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At least 721 records · Page 40Linked to original sources
PubMed1981

Amniography in prenatal diagnosis.

The increasing use of prenatal diagnostic methods, including sonography and amniotic fluid analysis, has made it possible to suspect certain fetal defects at an early gestational age. In selected cases, accurate diagnosis of the specific malformation may have an effect on fetal and neonatal prognosis, and on prenatal counseling of the parents. As part of a large regional screening program for neural tube defects, we performed 28 midtrimester amniograms. We found 14 neural tube defects (nine spina bifida, four anencephaly, one Meckel syndrome), four abdominal wall defects, two tumors, and eight normal examinations. Radiographic examples of these malformations are presented, including previously undescribed findings in meningomyeloceles. The place of amniography in prenatal diagnosis is discussed.

Abdominal Muscles↗
PubMed1998

L-Arginine inhibits vasopressin-stimulated mesangial cell Ca2+.

L-Arginine (L-Arg) affects various parameters that modulate the progression of renal disease. These same factors [e.g., glomerular filtration rate, changes in mesangial cell (MC) tension, and production of NO] are all controlled at least in part by changes in MC intracellular Ca2+ concentration ([Ca2+]i). We therefore evaluated the effect of L-Arg on MC [Ca2+]i. We found that L-Arg inhibits the vasopressin-stimulated rise in MC [Ca2+]i both in rat and murine cell cultures. This effect does not appear to be due to metabolism of L-Arg to either NO or L-ornithine (L-Orn). Blocking the metabolism of L-Arg with Nomega-monomethyl-L-arginine, an NO synthase inhibitor, or with 20 mM L-valine (L-Val), an inhibitor of Orn formation, does not reverse the inhibition. However, other cationic amino acids, as well guanidine, the functional group of L-Arg, all inhibit the vasopressin-stimulated rise in [Ca2+]i, consistent with a structural basis for this effect. We conclude that 1) L-Arg inhibits vasopressin-stimulated murine and rat MC [Ca2+]i rise, 2) this inhibition is not mediated by metabolism of L-Arg to either NO or L-Orn, and 3) the effect of L-Arg is due to its cationic functional group, guanidine.

Animals↗
PubMed1975

Effect of physical training on the metabolism of thyroid hormones in man.

The effect of a 6-wk program of physical training (track running) on the peripheral metabolism of thyroxine (T4) and triiodothyronine (T3) was evaluated in a group of 11 men. Measurements were made of hormone turnover, urinay and fecal clearances, plasma hormone concentrations, and hormone binding by plasma proteins in all subjects before and after training, After training, metabolic clearance of T3 was increased 8.5% above the pretraining level due to an increased deiodinative clearance of this hormone. No significant change was observed in plasma T3 concentration. The absolute degradation of T3 increased 10.3% after training. In contrast, no significant change in the metabolic clearance of T4 was detected. Significantly decreased plasma concentration of total T4 after 4 and 6 wk of training was apparently not due to decreased hormone binding by plasma protein since no significant alteration in the dialyzable fraction of T4 was detected. The absolute degradation rate of T4 was decreased 8.8% after training. Possible implications of the observed differential impact of training on the degradation of T4 and T3 regarding thyroid hormone economy are discussed.

Adolescent↗
PubMed1975

Assessment of the degradation of thyroid hormones in man during bed rest.

The effect of bed rest on the absolute turnover rates of thyroid hormones, thyroxine (T4) and triiodothyronine (T3), was evaluated in man. Bed rest resulted in physical deconditioning, measured by a decreased rate of maximal oxygen consumption; physical deconditioning was associated with no significant alterations in the metabolic clearance of T4 and T3. Plasma concentrations of these iodothyronines were not changed as a result of bed rest. Absolute hormone turnover rates were similar in control and bed-rest subjects. The data suggest that the degradation of thyroid hormones is not influenced by physical deconditioning or hypodynamia.

Adolescent↗
PubMed1975

Circadian variations in concentrations of plasma thyroxine and triiodothyronine in man.

The plasma concentrations of thyroxine (T4), triiodothyronine (T3), and total protein (Pr) were measured at 2-h intervals in 8 male subjects during two 24-h periods. Plasma T4 and T3 levels varied significantly during the day. T4 values were highest at 0900 hours and thereafter declined rapidly reaching lowest levels at 1500-1700 hours (mean decrement, 13.2% of 0.00-hour value). Plasma T3 was highest at 0900 hours and lowest at 1700-1900 hours (mean decrement, 16.7% of 0900-hour value). Fluctuations observed in Pr were not significant. Variations in plasma T4 and T3 appeared concordant with respect to time, since no significant variation was detected in T3:T4 plasma concentration ratios. In view of previous studies that have demonstrated circadian variations in the binding of thyroid hormones by plasma proteins, it is suggested that the observed temporal variations in plasma concentrations of T3 and T4 reflect parallel changes in the capacity or affinity of specific plasma binding proteins of these iodothyronines.

Adolescent↗
PubMed2003

Novel index for invasively assessing the coronary microcirculation.

BACKGROUND: A relatively simple, invasive method for quantitatively assessing the status of the coronary microcirculation independent of the epicardial artery is lacking. METHODS AND RESULTS: By using a coronary pressure wire and modified software, it is possible to calculate the mean transit time of room-temperature saline injected down a coronary artery. The inverse of the hyperemic mean transit time has been shown to correlate with absolute flow. We hypothesize that distal coronary pressure divided by the inverse of the hyperemic mean transit time provides an index of microcirculatory resistance (IMR) that will correlate with true microcirculatory resistance (TMR), defined as the distal left anterior descending (LAD) pressure divided by hyperemic flow, measured with an external ultrasonic flow probe. A total of 61 measurements were made in 9 Yorkshire swine at baseline and after disruption of the coronary microcirculation, both with and without an epicardial LAD stenosis. The mean IMR (16.9+/-6.5 U to 25.9+/-14.4 U, P=0.002) and TMR (0.51+/-0.14 to 0.79+/-0.32 mm Hg x mL(-1) x min(-1), P=0.0001), as well as the % change in IMR (147+/-66%) and TMR (159+/-105%, P=NS versus IMR % change), increased significantly and to a similar degree after disruption of the microcirculation. These changes were independent of the status of the epicardial artery. There was a significant correlation between mean IMR and TMR values, as well as between the % change in IMR and % change in TMR. CONCLUSIONS: Measuring IMR may provide a simple, quantitative, invasive assessment of the coronary microcirculation.

Animals↗
PubMed2003

Comparison of coronary thermodilution and Doppler velocity for assessing coronary flow reserve.

BACKGROUND: Thermodilution coronary flow reserve (CFRthermo) is a new technique for invasively measuring coronary flow reserve (CFR) with a coronary pressure wire and is based on the ability of the pressure transducer to also measure temperature changes. Whether CFRthermo correlates well enough with absolute flow-derived CFR (CFRflow) to replace Doppler wire-derived CFR (CFRDoppler) remains unclear. METHODS AND RESULTS: In an open-chest pig model, CFRthermo was measured in the left anterior descending (LAD) artery and compared with CFRDoppler and CFRflow, measured with an external flow probe placed around the LAD. In 9 pigs, CFR was measured simultaneously by all 3 means in the normal LAD and after creation of an epicardial LAD stenosis. To determine the added effect of microvascular disease, measurements of flow reserve were also performed after disruption of the coronary microcirculation with embolized microspheres. Intracoronary papaverine (20 mg) was used to induce hyperemia. In a total of 61 paired measurements, CFRthermo correlated strongly with the reference standard CFRflow (r=0.85, P<0.001). CFRDoppler correlated less well with CFRflow (r=0.72, P<0.001). Bland-Altman analysis showed a closer agreement between CFRthermo and CFRflow. CONCLUSIONS: CFRthermo correlates better with CFRflow than does CFRDoppler.

Animals↗
PubMed2004

Microvascular resistance is not influenced by epicardial coronary artery stenosis severity: experimental validation.

BACKGROUND: The effect of epicardial artery stenosis on myocardial microvascular resistance remains controversial. Recruitable collateral flow, which may affect resistance, was not incorporated into previous measurements. METHODS AND RESULTS: In an open-chest pig model, distal coronary pressure was measured with a pressure wire, and the apparent minimal microvascular resistance was calculated during peak hyperemia as pressure divided by flow, measured either with a flow probe around the coronary artery (R(micro app)) or with a novel thermodilution technique (apparent index of microcirculatory resistance [IMR(app)]). These apparent resistances were compared with the actual R(micro) and IMR after the coronary wedge pressure and collateral flow were incorporated into the calculation. Measurements were made at baseline (no stenosis) and after creation of moderate and severe epicardial artery stenoses. In 6 pigs, 189 measurements of R(micro) and IMR were made under the various epicardial artery conditions. Without consideration of collateral flow, R(micro app) (0.43+/-0.12 to 0.46+/-0.10 to 0.51+/-0.11 mm Hg/mL per minute) and IMR(app) (14+/-4 to 17+/-7 to 20+/-10 U) increased progressively and significantly with increasing epicardial artery stenosis (P<0.001 for both). With the incorporation of collateral flow, neither R(micro) nor IMR increased as a result of increasing epicardial artery stenosis. CONCLUSIONS: After collateral flow is taken into account, the minimum achievable microvascular resistance is not affected by increasing epicardial artery stenosis.

Animals↗
PubMed2004

Overexpression of human copper/zinc superoxide dismutase (SOD1) suppresses ischemia-reperfusion injury and subsequent development of graft coronary artery disease in murine cardiac grafts.

BACKGROUND: Ischemia-reperfusion injury is an important risk factor for graft coronary artery disease (GCAD). We hypothesized that overexpression of SOD1 in donor hearts would suppress ischemia-reperfusion injury and thereby reduce GCAD. METHODS AND RESULTS: In one series, donor hearts of C57BL/6 (H-2b) transgenic mice overexpressing human SOD1 or C57BL/6 wild-type mice were heterotopically transplanted into C57BL/6 recipients and procured after 4 hours of reperfusion (n=6 each). Superoxide, TNF-alpha, and MCP-1/CCL2 production were significantly reduced in the SOD1 transgenic donor heart recipients, and graft injury determined by serum CPK-MB levels was significantly decreased. Cardiomyocyte apoptosis and caspase-3 and caspase-9 activities were significantly decreased in these recipients; caspase-8 activity was unchanged. Fas ligand but not Fas expression was also reduced. In a second series, transgenic and wild-type hearts were transplanted into C-H-2bm12KhEg (H-2bm12) recipients, and then procured on day 56 (n=7 each). Cardiac graft beating was significantly better in the SOD1 transgenic donor heart recipients on days 28, 42, and 56 (but not day 14). Significant reduction in luminal narrowing, the intima/media ratio, and the percentage of diseased vessels was seen in the SOD1 transgenic donor heart recipients, and MCP-1/CCL2, ICAM-1, and VCAM-1 production were significantly reduced. CONCLUSIONS: Overexpression of SOD1 attenuates both apoptosis and the inflammatory response during ischemia-reperfusion injury and therefore mitigates against the subsequent development of GCAD.

Animals↗
PubMed1974

Augmentation of the peripheral metabolism of L-triiodothyronine and L-thyroxine after acclimation to cold. Multifocal stimulation of the binding of iodothyronines by tissues.

Increased metabolism of thyroid hormones was observed in rats adapted to an ambient temperature of 4 degrees C. The increased hormonal degradation was manifested in enhanced metabolic, urinary deiodinative, biliary, and fecal clearances of iodothyronines. Increased metabolic clearances were due to stimulation of cellular hormonal disposition, evidenced by elevated intrinsic cellular clearances. After adaptation, the concentration of protein-bound iodine in plasma was decreased, and the binding of the hormones by plasma proteins was increased. The enhanced rate of metabolism of iodothyronines was associated with stimulation of the binding of these hormones by diverse tissues, suggesting the participation of extrahepatic degradative foci in the increased hormonal deiodination observed in vivo. Increased hepatocellular binding and a significantly enlarged hepatic distribution space of thyroxine were noted. Hepatocellular binding of triiodothyronine was similarly augmented, and a smaller but significant increase in the hepatic space of this iodothyronine was detected. Analysis of the hepatic subcellular partition of iodothyronines 35 min after the intravenous administration of isotopically labeled thyroid hormones disclosed increased hormonal binding by the microsomal fraction in cold-adapted animals and an attendant increase in the microsomal protein concentration. Partial microsomal subfractionation in a discontinuous sucrose gradient indicated that the observed stimulation of microsomal hormonal binding was associated with proliferation of the smooth endoplasmic reticulum.

Adaptation, Physiological↗
PubMed1978

The influence of fasting, diabetes, and several pharmacological agents on the pathways of thyroxine metabolism in rat liver.

As judged from both paper and column chromatography, slices or homogenates of liver from rats fasted for 48 h displayed a lesser rate of generation of (125)I-labeled 3,5,3'-triiodothyronine (T(3)) from (125)I-labeled thyroxine (T(4)) added to incubation media than did preparations from normal chow-fed animals. A similar defect in the conversion of T(4) to T(3) in the livers of fasted animals was observed when preparations were incubated with substrate concentrations of T(4) so that T(3) generation could be assessed by radioimmunoassay. The effect of fasting could be prevented, wholly or in part, by administration of glucose in the drinking water to otherwise fasted animals, and the degree of prevention appeared to be proportional to the concentration of glucose employed. Diminished generation of T(3) from T(4) was similarly evident in the livers of animals with streptozotocin-induced diabetes mellitus, and this defect was overcome by the provision of insulin in vivo, but not in vitro. Decreased formation of T(3) from T(4) was also observed in preparations of liver from animals given dexamethasone, amiodarone, and propylthiouracil. In no case could these effects on the net formation of T(3) from T(4) be explained by effects of the experimental conditions on the degradation of the T(3) generated, as judged from the rate of degradation of exogenous (125)I-T(3) measured in parallel incubates. An analysis of the rate of disappearance of (125)I-T(4) from reaction mixtures in relation to the rate of appearance of (125)I-T(3) and (125)I-iodide was employed to estimate the activity of the 5-monodeiodinating pathway of T(4) metabolism that leads to the formation of 3,3',5'-triiodothyronine (reverse T(3)). Such estimates indicated that reverse T(3) formation was actively proceeding in the preparations studied, was slightly enhanced by fasting, was unaffected by dexamethasone and amiodarone, and was markedly inhibited by propylthiouracil. In view of the similarities between the effect of these experimental manipulations on the generation of T(3) from T(4) by rat liver in vitro to their effects on the production rates and serum concentrations of T(3) in man, it is concluded that the rat liver system provides a suitable model for the study of factors that influence the conversion of T(4) to T(3) in man. In addition, the findings strongly indicate that this process, at least in the liver, is closely linked to the utilization of carbohydrate.

Animals↗
PubMed1979

Observations on the factors that control the generation of triiodothyronine from thyroxine in rat liver and the nature of the defect induced by fasting.

Studies were performed to explore the mechanism underlying the impaired generation of 125-I-3,5,3'-triiodothyronine (T3) from 125I-thyroxine (T4) (T3-neogenesis)) in preparations of liver from rats fasted for 48 h and the prevention of this effect by the feeding of glucose. T3-neogenesis in livers from fasted animals and those fed chow or glucose was assessed in various mixtures of crude microsomal fractions with either buffer or cytosols. T3-neogenesis was mediated by an enzyme present in the microsomal fraction whose activity was enhanced by cytosolic cofactor(s). In livers from animals fasted for 48 h, the supporting activity of cytosol was decreased, whereas the activity of the enzyme was unaffected. Administration of glucose as the sole nutritional source prevented the decrease in the supporting activity of hepatic cytosol that was regularly observed in the case of animals totally deprived of food. The diminished supporting activity for T3-neogenesis provided by liver cytosol from fasted animals was restored to normal by enrichment with either NADPH or GSH, but the two cofactors appeared to act at different loci. GSH stimulated T3-neogenesis in microsomes incubated in the absence of cytosol, i.e., in buffer, whereas NADPH did not. The stimulatory effect of both agents was blocked by the sulfhydryl oxidant, diamide, which also inhibited T3-neogenesis in mixtures of microsomes with cytosols. Taken together, these observations suggest that GSH acts directly on the enzyme in the crude microsomal fraction, whereas NADPH acts within the cytosol, possibly by increasing the concentration of GSH through the action of the enzyme glutathione reductase, for which NADPH is a cofactor. In this light, the decreased supporting activity of hepatic cytosol from starved animals appears to reflect, at least partly, a decreased concentration of one or both cofactors. The direct stimulation of enzyme activity by GSH, and the apparent lack of inhibition of unstimulated activity by diamide, suggests that the 5'-monodeiodinase for thyroxine that mediates T3-neogenesis may be a GSH transhydrogenase.

Animals↗