatment. The possible mechanism of the supra-additive effect of insulin and indomethacin on the edema formation induced by carrageenan is discussed.

Animals↗
PubMed1980

[Echocardiograhy in athletes].

The electrocardiogrammes and echocardiogrammes of 10 weight lifters and 20 endurance trained top class athletes (runners, basket ball players and cyclists) were analysed. The electrocardiogrammes confirmed the notion of a specific profile in endurance trained athletes with left ventricular diastolic overload pattern. The echocardiogrammes did not show increased left ventricular wall thickness in the resistance trained athletes. It did show however a clear increase in left ventricular internal diastolic dimension and posteror wall thickness--the anatomical substratum of the large heart in athletes--in some categories of endurance trained athletes (cyclists and basket ball players). No change in the indices of left ventricular performance was found in either group.

Adult↗
PubMed1979

[Severe pulmonary embolism and recurrent thrombophlebitis caused by hereditary antithrombin III deficiency].

Severe pulmonary embolism with thrombosis of the inferior vena cava was observed in a 16 year old girl with no risk factors and treated successfully by fibrinolytic therapy. Secondarily, despite heparino-therapy, upper limb venous thrombosis occurred. Investigation of the clotting factors in the patient and her family revealed a hereditary deficit of antithrombin III. The features of the haemotological diagnosis of this rare condition and the therapeutic implications are discussed.

Adolescent↗