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PubMed1991

Induction of human monocyte IL-1 mRNA and secretion during anti-CD3 mitogenesis requires two distinct T cell-derived signals.

The T cell signals that regulate the induction of human monocyte IL-1 during primary immune activation were investigated by using anti-CD3 mitogenesis. The induction of monocyte IL-1 alpha and beta mRNA during anti-CD3 mitogenesis was rapid (less than or equal to 1 h) and required the presence of both T cells and anti-CD3. The addition of T cells plus a nonmitogenic anti-CD5 antibody failed to induce IL-1 alpha or beta mRNA, indicating that IL-1 mRNA induction by anti-CD3 required T cell activation. Experiments using double chamber culture wells revealed that the major initial phase of IL-1 alpha and beta mRNA induction (1 to 12 h) required direct cell contact between monocytes and T cells. A subsequent minor late phase (greater than or equal to 12 h) of IL-1 mRNA was induced independently of cell contact in monocytes that received only soluble factors generated during anti-CD3 mitogenesis and was temporally associated with the appearance in culture supernatants of the late phase IL-1-inducing cytokines, IL-2, IFN-gamma, and TNF-alpha. Metabolic inactivation of T cells using paraformaldehyde demonstrated that the ability of T cells to induce IL-1 mRNA via cell contact was acquired only after activation of T cells via solid phase anti-CD3. Furthermore, pretreatment of T cells with the protein synthesis inhibitor emetine had no effect on T cell-mediated induction of monocyte IL-1 mRNA or cell-associated IL-1 alpha and beta, indicating that the expression of the IL-1 inductive signal did not require protein synthesis. Despite their ability to induce monocyte IL-1 alpha and beta mRNA, activated T cells treated with paraformaldehyde or emetine were no longer able to induce monocytes to secrete IL-1 beta into culture supernatants. However, supernatants from purified T cells that were activated with solid-phase anti-CD3 restored the ability of paraformaldehyde or emetine-treated T cells to induce IL-1 secretion. These studies provide evidence that supports a two-signal model of monocyte IL-1 production during primary immune activation. The first signal leads to the induction of monocyte IL-1 mRNA and is mediated by direct contact with activated T cells, and the second signal is provided by soluble T cell factors and results in IL-1 secretion.

Antibodies, Monoclonal↗

PubMed1991

[Determinants of susceptibility to the induction of autoimmune diabetes in inbred strains of rats].

Interleukin 2 (IL 2) proved to be important for the generation of autoreactive T cells in the pathogenesis of different autoimmune disorders, including diabetes. Also, we have previously shown that lymphoid cells obtained from inbred strains of rats Dark August (DA) and Albino Oxford (AO) exhibited a genetically determined difference in their ability to produce IL 2. In this study, in DA and AO rats, we analysed the susceptibility to the induction of autoimmune diabetes with multiple subdiabetogenic doses of alloxan. Rats were injected i.v. with 25 mg/kg b.w. of alloxan in 5 consecutive days. All DA rats developed moderate and persistent hyperglycaemia 15 days after the induction. In contrast, AO rats failed to develop the disease after the same regimen of induction. When the induction was made in (AO x DA)F1 rats, all of them developed the disease similar to the susceptible parental DA strain. However, the onset was delayed (the 40th day after the induction) and the glycaemia was constantly lower than in DA rats. Our results indicate that the difference in the response to the induction of autoimmune diabetes between susceptible DA strain, being high IL 2 producer, and resistant AO strain, being low IL 2 producer, is genetically determined. The results also suggest that this control could involve the gene determining the level of IL 2 production in DA and AO rats, thus signifying that the susceptibility to the induction of this form of autoimmune diabetes could be related to the level of IL 2 activity.

Alloxan↗

PubMed1990

[Anesthesia induction in children: propofol in comparison with thiopental following premedication with midazolam].

Propofol provides smooth and rapid induction of anesthesia in adults and guarantees rapid recovery. The use of propofol in adults is frequently associated with pain on injection, but this can be reduced by: (1) injection into the relatively large veins in the forearm or the antecubital fossa: (2) addition of lignocaine to the propofol; or (3) injection of an opioid (alfentanil) before propofol. Compared with experience in adults, there is very little experience with propofol in pediatric anesthesia. The aim of this random prospective study was to compare the induction characteristics of propofol and thiopentone in pediatric anesthesia. Vigilance and behavior in the postoperative period were also compared. METHOD. A total of 75 healthy children aged 3-12 years who were undergoing elective operations were studied. All the children received premedication with 0.5 mg/kg midazolam with 0.02 mg/kg atropine by the rectal route. The children were divided randomly into 3 groups and received: group A, thiopentone 3-6 mg/kg; group B, propofol 1-3 mg/kg mixed with lignocaine (10/200 mg); group C, propofol 1-3 mg/kg, followed 1 min later by alfentanil 0.01 mg/kg. The induction agent was injected over 30 s, if possible into the vein in the forearm or the antecubital fossa. The immediate reaction on vein puncture and any discomfort during the injection were noted. After intubation the anesthesia was maintained with 1 vol% halothane, nitrous oxide and oxygen (2:1). Arterial pressure was measured on arrival in the induction room, immediately after the induction of anesthesia, immediately after intubation and thereafter at 5-min intervals throughout the anesthesia. Heart rate (ECG) and arterial oxygen saturation (saO2) were measured continuously. The existence of any anterograde amnesia was tested (age over 4 years) by means of one of 6 pictures shown to each before operation. The ability to recall the picture shown was recorded 2-5 h postoperatively. The completeness of recovery was assessed at 10-min intervals up to 1 h, and thereafter at 1-h intervals. In the postoperative period a recovery test (postbox test) was performed. The incidence of side effects during the induction of anesthesia and also during recovery and the postoperative period (for 5 h) was recorded. RESULTS. There was no significant difference between the children in the 3 different groups with regard to age, body weight, type of operation, or duration of anesthesia. Among the total of 75 children, 66.7% accepted the vein puncture very well, and 24% well. In some children in each group we observed obstruction of the respiratory tract (group A, 36%; group B, 48%; group C, 64%). Apnea for 20 s was observed only in groups B and C (2 and 3 children respectively). During spontaneous respiration with room air there was a significant decrease of the arterial oxygen saturation about 1 min after induction in all groups. In children ventilated with oxygen by mask, the SaO2 remained nearly constant...

Administration, Rectal↗

PubMed1989

Induction of lymphokine-activated killer activity by interleukin 4 in human lymphocytes preactivated by interleukin 2 in vivo or in vitro.

In an attempt to augment the generation of human cytotoxic effector cells for potential cancer therapy with interleukin 2 (IL2) and lymphokine-activated killer (LAK) cells, the effect of interleukin 4 (IL4) on LAK cell induction was studied. In normal human peripheral blood lymphocytes (PBL), IL4 does not induce LAK activity and inhibits LAK induction by IL2. However, since lymphocyte activation, such as with antigen or mitogen, can render them responsive to IL4, the ability of IL4 to induce LAK activity in lymphocytes preactivated in vivo or in vitro with IL2 was investigated. PBL obtained from 12 patients with advanced cancer 1 to 3 days after IL2 therapy and from eight healthy control subjects were cultured 4 to 5 days with or without IL4 and/or IL2 and then tested for LAK activity as assessed by lysis of Daudi in a 4-h 51Cr release assay. In normal PBL, IL4 failed to induce LAK activity and consistently inhibited LAK induction by a suboptimal concentration of IL2 (10 units/ml). By contrast, IL4 induced LAK activity in PBL from seven of twelve IL2-treated patients and augmented LAK induction by the suboptimal IL2 in PBL from five of twelve IL2-treated patients. With an optimal LAK-inducing concentration of IL2 (1000 units/ml), IL4 less consistently inhibited LAK induction in normal PBL and had a variable effect upon LAK induction in PBL from IL2-treated patients. IL4 induced LAK activity in PBL obtained from a cancer patient after, but not before, systemic IL2 therapy. Similarly, IL4 induced LAK activity in normal PBL only after they had been preincubated with IL2. Thus, IL4 induces LAK activity in lymphocytes preactivated by IL2 in vivo or in vitro. Fluorescence-activated cell sorting revealed that the LAK activity, whether induced by IL4 or by IL2, was mediated largely by non-T (CD5-) natural killer-like (CD56+) cells. The results suggest a regulatory relationship between IL2 and IL4 in the induction and/or maintenance of LAK activity, which might be exploited to augment the generation of cytotoxic cells for lymphokine-mediated immunotherapy of human cancer.

Antigens, CD↗

PubMed1989

Induction of class II MHC antigen expression in macrophages by Mycoplasma species.

Several different Mycoplasma species have been shown to act as mitogens for either T or B cells and as stimulators of macrophage tumoricidal activity. In this report, we show that at least five different species of Mycoplasma are capable of inducing class II MHC expression on macrophages. We have observed significant induction of class II MHC surface expression on the myelomonocytic cell line, WEHI-3, as early as 24 h after deliberate infection of cultures, reaching maximal levels by 4 days. This induction was also apparent at the mRNA level as assessed by Northern blot analysis by using A alpha, E alpha, and A beta probes. However, unlike many other previously described MHC-inducing agents, mycoplasmas failed to induce class I MHC expression at either the cell surface or mRNA levels. Kinetic analysis revealed that induction of class II mRNA by mycoplasmas was slower than induction by IFN-gamma requiring 24 h rather than 8 h for significant increases to be noted. Induction by mycoplasmas does not require the presence of live organisms and remains active after heat treatment of 90 degrees C for 30 min. We have also demonstrated that mycoplasma infection of primary bone marrow macrophage cultures leads to the induction of both class I and class II genes and, as in the case of WEHI-3, this induction does not require the presence of live organisms. These data indicate that several Mycoplasma species have the capacity to induce class II MHC expression in WEHI-3 and both class I and class II MHC expression in bone marrow macrophage cultures in the absence of any T cell products.

Animals↗

PubMedDate not supplied

[Hemodynamic reaction in the ultrarapid induction and protection realized with fentanyl].

The hemodynamic response caused by the orthotracheal intubation and also the fentanyl-induced protection were determined in the patients with ultrarapid anesthetic induction. 60 patients were randomly distributed in 3 groups, each of 30 patients: group I, control, with sequential induction, group II, with ultrarapid induction, and group III with ultrarapid induction protected by fentanyl administration. In the patients in the groups II and III the hydrocortisone in the blood, taken 1 minute before induction and 3 minutes after intubation was dosed radioimmunologically. Measurement of the hemodynamic constants showed the increase of the systolic and diastolic AT, and of the pulse during laryngoscopy and in the first two minutes after intubation in all the patients investigated. The hemodynamic response was stronger in the lot with rapid induction, with important differences in comparison with the group with sequential induction. In the IIIrd group, the previous injection with fentanyl, 5 mcg/kg led to a less intense hemodynamic response to laryngoscopy and intubation, close to that of the control group. Likewise, the injection of the anesthetic was followed by an important decrease in the plasmatic hydrocortisone in comparison with the preinduction values.

Adult↗

PubMedDate not supplied

[The effect of fentanyl as an adjuvant to etomidate and thiopental on the hemodynamic response to the induction of anesthesia and endotracheal intubation].

The hemodynamic modifications during anesthesia induction with etomidat or thiopentalum, with and without pretreatment with fentanyl, were studied in 60 ASA I-II patients. The patients were randomly divided into six subgroups, as a function of the induction agent (etomidat, 0.15 mg/kg, or thiopentalum, 3 mg/kg) and of the pretreatment used (fentanyl, 5 micrograms/kg, or 0.9% 1 ml/kg saline solution). Systolic, diastolic ATs and pulse were followed and measured during induction and after tracheal intubation. During induction the presence or absence of the thoracic rigidity, after fentanyl administration, and also the appearance of myoclonias and of local pain after etomidat injection were noted. Measurement of hemodynamic constants showed, in the control subgroups unprotected by fentanyl, that AT and pulse frequency increase following laryngoscopy and intubation irrespective of the induction agent used. Association of thiopentalum with fentanyl influenced partially tachycardia and postintubation hypertension. Administration of 5 micrograms/kg fentanyl prevented the SAT and pulse modifications but not the DAT variation. Association of 10 micrograms/kg fentanyl ensured a complete protective effect versus the tracheal intubation but, it led, first, to a SAT decrease by intensification of the myocardial depressing effect of the barbiturate. On the other hand, use of fentanyl as induction adjuvant with etomidat ensured the blockage of the pressure response to intubation, with hemodynamic stability during anesthesia induction, irrespective of the dose of fentanyl injected. Thoracic rigidity and the side effects generated by etomidate were absent.

Anesthesia, General↗

PubMed1989

Potentiation of interferon induction of class I major histocompatibility complex antigen expression by human tumor necrosis factor in small cell lung cancer cell lines.

The response of class I major histocompatibility complex antigen expression to in vitro administration of interferon and tumor necrosis factor alpha (TNF-alpha) was measured using class I major histocompatibility complex-deficient small cell lung cancer cell lines. Significant induction also was observed using gamma interferon (IFN-gamma) alone, whereas TNF-alpha alone yielded only modest induction. Classic small cell lung cancer cell lines NCI-H146 and NCI-H209 best demonstrated synergistic HLA and beta 2-microglobulin antigen induction with IFN-gamma and TNF-alpha with the following dose schedule: 3-6 days of TNF-alpha (200 units/ml) followed by 48 h of IFN-gamma (100 IU/ml). Induction was quantitated using an 125I-Protein A radioimmunoassay. Synergistic induction of the HLA and beta 2-microglobulin surface antigens on NCI-H146 was also possible with alpha interferon and TNF-alpha but required a higher concentration of the interferon, i.e., 3-6 days of TNF-alpha (200 units/ml) followed by 48 h of alpha interferon (1000 units/ml). Small cell lung cancer cell line NCI-H146 was further studied for expression of major histocompatibility complex messenger RNA using the optimal doses and sequence of addition of IFN-gamma and TNF-alpha as indicated above. A significant induction with IFN-gamma alone and synergistic induction with both IFN-gamma and TNF-alpha was quantitated for both HLA-A2 and beta 2-microglobulin transcripts using Northern blot analysis. Incubation with relatively low subcytotoxic doses of IFN-gamma and TNF-alpha also resulted in a marked synergistic decrease in c-myc message.

Animals↗

PubMed1987

Induction of asynchronous replication of polyoma DNA in rat cells by ultraviolet irradiation and the effects of various inhibitors.

The ability of various DNA damaging agents to induce asynchronous replication of polyoma DNA (APR) in rat cells carrying integrated copies of these DNA sequences may provide a useful model for understanding mechanisms of gene amplification. The present study has explored in detail the ability of UV irradiation to induce APR in the polyoma transformed rat fibroblast cell line H3. We have found that the optimum condition for induction of APR was obtained by irradiating the H3 cells with UV-C (wavelength, 254 nm) at 1-2 J/m2. Irradiation with UV-B (270-360 nm) was much less effective, and no induction of APR was obtained with even high doses of UV-A (345-440 nm). This action spectrum provides evidence that the critical target for induction of APR is DNA. We found that when normal rat fibroblasts were irradiated with UV-C and then fused to H3 cells, this also led to induction of APR. These results provide evidence that the induction of APR by UV-C is mediated by a trans-acting factor. The induction of APR by UV-C was inhibited by high doses of cycloheximide or actinomycin D, suggesting that the production of this trans-acting factor requires de novo protein and RNA synthesis. On the other hand, low doses of cycloheximide or actinomycin D alone were able to induce APR, perhaps by blocking the synthesis of cellular factors that normally inhibit APR. Thus, induction of APR by UV-C provides a useful system for identifying cellular factors that might mediate or prevent the asynchronous replication of various DNA sequences.

Animals↗

PubMed1987

Effects of human alveolar macrophages on the induction of lymphokine (IL 2)-activated killer cells.

Normal human alveolar macrophages (AM) significantly and reproducibly suppress induction of IL 2-activated killer (LAK) cell activity against allogeneic Burkitt's lymphoma (Daudi) cells. Incubation of purified peripheral blood lymphocytes for 4 days with autologous AM and 1 U/ml of IL 2 resulted in AM-mediated suppression of LAK activity, whereas peripheral blood monocytes isolated freshly by centrifugal elutriation from the same donor potentiated induction of LAK activity by IL 2. The suppression of LAK cell induction by human AM was dependent on the density of AM added to the lymphocyte cultures. Recombinant IFN-gamma did not affect AM-mediated suppression of LAK cell induction by IL 2. Both AM and monocytes stimulated with lipopolysaccharide markedly suppressed LAK cell induction by IL 2. AM-mediated down-regulation was seen only when AM were added immediately after the start of incubation of lymphocytes with IL 2; AM potentiated LAK activity when added 1 day later. Similar AM-mediated suppression of LAK cell induction was observed with four lines of allogeneic lung cancer cells as targets for LAK activity. These results indicate that AM may be important in regulation of in situ induction of LAK activity in the lung.

Cells, Cultured↗

PubMed1986

In vitro induction of proteins by alpha-interferon in hairy cell leukemia.

The striking clinical response of hairy cell leukemia to alpha-interferon led us to investigate the effects of interferon on hairy cells in vitro. We examined the nature of protein induction by interferon in the target hairy cells. To do this, we analyzed whole cell lysates of hairy cells from 11 patients by one-dimensional polyacrylamide gel electrophoresis. With this method, we showed the induction of 16 proteins, which ranged from Mr 140,000 to 12,000. Exposure to alpha-interferon caused very rapid induction of specific proteins in hairy cells, and induction continued for at least 9 days. Proteins were induced at extremely low interferon concentrations, and a dose-response effect was seen with increasing concentrations. A larger number of proteins was induced in hairy cells than in other lymphoid cells under the same conditions. Induction of most proteins was inhibited by actinomycin D, showing that new messenger RNA synthesis was required for their induction to occur. The number or pattern of induced proteins, or their prolonged induction, may be relevant to a change in the target hairy cells which is part of the process resulting in the antiproliferative effect of interferon in hairy cell leukemia.

Dactinomycin↗

PubMed1985

[Clinical evaluation of cases of remission induction failure in acute myelogenous leukemia].

Among 73 patients who were admitted to our hospital between 1972 and 1983, 9 died before starting chemotherapy, 29 achieved complete remission (CR) with an initial regimen of induction chemotherapy, while the remaining 35 patients failed to achieve CR with this initial regimen. Patients with high initial WBC counts (greater than 100,000/cmm), old age, temperature (greater than 38 degrees C) and antecedent hematological disorders, were more prone to failure of remission induction therapy. Comparing CR patients and non-CR patients, there seemed to be no difference in sex distribution, initial platelet counts, initial LDH, percentage of blasts in the blood and bone marrow, the incidence of DIC and the regimen used for remission induction. According to Preisler's criteria, remission induction failure cases were further subdivided into various types and the numbers of each type were as follows: Type I (absolute drug resistance) 1, Type II (relative drug resistance) 16, Type III (regeneration failure) 0, Type IV (hypoplastic death) 6 and Type V (early death) 11. Among 18 M1 cases, 8 were Type II or Type V. Four out of 7 M2 cases belonged to Type II and all 3 M3 cases were Type V. Six out of the 35 remission induction failure patients entered CR with the 2nd chemotherapy regimen and 19 patients died during induction treatment with the initial induction regimen. Causes of death were infection (5 cases), bleeding (6 cases), infection and bleeding (3 cases) and organ failure (5 cases).

Adolescent↗

PubMed1985

Dose response for induction of two cytochrome P-450 isozymes and their mRNAs by 3,4,5,3'4'5'-hexachlorobiphenyl indicating coordinate regulation in rat liver.

The present study compares the time course and dose-response curves for induction of the two major 3-methylcholanthrene (3-MC)-inducible isozymes of cytochrome P-450 and their mRNAs in livers of male rats after administration of 3,4,5,3'4'5'-hexachlorobiphenyl (HCB). Isozyme concentrations were measured by radioimmunoassay. The corresponding translatable mRNAs were measured by translation of polysomes in a cell-free translational system followed by immunoprecipitation and electrophoretic analysis of the translational products. The time course for induction of the two isozymes by HCB indicated that cytochrome P-448MC (P-450c) peaked sooner than P-448HCB (P450d). However, the time course for induction of the two mRNAs was identical. The dose-response curves for induction of the two isozymes and their mRNAs demonstrated that the ED50 for induction of P-448MC was identical to that of P-448HCB, suggesting that the two proteins are induced coordinately by this compound in liver. HCB did not induce P-450PB (the major phenobarbital-inducible isozyme) or affect mRNA levels for this isozyme. Although cytochrome P-448HCB is the predominant cytochrome in liver microsomes from HCB-induced rats, the magnitude of the induction of this isozyme (40-fold) is lower than that of P-448MC (600-fold), because cytochrome P-448HCB is present in higher concentrations in livers of untreated rats than P-448MC (90 versus 3 pmol/mg). Polysomes from control rats also contain more translationally active P-448HCB mRNA than P-448MC mRNA (0.009 versus 0.003% of the total translational products). The increase in the translatable mRNAs (12-fold for P-448HCB mRNA and 40-fold for P-448MC mRNA) was less than the increase in the isozymes. The discrepancy between the magnitude of the induction of the isozymes and their respective mRNAs suggests that factors other than an increase in mRNA influence the magnitude of the increase of the isozymes by HCB. However, HCB did not affect translational efficiency of total mRNA as measured in vitro in the present study. Differences in half-lives of the proteins or effects of HCB on the stability of the proteins might account for the magnitude of the increase in the isozymes after HCB treatment.

Animals↗

PubMed1982

The capacity of activated murine macrophages for augmented binding of neoplastic cells: analysis of induction by lymphokine containing MAF and kinetics of the reaction.

The capacity for augmented binding of tumor cells is an initial and necessary part of macrophage-mediated tumor cytotoxicity. To study the induction of binding capacity, we obtained FCS-elicited, inflammatory macrophages from C57BL/6J mice. Exposure of these macrophages to lymphokine(s) containing MAF induced augmented binding capacity in a dose-dependent fashion. Resident peritoneal macrophages did not respond to lymphokine, and endotoxin did not appreciably influence induction of binding. Maximum induction of binding required continuous interaction between macrophages and lymphokine for 6 to 10 hr. The conditions necessary for induction of binding closely paralleled those for induction of priming or cytolysis. Exposure of FCS-elicited macrophages from C3H/HeJ mice, although not of macrophages from A/J mice, induced augmented binding. The data suggest that the augmented capacity for binding tumor cells is induced by lymphokine(s) and that a major part of induction of priming for cytolysis by MAF is induction of such binding.

Animals↗

PubMed1983

Induction of mRNA specific for cytochrome P1-450 in wild type and variant mouse hepatoma cells.

We have used a cDNA probe specific for an aromatic hydrocarbon-inducible form of cytochrome P-450 to analyze the accumulation of enzyme-specific mRNA in wild type Hepa 1c1c7 cells and in variant cells defective in aryl hydrocarbon hydroxylase induction. In wild type cells, 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) produces a 25-50-fold increase in the steady state concentration of cytochrome P1-450-specific RNA. This RNA binds to oligo(dT)-cellulose and migrates in agarose gels as a single species of about 2900 nucleotides. Dot hybridization analyses of total RNA indicate that half-maximal induction of P1-450 mRNA occurs at about 10 pM TCDD; maximal induction occurs at about 100 pM TCDD. Parallel increases occur in aryl hydrocarbon hydroxylase activity. RNA induction precedes aryl hydrocarbon hydroxylase induction by 2-4 h. Kinetic analyses of mRNA induction in response to submaximal concentrations of TCDD reveal no change in the degradation of P1-450 mRNA during induction. We detect an increase in P1-450 mRNA 30 min after TCDD administration. Full accumulation of mRNA occurs in cells in which protein synthesis is inhibited by 95-97%. Variant cells with decreased TCDD receptors exhibit decreased basal and inducible levels of P1-450 mRNA. Variant cells with a defect in nuclear localization of the inducer-receptor complex exhibit virtually no basal or inducible levels of P1-450 mRNA. Hybrid cells formed by fusing these different variants contain wild type basal and inducible levels of P1-450 mRNA. We conclude that expression of the cytochrome P1-450 gene is under transcriptional control and requires nuclear localization of the TCDD receptor.

Animals↗

PubMed1981

Awakening characteristics following anesthesia induction with midazolam for short surgical procedures.

8-Chloro-6-(2-fluorophenyl)-1-methyl-4H-imidazol[1,5-a][1,4]benzodiazepine (midazolam maleate, Ro 21-3981, Dormicum) or thiopental were administered to 99 women undergoing short gynecological surgical procedures for induction and maintenance of anesthesia along with 67% nitrous oxide. Either fentanyl 1.5 microgram kg-1 or a saline placebo were given i.v. as acute premedication 5 min before induction. We measured the quality of induction and maintenance. Induction was more rapid after thiopental but thiopental produced more apnea especially when combined with fentanyl. Fentanyl premedication reduced the dose of hypnotics necessary to keep patients asleep. It was difficult to keep patients from moving during the procedure when only the hypnotics and nitrous oxide were used, so the use of these drugs for both induction and maintenance is recommended only when combined with narcotics or other analgesics. Although recovery after midazolam was slower than after thiopental, it was without untoward reactions such as hallucinations or excitement. Vomiting was less frequent after midazolam. Midazolam produced a profound period of amnesia for 1-2 h, so important instructions could not be given to patients during this time. All patients were awake enough to discharge from the hospital 200 min after the last dose of hypnotic was given. We would recommend a combination of midazolam, fentanyl and nitrous oxide for induction and maintenance of anesthesia for short surgical procedures except when a rapid induction is desired, then thiopental is preferred as the hypnotic.

Adult↗

PubMed1995

Cost-effectiveness of induction of labour versus serial antenatal monitoring in the Canadian Multicentre Postterm Pregnancy Trial.

OBJECTIVE: To determine the cost-effectiveness of induction of labour versus serial fetal monitoring while awaiting spontaneous labour in postterm pregnancies. DESIGN: Cost-effectiveness and cost-minimization analyses conducted as part of a Canadian multicentre randomized clinical trial. SETTING: Twenty-two Canadian hospitals, of which 19 were teaching hospitals and 3 were community hospitals. PATIENTS: Women with uncomplicated pregnancies of 41 or more weeks' gestation were randomly assigned to induction of labour or serial antenatal monitoring. Of the 3418 women enrolled, no data were received on 11. Therefore, results were based on data from 1701 women in the induction arm of the study and 1706 women in the monitoring arm. MAIN OUTCOME MEASURES: Perinatal mortality and neonatal morbidity, rates of cesarean section and health care costs. Hospital costing models were developed specifically for the study. Data on use of major resources (e.g., length of hospital stay, surgical procedures, major diagnostic tests and procedures, and medications) for all trial participants were collected and combined with data on minor tests and procedures (e.g., laboratory tests) abstracted from a detailed review of medical records of a sample of patients. RESULTS: Because the results of the clinical trial showed a nonsignificant difference in perinatal mortality and neonatal morbidity between the induction and monitoring arms, the authors conducted a cost-minimization rather than a cost-effectiveness analysis. The mean cost per patient with a postterm pregnancy managed through monitoring was $3132 (95% confidence interval [CI] $3090 to $3174) and per patient who underwent induction of labour was $2939 (95% CI $2898 to $2981), for a difference of $193. The significantly higher (p < 0.0001) mean cost per patient in the monitoring arm was due mainly to the costs of additional monitoring and the significantly higher rates of cesarean section among these patients. Estimated conservatively, the savings resulting from a universal policy of managing postterm pregnancies by induction of labour in Canada may be as high as $8 million a year. CONCLUSIONS: A policy of managing postterm pregnancy through induction of labour not only results in more favourable outcomes than a monitoring strategy but does so at a lower cost.

Cost Control↗

PubMed1994

Rapid inhalation induction with high concentration of sevoflurane using a new vaporizer.

Sevoflurane allows a moderately rapid induction with only slight problems of induction. However, it has not been possible to conduct tests with more than 2.6 minimum alveolar concentration (MAC) of sevoflurane (4.5%) because of the limitations in the performance of the currently available vaporizer. We tested the performance of a new vaporizer and tried it with single breath induction. The new vaporizer could deliver a 4.3 MAC (7.5%) sevoflurane through oxygen of 8 liter/min. Twenty-one unpremedicated volunteers breathed 7.5% sevoflurane in oxygen. The mean time for induction of anesthesia was 48 +/- 16 seconds, reflecting its high concentration and low blood/gas solubility. Although coughing was observed in two subjects, laryngospasm, breath holding, and secretions did not occur during induction by this method. All subjects except one would be willing to undergo similar induction again. This study demonstrate that the new vaporizer can be used to administer 7.5% concentration of sevoflurane and to adequately perform smooth and rapid inhalation induction of anesthesia in young volunteers without premedication.

Adult↗