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Biomedical subjects

C V Smith

Publications and source records attributed to C V Smith.

At least 145 records · Page 8Linked to original sources
PubMed1989

Randomized comparison of meperidine and fentanyl during labor.

This randomized investigation compared the efficacy of the conventional narcotic, meperidine, and a more potent and short-acting analgesic, fentanyl, during labor. One hundred five women with uncomplicated term pregnancies in active labor were randomly assigned to receive either intravenous fentanyl (50-100 micrograms every hour) or meperidine (25-50 mg every 2-3 hours) in a non-blinded manner. The analgesics were rated equivalent in efficacy. Maternal nausea, vomiting, and prolonged sedation occurred more frequently in the meperidine group. Naloxone use was significantly less in fentanyl- than in meperidine-exposed infants (one of 49 versus seven of 56; P less than .05). Neuroadaptive testing at approximately 2 hours and 24 hours postnatally revealed similar averaged scores in the two groups. Using the described intravenous dosing schedule, fentanyl was preferable to meperidine during labor because there was no prolonged maternal sedation or vomiting necessitating therapy and the requirement for neonatal naloxone was reduced.

Analgesia↗
PubMed1988

Alkylation of the liver plasma membrane and inhibition of the Ca2+ ATPase by acetaminophen.

Acetaminophen is activated metabolically to yield reactive species that bind covalently to liver cell macromolecules. The extent of covalent binding correlates with the occurrence and severity of hepatic necrosis. We reported previously [J. O. Tsokos-Kuhn, E. L. Todd, J. B. McMillin-Wood and J. R. Mitchell, Molec. Pharmac. 28, 56 (1985)] that active Ca2+ accumulation of isolated liver plasma membranes is decreased 60-75% after a hepatotoxic dose of acetaminophen in vivo. We now report that the protein of isolated liver plasma membranes was substantially labeled with drug metabolites after administration of [3H]acetaminophen. There was no increase in passive membrane permeability that might cause diminished Ca2+ accumulation. Intravesicular volume and relative purity of the vesicle preparations after acetaminophen were not different from controls. However, (Ca2+,Mg2+)-ATPase, a possible biochemical expression of the Ca2+ pump, was decreased 31% (P less than 0.025) after acetaminophen treatment. ATPase activity in both control and treated groups was enhanced by isolating membranes in the presence of 5 mM reduced glutathione (GSH), but the effects of drug treatment were not reversed. A similar effect of GSH on Ca2+ accumulation was observed previously [J. O. Tsokos-Kuhn, E. L. Todd, J. B. McMillin-Wood and J. R. Mitchell, Molec. Pharmac. 28, 56 (1985)]. These data are consistent with a hypothesis wherein alkylation of membrane proteins by reactive acetaminophen metabolites is a factor in the onset of hepatic necrosis after acetaminophen. They are not consistent with an oxidative stress hypothesis where thiol S-thiolation of membrane components is postulated to produce altered membrane permeability or thiol-reversible alterations in membrane protein structure and enzymatic function.

Acetaminophen↗
PubMed1988

Hypoxic damage generates reactive oxygen species in isolated perfused rat liver.

The aim of the present study was to investigate the possible role of reactive oxygen species in the pathogenesis of hypoxic damage in isolated perfused rat liver. One hour of hypoxia caused severe cell damage (lactate dehydrogenase release of greater than 12,000 mU/min/g liver wt) and total irreversible cholestasis which was accompanied by a loss of cellular ATP and a marked decrease in lactate efflux. Tissue glutathione disulfide (GSSG) content and GSSG efflux as a measure of hepatic reactive oxygen formation was less than 1% of total glutathione before and during hypoxia. Upon reoxygenation, however, hepatic GSSG content increased sharply to about twice the control values and GSSG efflux increased several-fold to around 3-4 nmol GSH-equivalents/min/g. The release of lactate dehydrogenase decreased upon reoxygenation and tissue ATP content recovered partially. When livers were reoxygenated at an earlier time interval than 1 hr of hypoxia, i.e., before the onset of damage, no enhanced GSSG formation was observed. The results demonstrate that hypoxic damage is a prerequisite to reactive oxygen formation during the subsequent reoxygenation period. Thus, reactive oxygen species appear unlikely to play a crucial role in the pathogenesis of hypoxic liver damage in the hemoglobin-free, isolated perfused liver model.

Adenosine Triphosphate↗
PubMed1988

Reactive oxygen species during ischemia-reflow injury in isolated perfused rat liver.

The hypothesis that intracellular generation of reactive oxygen species in hepatocytes or reticuloendothelial cells may cause ischemia-reperfusion injury was tested in isolated perfused livers of male Fischer rats. GSSG was measured in perfusate, bile, and tissue as a sensitive index of oxidative stress. After a preperfusion phase of 30 min, the perfusion was stopped (global ischemia) for various times (30, 120 min) and the liver was reperfused for another 60 min. The bile flow (1.48 +/- 0.17 microliters/min X gram liver weight), the biliary efflux of total glutathione (6.54 +/- 0.94 nmol GSH eq/min X g), and GSSG (1.59 +/- 0.23 nmol GSH eq/min X g) recovered to 69-86% after short-term ischemia and to 36-72% after 2 h of ischemia when compared with values obtained from control livers perfused for the same period of time. During reperfusion, the sinusoidal efflux of total glutathione (16.4 +/- 2.1 nmol GSH eq/min X g) and GSSG (0.13 +/- 0.05 nmol GSH eq/min X g) did not change except for an initial 10-30-s increase during reperfusion washout. No increased GSSG secretion into bile was detectable at any time during reperfusion. The liver content of total glutathione (32.5 +/- 3.5 nmol GSH eq/mg protein) and GSSG (0.27 +/- 0.09 nmol GSH eq/mg protein) did not change significantly during any period of ischemia or reperfusion. We conclude, therefore, that at most only a minor amount of reactive oxygen species were generated during reperfusion. Thus, reactive oxygen species are unlikely to cause ischemia/reperfusion injury in rat liver by lipid peroxidation or tissue thiol oxidation.

Adenosine Triphosphate↗
PubMed1988

Fetal acoustic stimulation testing. III. Predictive value of a reactive test.

The nonstress test (NST) is a helpful adjunct to the management of high-risk pregnancies. However, fetal sleep states may lead to falsely nonreactive tests. We assessed the usefulness of transabdominal acoustic stimulation of the fetus and demonstrated an approximately 50% reduction in the number of nonreactive tests and a shorter testing time. No change in the predictive reliability of a reactive test was observed. With regard to the intrapartum and neonatal outcome in women delivering within seven days of a reactive test, no difference between the incidence of meconium-stained amniotic fluid, depressed one- or five-minute Apgar scores or operative intervention for fetal distress could be identified. A reactive test evoked by acoustic stimulation is as reliable as the NST. It offers the additional benefits of reduced testing time and a lower incidence of nonreactive tests.

Acoustic Stimulation↗
PubMed1988

Continuing experience with the fetal acoustic stimulation test.

Antepartum fetal heart rate testing remains a useful method with which to assess fetal well-being in high-risk pregnancies. Recently the adjunctive use of transabdominal acoustic stimulation was proven effective in reducing the number of nonreactive nonstress tests (NSTs) without changing the predictive reliability of the test. Our continuing experience with this method involved 1,503 women undergoing 3,935 tests. A reactive test occurred in 93%, and the fetal death rate was 1.3/1,000. In an attempt to evaluate the incidence of mortality in a large population, data from the current investigation were pooled with those from other reports from our institution. In our aggregate experience of 7,763 tests, fetal death occurred within seven days of a reactive test with an incidence of 1.9/1,000 in patients receiving acoustic stimulation. This finding contrasts favorably with a death rate of 1.6/1,000 in fetuses with spontaneous reactivity. Fetal acoustic stimulation testing seems to offer advantages over the more traditional NST, and the predictive values of normal tests seem to be equivalent.

Acoustic Stimulation↗
PubMed1988

Liver membrane calcium transport in diquat-induced oxidative stress in vivo.

Hepatic necrosis is produced rapidly by 0.1 mmol/kg diquat in male Fischer-344 rats but not Sprague-Dawley rats, yet massive oxidant stress is caused by diquat in both strains of rat. Liver plasma membrane calcium uptake was unaltered by diquat treatment in either strain. However, diquat inhibited ATP-dependent calcium sequestration by hepatic microsomes from Fischer rats by 33% (33 +/- 2 versus 50 +/- 2 nmol/mg/20 min), whereas liver microsomal calcium uptake in Sprague-Dawley rats was not decreased by diquat treatment. Microsomes of diquat-treated Fischer rats showed marked increases in calcium efflux versus controls (k efflux = 0.115 +/- 0.027 versus 0.051 +/- 0.005 min-1; p less than 0.025), but microsomes of diquat-treated Sprague-Dawley rats exhibited no significant change in efflux rate. Calcium uptake by the endoplasmic reticulum of saponin-permeabilized isolated hepatocytes was diminished in parallel with diquat cytotoxicity. Significant increases in 11-, 12-, and 15-hydroxy 20:4 fatty acids were found in liver microsomes isolated after diquat treatment in vivo and administration of desferrioxamine (0.24 mmol/kg, intraperitoneally) administered before diquat significantly protected against the inhibition of microsomal calcium uptake. These data suggest a possible role for Fenton chemistry and lipid peroxidation in this feature of diquat-generated hepatic damage in vivo.

Animals↗
PubMed1987

Effect of BCNU pretreatment on diquat-induced oxidant stress and hepatotoxicity.

Diquat administration produces hepatic necrosis in male Fischer-344 rats, and minimally in male Sprague-Dawley rats, with massive oxidant stress observable in both strains as evidenced by increased biliary efflux of glutathione disulfide (GSSG). Pretreatment of both strains of rats with 80 mg/kg of 1,3-bis(2-chloroethyl)-N-nitrosourea (BCNU) inhibited hepatic glutathione reductase by 75 percent and increased dramatically the biliary efflux of GSSG produced by administration of diquat. BCNU pretreatment markedly potentiated diquat hepatotoxicity in the Fischer rats and modestly in Sprague-Dawley rats. BCNU-pretreated Fischer rats did not show an enhanced depletion of nonprotein sulfhydryls in response to diquat, in spite of the dramatic potentiation of the hepatic necrosis produced, nor were protein thiols depleted. The effects of BCNU on diquat hepatotoxicity in the Fischer rat are consistent with a critical role for reactive oxygen species in the pathogenesis of the observed hepatic necrosis and for the protective role of the glutathione peroxidase/reductase system. The data suggest that shifts in thiol-disulfide equilibria are not responsible for the cell death produced by oxidant stress in vivo, but are consistent with a role for lipid peroxidation in the pathogenesis of the lesion.

Animals↗
PubMed1987

Antepartum fetal surveillance in the patient with decreased fetal movement.

Whenever a patient has the subjective perception of decreased fetal movement, prompt evaluation in the form of antepartum fetal surveillance has been undertaken. The purpose of this report is to describe our experience with 489 pregnant women who came between Jan. 1 and Dec. 31, 1985 to our Antepartum Fetal Surveillance Clinic with this complaint alone or in association with another indication for fetal surveillance. Overall, 838 nonstress tests were performed, and the results were reactive, 93.2%; nonreactive, 6.8%; and fetal heart rate decelerations, 6.1%. Comparison of the first nonstress test results between those with decreased fetal movement alone or in combination with another diagnosis demonstrated a similar incidence of nonreactivity and fetal heart rate decelerations. In those patients whose indication was decreased fetal movement alone, there was a 3.7 times greater likelihood of diminished amniotic fluid volume. When the last test within 7 days of delivery was analyzed, the decreased fetal movement alone group had a lower incidence of cesarean delivery, cesarean delivery for fetal distress, and Apgar scores less than 7 than patients with an additional indication for testing. In summary, decreased fetal movement continues to be an acceptable indication for fetal surveillance. Based on our retrospective experience, the most reasonable approach appears to be a combination of nonstress test and amniotic fluid volume assessment. Unless the patient has additional indications for fetal surveillance, the patient with decreased fetal movement with a reactive nonstress test and a normal amniotic fluid volume does not appear to warrant additional testing.

Amniotic Fluid↗
PubMed1987

Methods for determination of lipid peroxidation in biological samples.

Interest in the pathological consequences of lipid peroxidation has led to the development of a number of analytical approaches to the quantitation of products. However, the various analytical methodologies employed often do not measure the same chemical classes of products, and apparent discrepencies have been observed, particularly in studies of lipid peroxidation in biological systems. This review provides a brief discussion of some of the strengths and weakness of methods currently used for the determination of lipid peroxidation in biological tissues.

Animals↗
PubMed1987

Antepartum cardiotocography.

Antepartum cardiotocography remains a valuable adjunct in the management of the high-risk gravida. Twice weekly use of NST coupled with real-time ultrasound assessment of amniotic fluid volume appear reasonable approaches to testing. More controversial is the use of testing in all pregnancies. Clearly, if one could reduce the perinatal mortality to 1-2/1000, such universal application of testing could be justified. However, more pragmatic concerns, such as personnel and cost constraints have all but prohibited the adoption of this policy. Secondly, in an attempt to improve the predictive reliability of antenatal testing additional evaluation of patients demonstrating diminished AFV or variable decelerations should be considered. More frequent testing or consideration for delivery are reasonable management plans. Finally, the use of acoustic stimulation to reduce the frequency of persistently non-reactive NSTs offers considerable promise. Investigations in this and other techniques of surveillance are ongoing. The best single method remains to be discovered, but utilization of current techniques offers the obstetrician a reliable technique by which to assess fetal well-being.

Acoustic Stimulation↗
PubMed1987

Amniotic fluid volume assessment with the four-quadrant technique at 36-42 weeks' gestation.

An ultrasound approach was developed to identify normal amniotic fluid volume. The uterine cavity was divided into four quadrants. With the use of linear-array, real-time B-scanning, the vertical diameter of the largest pocket in each quadrant was measured. The sum of these four quadrants was used to provide a single number for the amniotic fluid volume and termed the amniotic fluid index. This approach is simple, requires little time and gives a semiquantitative estimate of amniotic fluid volume. Based on our observations, the normal amniotic fluid index in term gestation is 12.9 +/- 4.6 cm. Evaluation of the relationship between amniotic fluid volume and fetal outcome is under investigation.

Amniotic Fluid↗
PubMed1987

The four-quadrant assessment of amniotic fluid volume: an adjunct to antepartum fetal heart rate testing.

Amniotic fluid volume assessment using a semiquantitative four-quadrant technique, the amniotic fluid index, was evaluated in relationship to fetal heart rate (FHR) testing and perinatal morbidity in 330 high-risk pregnancies. An inverse relationship was found between the amniotic fluid index and nonreactive nonstress tests (NST), FHR decelerations, meconium staining, cesarean section for fetal distress, and low Apgar scores. More important, adverse perinatal outcome was significantly more frequent with diminished compared with normal amniotic fluid volume, even if the NST was reactive.

Amniotic Fluid↗
PubMed1987

Four-quadrant assessment of amniotic fluid volume. Interobserver and intraobserver variation.

While the use of the four-quadrant technique, or the amniotic fluid index (AFI), for amniotic fluid volume assessment has been shown to correlate with perinatal outcome, one concern among clinicians is the reliability of a single AFI measurement. The purpose of this investigation was to ascertain the margin of error using this technique among 23 term and postterm women. The AFI was obtained using linear array real-time B-scan ultrasound to measure the vertical diameter of the largest amniotic fluid pocket in each of the four quadrants. The sum of these measurements was expressed as the AFI. Eight women underwent ten consecutive AFI measurements by the same sonographer to determine intraobserver variation. Interobserver variation between five sonographers was measured by assessing the AFI in 15 additional patients. With the amniotic fluid volume in the low or normal range, our results demonstrated the intraobserver and interobserver variations in AFI to average 1.0 and 2.0 cm, respectively. With an above-normal amniotic fluid volume, a 2.5- to 3-fold greater variation was observed. A relatively small margin of error appears to exist between observers using the four-quadrant technique to assess amniotic fluid volume.

Amniotic Fluid↗
PubMed1987

Amniotic fluid index measurements during pregnancy.

Amniotic fluid volume assessment has become an important part of antepartum fetal surveillance. The amniotic fluid index (AFI), or four-quadrant technique, has been suggested for this purpose. While previous reports have outlined this technique and correlated the results with pregnancy outcome, none have reviewed the changes in AFI throughout pregnancy. We studied AFI changes from 11 through 43 weeks' gestation. As part of the entry criteria, only patients with good dates were evaluated. The AFI was determined by the summation of the vertical diameter of the largest pocket in each of the four quadrants. All amniotic fluid studies were conducted using real-time linear array B-scan. During the study period, 197 patients with good dates confirmed clinically and sonographically underwent 262 AFI assessments. From 11 to 26 weeks the AFI rose progressively. Thereafter until term, the AFI remained approximately 16.2 +/- 5.3 cm. After 38 weeks the AFI appeared to gradually decline. Data obtained from this study population corroborate previously defined normal amniotic fluid volumes. These results also suggest that serial measurements of the AFI may be an effective means of assessing fetal status throughout pregnancy.

Amniotic Fluid↗