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PubMed2005

Induction of IFN-regulated factors and antitumoral surveillance by transfected placebo plasmid DNA.

Delivery of DNA encoding therapeutic genes in vivo has great potential for treating malignancy as well as genetic diseases. Delivery of placebo DNA without a transgene is used as a control in gene therapy studies. It is tacitly assumed by most investigators that the protein expressed from the transfected DNA has phenotypic consequences, but that the consequences are not from the DNA itself. Here, we demonstrate that transfection of control plasmid DNA (that does not express a gene product) into tumor cell lines induces a dramatic (>10-fold) increase in the expression of the interferon (IFN)-regulated genes IRF7, STAT1, MIG (approved gene symbol CXCL9), MHCI (MICA), and CD11a (ITGAL) in tumor cell lines. Induction of these genes inhibits tumor development and tumor growth in immunocompetent mice that are immunized with apoptotic tumor cells. The antibody depletion study indicates that the underlying mechanism by which transfection of control DNA induces IFN-regulated genes is the induction of a secreting factor(s) such as IFN-beta. Three lines of evidence indicate that DNA transfection-mediated induction of IFN-regulatory genes is independent of TLR9. The three lines of evidence are: (1) TLR9 is not expressed in either SCCVII or 4T1 cell line, (2) activation of TLR9 downstream signaling molecules is not associated with the induction of gene expression, and (3) the secretion factor(s) obtained from the conditioned medium of DNA-transfected SCCVII tumor cells induces the same type of gene expression in the 4T1 tumor cell line, which is refractory to the gene induction by DNA transfection. Our finding indicates that the 4T1 tumor cell line, which is resistant to the DNA transfection-mediated induction of IFN-regulated genes, can be used to determine the real therapeutic gene function.

Animals↗
PubMed1992

A prospective randomized clinical trial comparing two oxytocin induction protocols.

OBJECTIVE: Our objective was to compare the safety and efficacy of two accepted oxytocin induction protocols that differ in oxytocin dose increments. STUDY DESIGN: At the Carolinas Medical Center in Charlotte, North Carolina, 151 women with indications for induction of labor were prospectively randomized into one of two oxytocin induction protocols. Safety and efficacy of the two protocols were analyzed with two-tailed t tests and chi 2. RESULTS: Time from induction to establishment of a regular labor pattern was significantly shorter in the experimental group compared with the traditional group (p = 0.03). However, no significant difference was seen from onset of induction to time of delivery. Incidences of hyperstimulation were not significantly different between the two protocols, but there was a trend toward a higher incidence of fetal heart rate changes in the experimental group (p = 0.08). CONCLUSION: These data suggest that induction with larger dose increments will shorten time to adequate labor without an associated increase in uterine hyperstimulation or poor neonatal outcome. The differences in heart rate changes are concerning and merit further investigation. If confirmed by further studies, an increased risk of cord compression could outweigh the benefit of a faster onset of contractions.

Adult↗
PubMed1981

Oxytocin and the initiation of human parturition. I. Prostaglandin release during induction of labor by oxytocin.

Concentrations of plasma prostaglandins E and F and the 15-keto-13,14 dihydrometabolite of PGF2 alpha (PGFM) were determined by radioimmunoassay in 15 women who underwent induction of labor with oxytocin. Plasma PGFM rose significantly during the oxytocin infusion in nine women who went on to deliver vaginally but did not change in six women in whom induction of labor failed. Plasma PGE and PGF levels also rose during the infusion in the nine women with successful induction of labor but the changes were not statistically significant. In comparison to the six women in whom induction failed, however, plasma PGE in the nine women with successful induction reached significantly higher levels. Oxytocin infusions elicited uterine contractions of similar frequency in both groups of women, but the cervix failed to dilate in the six women in whom induction failed. The oxytocin-induced rise in plasma PGFM is, therefore, not simply a consequence of uterine contractions. We suggest that oxytocin stimulates PGF production in the pregnant uterus when it is appropriately sensitized to oxytocin, causing a potentiation of the oxytocin-induced contractions which is necessary for the contractions to become efficient in dilating the cervix. We further suggest that the stimulation of PGF production by oxytocin is mediated by oxytocin receptors, probably in the decidua.

Dinoprost↗
PubMed1996

The presence of fetal fibronectin in the cervicovaginal secretions of women at term--its role in the assessment of women before labor induction and in the investigation of the physiologic mechanisms of labor.

OBJECTIVE: Our purpose was to determine whether the presence of fetal fibronectin in cervicovaginal secretions of patients undergoing induction of labor reflected the cervical state and ultimately the ease of induction of labor. STUDY DESIGN: A prospective observational study of 103 patients undergoing induction of labor at term was conducted at Liverpool Maternity Hospital, a large university teaching hospital. We studied the women after 37 completed weeks of pregnancy. A Dacron (Adeza Biomedical, Sunnyvale, Calif.) polyester swab specimen was first taken from the endocervix for assessment of the presence of the fetal fibronectin. The cervix was then assessed by digital vaginal examination and scored with a modified Bishop's score. The fetal fibronectin swab was processed at the bedside with a membrane immunoassay kit specific for fetal fibronectin. A score was ascribed depending on the strength of the fibronectin reaction determined by the intensity of the color change on the plate, the presence of fetal fibronectin resulting in a score of 1 to 4. The patient was subsequently managed according to the standard induction protocol of the unit. The clinicians involved in the patient's care were blind to the result of the fetal fibronectin swab. RESULTS: There was a good correlation between the modified Bishop's score and the fetal fibronectin score (r = 0.58, p < 0.001). To predict a latent phase of < 8 hours, a fetal fibronectin score of 3 or 4 has a sensitivity of 73% with a specificity of 83% and a modified Bishop score of > or = 4 has a sensitivity of 75% and a specificity of 73%. For delivery within 12 hours of induction of labor a fetal fibronectin score of > or = 3 has a sensitivity of 61% and specificity of 83% compared with the modified Bishop score of > or = 4, which has a sensitivity of 76% and a specificity of 72.5%. CONCLUSIONS: The fetal fibronectin score is as good as the modified Bishop score as an index of the ease with which induction of labor may be performed. This would imply that it also reflects the proximity of the onset of labor. The presence of fetal fibronectin cervicovaginal secretions is therefore a marker of the changes in the cervix and membranes that precede labor regardless of the gestational age.

Adolescent↗
PubMed1997

Induction of labor with use of a Foley catheter and extraamniotic corticosteroids.

OBJECTIVE: Our purpose was to examine the hypothesis that corticosteroids, when administered extraamniotically, can enhance the labor process and reduce the induction-to-delivery interval. STUDY DESIGN: A double-blind, randomized study was conducted on 98 women with a gestational age of 36 to 42 weeks, an unfavorable cervix, and medical indications for delivery, who were assigned to receive either 20 mg of dexamethasone in saline solution (study group, n = 50) or saline solution only (control group, n = 48) administered extraamniotically through an intracervical inflated Foley balloon catheter. The net effect of steroids was assessed with use of multivariant logistic regression analysis. RESULTS: The mean time intervals between induction of labor to the active phase and between induction of labor to delivery were significantly shorter in the study group compared with those of the control group (7.8 +/- 3.1 hours vs 9.9 +/- 3.9 hours, p < 0.03, 11.9 +/- 3.0 hours vs 14.5 +/- 4.8 hours, p < 0.01, respectively). Those not receiving steroids were at a 3.2 higher risk of having a longer time interval of induction to delivery (95% confidence interval 1.1 to 9.5). The general success rate in achieving vaginal delivery was, however, similar between the groups. CONCLUSIONS: Induction of labor with use of an intracervical Foley balloon catheter and extraamniotic corticosteroids reduces the time interval from induction of labor to delivery. This may indicate a possible role for corticosteroids in the parturition process.

Adult↗
PubMed1999

A comparison of orally administered misoprostol with vaginally administered misoprostol for cervical ripening and labor induction.

OBJECTIVE: Our purpose was to compare orally administered with vaginally administered misoprostol for cervical ripening and labor induction. MATERIAL AND METHODS: Two hundred twenty subjects with medical or obstetric indications for labor induction and undilated, uneffaced cervices were randomly assigned to receive orally administered or vaginally administered misoprostol. Fifty micrograms of oral misoprostol or 25 microgram of vaginal misoprostol was given every 4 hours. If cervical ripening (Bishop score of >/=8 or cervical dilatation of >/=3) or active labor did not occur, repeated doses were given to a maximum of 6 doses or 24 hours. Thereafter, oxytocin was administered intravenously by a standardized incremental infusion protocol to a maximum of 22 mU/min. RESULTS: Of the 220 subjects evaluated, 110 received orally administered misoprostol and 110 received vaginally administered misoprostol. Fewer subjects who received the oral preparation (34/110, 30.9%) were delivered vaginally within 24 hours of initiation of induction, in comparison with those who received the vaginal preparation (52/110, 47.3%) (P =.01). The average interval from start of induction to vaginal delivery was nearly 6 hours longer in the oral treatment group (mean and SD 1737.9 +/- 845.7 minutes) than in the vaginal treatment group (mean and SD 1393.2 +/- 767.9) (P =.005, log-transformed data). Orally treated patients required significantly more doses than vaginally treated patients (orally administered doses: mean and SD 3.3 +/- 1.7; vaginally administered doses: mean and SD 2.3 +/- 1.2) (P <.0001). Oxytocin administration was necessary in 83 (75.4%) of 110 orally treated subjects and in 65 (59.1%) of 110 vaginally treated subjects (P =.01, relative risk 1. 28, 95% confidence interval 1.06-1.54). Vaginal delivery occurred in 95 (86.4%) orally treated subjects and in 85 (77.3%) vaginally treated subjects (P =.08, relative risk 1.12, 95% confidence interval 0.99-1.27), with the remainder undergoing cesarean delivery. There was no difference in the incidence of uterine contractile abnormalities (tachysystole, hypertonus, or hyperstimulation), intrapartum complications, or neonatal outcomes between the 2 groups. CONCLUSIONS: Oral administration of 50-microgram doses of misoprostol appears less effective than vaginal administration of 25-microgram doses of misoprostol for cervical ripening and labor induction. Further investigation is needed to determine whether orally administered misoprostol should be used for cervical ripening and labor induction.

Administration, Intravaginal↗
PubMed2002

Delayed induction of delta-6 and delta-5 desaturases by a peroxisome proliferator.

Delta-6 desaturase (D6D) is the key enzyme for the synthesis of highly unsaturated fatty acids (HUFA) such as arachidonic acid (AA) and docosahexaenoic acid (DHA) in mammals. Transcription of D6D gene is activated by both sterol regulatory element binding protein-1c (SREBP-1c) and peroxisome proliferators (PP). This response of D6D is paradoxical because SREBP-1c transactivates genes for fatty acid synthesis in liver, while PP induce enzymes for fatty acid oxidation. We hypothesized that the induction of D6D gene by PP is a compensatory response to the increased HUFA demand caused by peroxisome proliferation and induction of fatty acid oxidation. We investigated the time-course effects of a PP, Wy14643, on the induction of HUFA metabolizing genes and HUFA profile in rat liver. The mRNA of fatty acid oxidation enzymes in the Wy14643 fed group became significantly higher than controls at 4 h and reached maximum within 28 h. In contrast, the mRNA of delta-6 and delta-5 desaturases in the Wy14643 group was not significantly higher than control at 4 h and took >28 h to reach the maximum. Despite the induction of HUFA synthetic pathway, the concentration of end products (AA and DHA) remained unchanged throughout the 4-day period in liver phospholipids and non-esterified fatty acids. Taken together, this study supports our hypothesis and suggests that peroxisome proliferation and induction of fatty acid oxidation enzymes are the major mechanisms of the induction of HUFA synthesis by PP.

Animals↗
PubMed2003

Essential roles for NF-kappa B and a Toll/IL-1 receptor domain-specific signal(s) in the induction of I kappa B-zeta.

I kappa B-zeta, a new negative-regulator of nuclear factor-kappa B (NF-kappa B), is strongly induced by lipopolysaccharide or interleukin-1 beta stimulation, but not by tumor necrosis factor-alpha. Here, we analyzed the mechanisms for transcriptional induction of I kappa B-zeta. I kappa B-zeta mRNA was induced by overexpression of MyD88 or TRAF6, but not TRAF2. Stimulation of macrophages with peptidoglycan or CpG DNA, which activated Toll-like receptor 2 or 9, respectively, also resulted in I kappa B-zeta induction. Thus, activation of the MyD88-dependent signaling pathway, commonly found downstream of different Toll/interleukin-1 receptor (TIR) domains, is sufficient for I kappa B-zeta induction. The induction was inhibited by treatment with various inhibitors of NF-kappa B activation or by overexpressing I kappa B-alpha or beta, indicating essential roles for NF-kappa B in I kappa B-zeta induction. However, overexpression of the NF-kappa B subunits induced I kappa B-alpha, but not I kappa B-zeta. These results indicate the existence of another signal essential for I kappa B-zeta induction, which is specifically mediated by the TIR domain-mediated signaling pathway.

Adaptor Proteins, Signal Transducing↗
PubMed2001

Acute and chronic nicotine exposure reverse age-related declines in the induction of long-term potentiation in the rat hippocampus.

Long-term potentiation (LTP) is widely considered to be the cellular substrate of learning and memory. The induction of LTP becomes more difficult with age in parallel with declining learning and memory ability. Because nicotine improves learning and memory in aged rats, we examined the effects of acute and chronic nicotine exposure on age-related declines in LTP induction. We found that acute nicotine exposure lowered the threshold for LTP induction in the aging hippocampus. The effect of nicotine was mimicked by the alpha7 nicotinic acetylcholine receptor (nAChR) antagonist methyllycaconitine and blocked by the non-alpha7 nAChR antagonist dihydro-beta-erythroidine, suggesting that both nicotine-mediated desensitization of alpha7 nAChRs and activation of non-alpha7 nAChRs contribute to the nicotine effect. The non-alpha7 nAChR agonist A85380 that facilitates the induction of LTP in the young hippocampus had no effect, however, suggesting that at least one pathway involving non-alpha7 nAChRs was altered by aging. Chronic nicotine treatment of aged rats also lowered the threshold for LTP induction and acute nicotine exposure lowered the threshold further in the chronic-nicotine-treated aged hippocampus. These results not only suggest that the mechanisms mediated by acute and chronic nicotine exposure are different, but also demonstrate that age-associated declines in LTP induction can be reversed with nicotine treatment.

Aconitine↗
PubMed1997

Attenuation of nitric oxide synthase induction in IRF-1-deficient glial cells.

Nitric oxide (NO) produced by inducible nitric oxide synthase (iNOS) exerts inhibitory and cytotoxic effects on various cells including neuronal cells. Glial NO production, mediated via induction of iNOS, is thought to facilitate neuronal damage during cerebral ischemia. Recently, interferon regulatory factor-1 (IRF-1) has been reported to be an essential transcription factor for iNOS mRNA induction in murine macrophages. However, expression of IRF-1 and its role in the central nervous system have not been examined. In the present study, by using primary glial cell cultures from mice with targeted disruption of the IRF-1 gene, we investigated whether IRF-1 is involved in iNOS mRNA induction in glial cells. After stimulation with lipopolysaccharide and interferon-gamma, IRF-1 mRNA was strongly induced in wild-type (IRF-1 +/+) glial cells. iNOS mRNA induction and nitrite production in IRF-1 -/- glial cells were reduced as compared with those observed in IRF-1 +/+ glial cells. Diethyldithiocarbamate, a selective inhibitor of nuclear transcription factor kappa B (NF-kappa B), completely inhibited iNOS mRNA induction. These results suggest that not only NF-kappa B but also IRF-1 play important roles in iNOS mRNA induction in the central nervous system.

Animals↗
PubMed1998

Stimulant-mediated c-fos induction in striatum as a function of age, sex, and prenatal cocaine exposure.

Induction of the immediate-early gene c-fos by the stimulants cocaine and amphetamine (AMPH) was analyzed by Fos immunocytochemistry at different ages in the brains of prenatally cocaine-treated and control rats. Cocaine and AMPH induced c-fos in patches of striatal neurons during the first postnatal week, and thereafter produced a progressively more homogeneous pattern that was more dense medially. Quantification of Fos-immunoreactive cells in older rats revealed differences related to sex and prenatal cocaine treatment. Both cocaine and AMPH produced dose-dependent increases in the number of Fos-immunoreactive cells in striatum. Prenatal cocaine exposure resulted in increased Fos in males in response to AMPH (2 mg/kg) at P18 and cocaine (10 mg/kg) at 1-2 months. In females, prenatal cocaine treatment resulted in a reduced response to cocaine at 1-2 months. Increased c-fos induction was observed in control females compared to control males in response to low doses of stimulants; no such sex difference was observed in prenatally cocaine-treated rats. The dopamine D1 antagonist SCH23390 blocked cocaine-mediated c-fos induction in all groups. The NMDA antagonist MK-801 blocked cocaine-mediated c-fos induction in the medial striatum. In females only, MK-801 pretreatment resulted in a dramatic increase in the number of Fos-immunoreactive cells in lateral striatum. These findings indicate differences in the neural basis of c-fos induction in males and females, and changes in stimulant-mediated c-fos induction resulting from prenatal cocaine exposure.

Aging↗
PubMed1997

Oral mifepristone 600 mg and vaginal gemeprost for mid-trimester induction of abortion. An open multicenter study. UK Multicenter Study Group.

This open multicenter study was performed in 20 hospital gynecological units in the UK. The effects of 600 mg oral mifepristone as pretreatment to vaginal prostaglandin induction of second trimester abortion was studied in 267 women. The primary efficacy variable was the abortion induction interval, defined as the time taken to expel the fetus from the time of administration of the first prostaglandin pessary. Induction was commenced 36 to 48 hours following mifepristone intake. The mean abortion induction interval was 7 h. A total of 81.9% of women aborted within 12 h. There was a significant relationship between abortion induction interval and age of gestation, and a significant inverse relationship between abortion induction interval and parity. Vomiting, pelvic pain, and nausea were the most frequently reported adverse events. Two patients required transfusion and one patient with a uterine scar from a previous cesarean section suffered a ruptured uterus and hysterotomy.

Abortifacient Agents, Nonsteroidal↗
PubMed1991

Homeogenetic neural induction in Xenopus.

Neural induction is known to involve an interaction of ectoderm with dorsal mesoderm during gastrulation, but several kinds of studies have argued that competent ectoderm can also be neutralized via an interaction with previously neuralized tissue, a process termed homeogenetic neural induction. Although homeogenetic neural induction has been proposed to play an important role in the normal induction of neural tissue, this process has not been subjected to detailed study using tissue recombinants and molecular markers. We have examined the question of homeogenetic neural induction in Xenopus embryos, both in transplant and recombinant experiments, using the expression of two neural antigens to assay the response. When ectoderm that is competent to be neuralized is transplanted to the region adjacent to the neural plate of early neurula embryos, it forms neural tissue, as assayed by staining with antibodies against the neural cell adhesion molecule, N-CAM. Transplants to the ventral region, far from the neural plate, do not express N-CAM, indicating that neuralization is not occurring as a result of the transplantation procedure itself. Because this response might be occurring as a result of interactions of ectoderm with either adjacent neural plate tissue, or with underlying dorsolateral mesoderm, recombinant experiments were performed to determine the source of the neuralizing signal. Ectoderm cultured in combination with neural plate tissue alone expresses neural markers, while ectoderm cultured in combination with dorsolateral mesoderm does not. We conclude that neural tissue can homeogenetically induce competent ectoderm to form neural tissue and argue that this induction occurs via planar signaling within the ectoderm, a mechanism that, in normal development, may be involved in interactions within presumptive neural ectoderm or in specifying structures that lie near the neural plate.

Animals↗
PubMed2003

Loss of activity of the selenoenzyme thioredoxin reductase causes induction of hepatic heme oxygenase-1.

The stress response enzyme heme oxygenase (HO)-1 is induced in livers of selenium-deficient rodents, probably to compensate for loss of certain selenoproteins. We sought to identify those selenoproteins. Selenium-replete mice with genetic deletion of selenoprotein P or glutathione peroxidase-1 did not have elevated hepatic HO activity, thus ruling out involvement of those selenoproteins in HO-1 induction by selenium deficiency. However, inhibition of thioredoxin reductase (TrxR) by a low dose of gold in the form of aurothioglucose led to induction of hepatic HO activity. Moreover, further induction by phenobarbital was observed. This HO-1 induction pattern is also seen in selenium-deficient mice. In the rat hepatoma cell line H4IIE, inhibition of TrxR by aurothioglucose or by 1-chloro-2,4-dinitrobenzene led to induction of HO-1. We conclude that loss of TrxR is responsible for the induction of HO-1 by selenium deficiency.

Animals↗
PubMed2002

Labor induction with vaginal misoprostol and extra-amniotic prostaglandin F2alpha gel.

OBJECTIVE: To compare the effectiveness of vaginally administered misoprostol with extra-amniotic prostaglandin F2alpha (PGF2alpha) gel for induction of labor. METHOD: A randomized controlled trial, with women allocated to receive either misoprostol 50 microg intra-vaginally or extra-amniotic PGF2alpha gel 5 mg, was conducted in Harare Maternity Hospital. A total of 152 women were admitted for induction of labor with a term singleton, pregnancy and cephalic presentation were recruited. The main outcome was duration of induction. RESULTS: There were no differences in the characteristics of women in the two groups at recruitment. In the misoprostol group there was a significantly reduced need for augmentation of labor with oxytocin (OR=0.36; 95% C.I. 0.17-0.73) and delivery by cesarean section for failure to progress (OR=0.11; 95% C.I. 0.00-0.88). The risk for duration of induction to vaginal delivery exceeding 12, 18 or 24 h was reduced by 18%, 38% and 68%, respectively, but only the risk for duration >24 h was significantly reduced (OR=0.32; 95%C.I. 0.11-0.91). The mean duration of induction was shorter in the misoprostol group, 15.2 vs. 23.6 h (P=0.02). There were no differences in fetal outcome. CONCLUSION: Misoprostol 50 microg was associated with less use of oxytocin in labor, a shorter induction to delivery interval and fewer cesarean sections for failure to progress when compared with extra-amniotic PGF2alpha gel.

Administration, Intravaginal↗
PubMed2002

Induction of labor in twin pregnancy after 36 weeks does not increase maternal-fetal morbidity.

OBJECTIVE: To compare maternal and perinatal outcomes in twin pregnancy patients without any fetal or maternal disease, managed by labor induction or expectant management after 36 weeks gestation. METHODS: We conducted a case-control study of 81 patients: labor induction (n=36) vs. expectant management (n=45). Labor was induced using oxytocin (n=18), vaginal prostaglandins (n=6) or intrauterine balloon catheter (n=12) according to the Bishop score. Maternal and perinatal outcome variables were compared among both groups. RESULTS: The characteristics of the labor induction group and the expectant management group were not statistically different, except for the rate of nulliparae (55.6% vs. 33.3%) and the rate of epidural analgesia (100% vs. 80%). There was no significant difference in labor time (6.5+/-2.8 h vs. 6.0+/-3.6 h), cesarean section rate (8.3% vs. 13.3%) or duration of maternal hospitalization (7.3+/-2.0 days vs. 7.5+/-2.3 days) in the labor induction group and in the expectant management group, respectively. The birth weight was higher in the labor induction group than in the expectant management group (2639+/-352 g vs. 2463+/-298 g, P<0.001). The rate of Apgar score <7 at 5 min was 0% and 3.3%, respectively. Neonatal intensive care unit admission occurred in 30.5% and 26.6% of the groups, respectively. No perinatal death was reported. CONCLUSION: Induction of labor may be proposed to patients with uneventful twin pregnancy after 36 weeks gestation without increasing maternal-fetal morbidity.

Apgar Score↗
PubMed1987

Comparison of respiratory inductive plethysmography and thoracic impedance for apnea monitoring.

Thoracic impedance apnea monitors may fail to detect obstructive apnea, may falsely alarm when the infant is breathing, and may confuse cardiac artifact with respiratory impedance. Therefore, we compared the performance of a respiratory inductive plethysmograph and a thoracic impedance monitor with a reliable measure of airflow, either nasal CO2 or pneumotachograph, during 29 studies in 28 patients referred for sleep laboratory evaluation. Sleep time averaged 72 +/- 37 (SD) minutes. The inductance plethysmography and the impedance monitor detected 99.6% +/- 0.6% and 98.3% +/- 3.0% of breaths, respectively. However, in two studies, the impedance monitor detected many extra breaths, once because of cardiac-induced impedance changes and once because of partial airway obstruction-induced impedance changes. In 11 studies, cardiac artifact was sometimes misinterpreted as a breath by the impedance monitor. The impedance monitor, but not the inductance plethysmograph, missed breaths following sighs in 16 of 29 studies. Both monitors detected all 60 episodes of central apnea. The inductance plethysmography detected 35 of 38 episodes of obstructive apnea, but the impedance monitor identified only two such events. Apnea was detected falsely four times by the inductance plethysmograph and 14 times by the impedance monitor. These results suggests that a respiratory inductive plethysmograph would have significant advantages over impedance monitoring, including the ability to detect obstructive apnea, and freedom from cardiac artifact.

Apnea↗
PubMed1998

Relative induction of heat shock protein in coronary endothelial cells and cardiomyocytes: implications for myocardial protection.

OBJECTIVES: Induction of the 70 kd heat shock protein in the heart is known to exert a protective effect against postischemic mechanical and endothelial dysfunction. However, the exact site of induction and the mechanisms involved remain unknown. The aim of this study was to investigate the relative capacity of endothelial and myocardial cells to express the 70 kd heat shock protein in response to heat stress, as well as their significance. METHODS: (1) Postischemic recovery of cardiac mechanical and endothelial function was studied in isolated rat hearts with and without endothelial denudation with saponin. (2) Semiquantitative determination of induction of 70 kd heat shock protein by Western immunoblotting was performed in the whole cardiac homogenate, in isolated cardiac myocytes, and in coronary endothelial cells. (3) Immunocytochemistry was used to visualize the distribution of induction of 70 kd heat shock protein in both cell types. RESULTS: Postischemic recovery (percent preischemic value +/- standard error of the mean) of cardiac output in hearts from heat-stressed animals was significantly improved (66.7 +/- 6.9 vs 44.5 +/- 4.5 in the control group, p < 0.01). In heat-stressed hearts treated with saponin no improvement in the recovery of cardiac output was noted (44.7 +/- 6.9 in heat-stressed hearts vs 38.0 +/- 4.0 in heat-stressed, saponin-treated hearts, p = not significant). Endothelial function (as assessed by the vasodilatory response to the endothelium-dependent vasodilator 5-hydroxytryptamine) improved from 31.0 +/- 5.2 in the control group to 65.8 +/- 7.1 in heat-stressed hearts (p < 0.02 vs control) and dropped to -1.9 +/- 3.8 in heat-stressed hearts treated with saponin. Immunocytochemistry showed that only sections of hearts from heat-treated rats showed a strong specific reaction with heat shock protein antibody. The positive staining was seen in endothelial cells. Induction of 70 kd heat shock protein content in the whole cardiac homogenate from heat-stressed rats as measured by Western immunoblotting was 5.2 +/- 1.9 (vs 0.0 in non-heat-stressed rats, p < 0.0001) and dropped to 0.0 in heat-stressed hearts treated with saponin. The tentative amount of 70 kd heat shock protein was 18.1 +/- 7.8 in isolated endothelial cells from heat-stressed hearts and 2.3 +/- 2.3 in isolated cardiac myocytes (p < 0.01 vs endothelial cells). CONCLUSIONS: Coronary endothelial cells are the main site of induction of 70 kd heat shock protein in the heart and appear to contribute to the protective effects of heat stress on the recovery of mechanical and endothelial function.

Animals↗