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Biomedical subjects

K Mikawa

Publications and source records attributed to K Mikawa.

At least 19 recordsLinked to original sources
PubMed1995

Lansoprazole reduces preoperative gastric fluid acidity and volume in children.

The purpose of this study was to explore the efficacy of lansoprazole, a proton pump inhibitor, in reducing the acidity and volume of gastric aspirate in children immediately following the induction of anaesthesia. One hundred healthy in-patients aged 3-11 yr undergoing elective surgery were randomly allocated to four groups (n = 25 each): lansoprazole-lansoprazole, placebo-placebo, placebo-lansoprazole, and lansoprazole-placebo. For each treatment regimen, the first medication was administered at 9:00 pm on the night before surgery and the second at 5:30 am on the morning of the day of surgery (three hours preoperatively). The dose of lansoprazole was 30 mg (approximately 1.4 mg.kg-1 mean). Children were offered 10 ml.kg-1 apple juice three hours before induction of anaesthesia. After induction of anaesthesia and tracheal intubation, gastric fluid was aspirated through a large-bore, multiorifice orogastric tube and analyzed for pH and total fluid volume. Lansoprazole increased gastric fluid pH and decreased gastric fluid volume regardless of whether it was administered before or after placebo. Two consecutive doses of lansoprazole was the most effective means of increasing the pH and reducing the volume of gastric aspirate; in this group, there were no subjects with gastric aspirate volume > 0.4 ml.kg-1 and pH < 2.5. Oral lansoprazole, at least 30 mg, given on the night before surgery or on the morning of surgery will improve the gastric environment at the time of induction of paediatric anaesthesia. The most effective regimen was two doses (at bedtime and on the morning) of lansoprazole.

2-Pyridinylmethylsulfinylbenzimidazoles↗
PubMed1995

Gastric fluid volume and pH after nizatidine in adults undergoing elective surgery: influence of timing and dose.

We conducted a prospective, randomized, double-blind study to investigate the effect of oral nizatidine (150-600 mg), a new potent H2 antagonist, on preoperative gastric fluid pH and volume in adults undergoing elective surgery. One hundred and seventy-five healthy adults (21-68 yr) were randomly allocated to seven treatment groups (n = 25); Placebo was administered at 21:00 and 06:30 the night before and on the day of surgery, respectively (0/0: control); nizatidine 150 mg at 21:00 and placebo at 06:30 (150/0); placebo at 21:00 and nizatidine 150 mg at 06:30 (0/150); nizatidine 150 mg at 21:00 and 06:30 (150/150); nizatidine 300 mg at 21:00 and placebo at 06:30 (300/0); placebo at 21:00 and nizatidine 300 mg at 06:30 (0/300); and nizatidine 300 mg at 21:00 and 06:30 (300/300). Each patient fasted overnight and took the drug and/or placebo with 20 ml water. After induction of anaesthesia, the pH and volume of gastric fluid obtained through an orogastric tube were measured. The mean pH of 0/150, 150/150, 300/0, 0/300, and 300/300 groups was higher than that of the control group (P < 0.05). Gastric volume in these groups was smaller than in the control (P < 0.05). The 150/0 group failed to decrease gastric fluid volume and increase pH. In the 300/0 group, the gastric pH was lower than other regimens which effectively decreased gastric acidity (P < 0.05). The number of patients with a pH < 2.5 and a volume > 0.4 ml.kg-1 in the 0/150, 150/150, 0/300, and 300/300 groups (0%) was less than in the control group (16%) (P < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗
PubMed1995

Improvement of the accuracy of references in the Canadian Journal of Anaesthesia.

A previous study indicated that there were many citation errors in the Canadian Journal of Anaesthesia. After this report, editors of the Journal requested any contributors, whose papers were accepted for publication, to verify the accuracy of reference citation by including a photocopy of the first page of each reference. The present study examined if the accuracy of the reference list had improved. We compared citation errors between volumes of 1990 and 1994. One hundred references from each year's publication were randomly selected. After citations of nonjournal articles were excluded, the remaining 190 citations were carefully scrutinized. Authors' names, article title, journal title, volume number, page numbers, and year were examined in each selected reference. A reference was deemed correct if each element of the citation was identical to its source. Of the examined references, 48% and 22% contained one or more errors in 1990 and 1994, respectively. Errors in the title and author field of citation were most common in the either of the two years, occurring in about 70% of the references which contained some errors. Citation errors in Canadian Journal of Anaesthesia were considerably improved after the request to verify citation accuracy. Although this check-system probably contributes to the improvement of accuracy of reference citation, the rate of citation errors remains high. We believe that contributors' efforts will enhance the value of the journal.

Anesthesiology↗
PubMed1995

The efficacy of guanfacine in reducing perioperative hemodynamic changes and volatile anesthetic requirement.

STUDY OBJECTIVE: To evaluate the efficacy of guanfacine, an alpha 2-adrenergic agonist, for attenuating hemodynamic changes associated with tracheal intubation or extubation, providing intraoperative hemodynamic stability, and reducing inhalation anesthetic requirement in patients undergoing gynecologic surgery. DESIGN: Randomized, double-blind, placebo-controlled study. SETTING: Inpatient gynecology at a university hospital. PATIENTS: 45 women (ASA I) undergoing elective abdominal hysterectomy. INTERVENTIONS: Guanfacine and placebo supplementation. Oral guanfacine at 0.5 or 1 mg or a placebo (control) 3 hours before induction of anesthesia. Anesthesia was induced with thiamylal 5 mg/kg and vecuronium 0.2 mg/kg, and maintained with isoflurane and 50% nitrous oxide (N2O) in oxygen. The inspired isoflurane concentration was maintained at 1% during the first 5 minutes following induction of anesthesia and titrated to the concentration required to maintain hemodynamic stability [defined as +/- 10% of systolic blood pressure (SBP)]. The end-tidal concentration of isoflurane was monitored throughout anesthesia. On completion of surgery, N2O and isoflurane were discontinued. Following confirmation of recovery from anesthesia and muscle relaxation, the endotracheal tube was removed. MEASUREMENTS AND MAIN RESULTS: Patients in the control group showed significant increases in SBP and diastolic blood pressure (DBP) and heart rate (HR) associated with tracheal intubation 50 +/- 5, 57 +/- 6.3, and 45 +/- 4.6 (%, mean +/- SEM, p < 0.05 for any variables), respectively. Plasma norepinephrine and epinephrine concentrations increased to 382 +/- 40 pg/ml and 49 +/- 4.2 pg/ml, respectively (p < 0.05 compared with basal values). These changes were attenuated in patients receiving 1 mg of guanfacine (29 +/- 4.2, 33 +/- 4.5, 25 +/- 3.2, 210 +/- 32, and 22 +/- 3.5, respectively (p < 0.05 for any variables compared with placebo group). Higher inspired concentrations of isoflurane (%) were required in the control and 0.5 mg guanfacine-treated groups (1.2 +/- 0.05 and 1.0 +/- 0.04, respectively) than in the 1 mg guanfacine-treated group (0.62 +/- 0.03) for hemodynamic stability (p < 0.05). Coefficient of variation in HR changes during surgery was 17.2, 13.9, and 8.8 in the placebo, guanfacine 0.5 mg, and guanfacine 1 mg treated groups, respectively. Compared with placebo, guanfacine 1 mg reduced the maximum changes (mean +/- SEM) in SBP (7 +/- 1.2 vs. 18 +/- 2.2) and in HR (23 +/- 2.1 vs. 44 +/- 3.6) occurring during tracheal extubation. The incidence of perioperative complications was similar among the three groups. CONCLUSION: Guanfacine 1 mg administered orally proved to be an effective premedicant for providing intraoperative hemodynamic stability, attenuating the increase in BP and HR associated with tracheal intubation and extubation, and reducing anesthetic requirements without increasing the incidence of perioperative complications.

Adult↗
PubMed1995

The antiemetic efficacy of prophylactic granisetron in gynecologic surgery.

Postoperative nausea and vomiting are common after recovery from anesthesia. We examined the prophylactic effect of granisetron on postoperative nausea and vomiting in 120 female patients (ASA physical status I) undergoing gynecologic surgery. They were randomly allocated to one of three groups (n = 40 for each): saline (as a control), granisetron 20 micrograms/kg, and granisetron 40 micrograms/kg. Saline or granisetron was given intravenously (IV) over 5 min approximately 30 min before the end of anesthesia. Nausea, vomiting, and safety assessments were performed during the 24-h recovery period. For the 24-h period after surgery, the number of emesis-free patients was significantly larger in the granisetron groups than in the control group (83%, 78%, and 20% of patients receiving granisetron 20 micrograms/kg and 40 micrograms/kg, and saline, respectively). Granisetron at both doses also was superior to the control for the prevention of nausea over the 24-h study period (nausea visual analog scales at 24-h postsurgery: 49 mm, 17 mm, and 18 mm in the control, granisetron 20 micrograms/kg, and granisetron 40 micrograms/kg groups, respectively). Fewer patients received "rescue" antiemetics in the granisetron groups than in the control group (10%, 10%, and 43% of patients in granisetron 20 micrograms/kg and 40 micrograms/kg, and the control groups, respectively). The adverse events in the granisetron groups were similar to those in the control group. The administration of granisetron had no significant effect on vital signs or clinical laboratory test profiles. Granisetron given at 20 or 40 micrograms/kg i.v. during anesthesia appears to be a simple, effective, and safe method for preventing postoperative nausea and vomiting.

Adult↗
PubMed1995

Attenuation of cardiovascular responses to tracheal extubation with diltiazem.

We conducted a randomized, double-blind study to examine the effects of intravenous (i.v.) diltiazem (0.1 or 0.2 mg/kg) on hemodynamic changes during tracheal extubation and emergence from anesthesia in 80 ASA physical status I patients undergoing elective gynecologic surgery. The effect of diltiazem was compared with that of lidocaine or saline. Anesthesia was maintained with 0.5%-1.5% isoflurane and 60% nitrous oxide (N2O) in oxygen. Muscle relaxation was achieved with vecuronium. The patients were randomly assigned to one of four groups (n = 20 for each group): saline (as a control), 0.1 mg/kg diltiazem, 0.2 mg/kg diltiazem, and 1 mg/kg lidocaine. These medications were given 2 min before tracheal extubation. Changes in heart rate (HR) and blood pressure (BP) were measured during and after tracheal extubation. The HR, systolic BP, and diastolic BP increased significantly during tracheal extubation in the control group (P < 0.05). Diltiazem, 0.1 and 0.2 mg/kg, and lidocaine attenuated the increases in these variables. The inhibitory effect on these cardiovascular responses was greatest with diltiazem 0.2 mg/kg, while the extent of attenuation by diltiazem 0.1 mg/kg was similar to that by lidocaine. We concluded that a bolus dose of i.v. diltiazem 0.1 or 0.2 mg/kg given 2 min before extubation was of value in attenuating the cardiovascular changes occurring in association with tracheal extubation and emergence from anesthesia. This alleviative effect of diltiazem was equal or superior to that of i.v. lidocaine 1 mg/kg.

Adult↗
PubMed1995

Oral clonidine premedication blunts the heart rate response to intravenous atropine in awake children.

BACKGROUND: Clonidine, which is known to have analgesic and sedative properties, has recently been shown to be an effective preanesthetic medication in children. The drug may cause side effects, including bradycardia and hypotension. This study was conducted to evaluate the ability of intravenous atropine to increase the heart rate (HR) in awake children receiving clonidine preanesthetic medication. METHODS: We studied 96 otherwise healthy children, 8-13 yr old, undergoing minor surgery. They received, at random, oral clonidine 2 or 4 micrograms.kg-1 or placebo 105 min before scheduled induction of anesthesia. Part I (n = 48, 16 per group): When hemodynamic parameters after insertion of a venous catheter had been confirmed to be stable, atropine was administered in incremental doses of 2.5, 2.5, and 5 micrograms.kg-1 every 2 min. The HR and blood pressure were recorded at 1-min intervals. Part II (n = 48, 16 per group): After the recording of baseline hemodynamic values, successive doses of atropine (5 micrograms.kg-1 every 2 min, to 40 micrograms.kg-1), were administered until HR increased by 20 beats.min-1. The HR and blood pressure were recorded at 1-min intervals. RESULTS: Part I: The increases in HR in response to a cumulative dose of atropine 10 micrograms.kg-1 were 33 +/- 3%, 16 +/- 3%, and 8 +/- 2% (mean +/- SEM) in children receiving placebo, clonidine 2 micrograms.kg-1, and clonidine 4 micrograms.kg-1, respectively (P < 0.05). Part II: The HR in the control group increased by more than 20 beats.min-1 in response to atropine 20 micrograms.kg-1 or less. In two patients in the clonidine 4 micrograms.kg-1 group, HR did not increase by 20 beats.min-1 even after 40 micrograms.kg-1 of atropine. CONCLUSIONS: Oral clonidine premedication (4 micrograms.kg-1) blunted the increase in HR after intravenous atropine in awake children, although clonidine 2 micrograms.kg-1 did not. A larger dose of atropine was required to increase the HR by 20 beats.min-1 in children receiving the premedicant in the larger dose.

Administration, Oral↗
PubMed1995

Does early posttreatment with lidocaine attenuate endotoxin-induced acute injury in rabbits?

BACKGROUND: It is well known that endotoxin causes acute lung injury, resulting in adult respiratory distress syndrome. Lidocaine pretreatment has recently been shown to attenuate endotoxin-induced lung injury in rabbits. The aim of the current study was to determine whether early postinjury treatment with intravenous lidocaine could attenuate acute lung injury induced by endotoxin in rabbits. METHODS: Thirty-two male anesthetized rabbits were randomly assigned to receive one of four treatments (n = 8 for each group): infusion of saline (group S-S), infusion of saline with lidocaine treatment (group S-L), infusion of Escherichia coli endotoxin (100 micrograms.kg-1 over a 60-min period) without lidocaine treatment (group E-S), or infusion of endotoxin with lidocaine treatment (group E-L). Ten minutes after the end of infusion of endotoxin (groups E-L and E-S) or saline (groups S-S and S-L), the animals received a bolus injection followed by continuous infusion of lidocaine (2 mg.kg-1 + 2 mg.kg-1.h-1 in groups S-L and E-L) or saline (groups S-S and E-S). The rabbits' lungs were ventilated with 40% O2. Hemodynamics, peripheral leukocyte and platelet counts, and arterial O2 tension (PaO2) were recorded during the ventilation period (6 h). After the observation, lung mechanics; the cell fraction of bronchoalveolar lavage fluid (BALF); and concentrations of activated complement components C3a and C5a, cytokines, and arachidonic acid metabolites in BALF were measured and analyzed. The ratio of lung wet weight to dry weight (W/D weight ratio) and albumin concentrations in BALF were analyzed as indexes of pulmonary edema. The Cypridina luciferin analogue-dependent chemiluminescence (representing O2 production) by neutrophils isolated from the pulmonary artery and light-microscopic findings of the lung were compared among the four groups. RESULTS: Endotoxin caused decreases in peripheral leukocyte and platelet counts, lung compliance, and PaO2. It caused increases in lung W/D weight ratio; polymorphonuclear cell counts in BALF; and albumin, C3a, C5a, tumor necrosis factor-alpha, interleukin (IL)-1 beta, IL-6, IL-8, and thromboxane B2 concentrations in BALF. Lidocaine attenuated the changes in W/D weight ratio and morphologic lung damage. The change in compliance, decrease in PaO2, and albumin concentrations in BALF were slightly but significantly less in rabbits receiving lidocaine after injury. The Cypridina luciferin analogue-dependent chemiluminescence by neutrophils was greater in rabbits receiving endotoxin without lidocaine than in those receiving endotoxin with lidocaine. CONCLUSIONS: These results indicate that early treatment with lidocaine attenuates endotoxin-induced lung edema in rabbits without affecting chemical mediators in BALF. However, the improvement is slight and likely to be of little clinical significance.

Animals↗
PubMed1995

Effects of exogenous intravenous glucose on plasma glucose and lipid homeostasis in anesthetized infants.

BACKGROUND: Whether intravenous glucose administration to infants during anesthesia is necessary remains to be resolved. The current study was designed to investigate the effect of exogenous glucose infusion on plasma glucose and lipid homeostasis in infants undergoing minor surgery. METHODS: Sixty infants (inpatients, ASA physical status 1) between 1 and 11 months of age were divided randomly into three groups as follows: LR group, lactated Ringer's solution (LR) alone; D2LR group, 2% glucose in LR; and D5LR group, 5% glucose in LR. Anesthesia was induced and maintained with halothane and nitrous oxide in oxygen. All fluids were infused at a rate of 6 ml.kg-1.h-1 until 1 h after surgery. Plasma concentrations of glucose, nonesterified fatty acids, ketone bodies, insulin, and cortisol were determined at induction of anesthesia, at the end of surgery, and 1 h after surgery. RESULTS: No infants in the three groups had hypoglycemia (< 50 mg.dl-1) throughout the study. In the LR group, plasma glucose concentration remained unchanged perioperatively compared with the basal values (at induction), whereas in the D2LR group, it increased during surgery but remained normoglycemic. In the D5LR group, plasma glucose concentration increased markedly both during and after surgery. In 6 of 20 infants, plasma glucose was greater than 200 mg.dl-1 at the end of surgery. In 8 of 20 infants receiving glucose-free infusion, plasma glucose concentrations decreased at the end of surgery. In contrast, the plasma glucose concentration increased in infants receiving glucose infusion. In the LR group, plasma concentrations of nonesterified fatty acids and ketone bodies increased at the end of and after surgery, suggesting lipid mobilization. The base excess decreased in the LR groups as concentration of the ketone bodies increased. Plasma insulin concentrations increased in the D2LR and D5LR groups and decreased after surgery in infants receiving a glucose-free solution. No intergroup differences in plasma cortisol concentrations existed at any sample point. CONCLUSIONS: These data indicate that, in otherwise healthy infants undergoing minor surgery, intravenous infusion of 2% glucose may be sufficient to maintain plasma glucose concentrations within physiologic ranges and to prevent a compensatory increase in lipid mobilization (lipolysis) when fluids are infused at a rate of 6 ml.kg-1.h-1. However, there are limitations in extrapolating the results to neonates.

Anesthesia↗
PubMed1995

Attenuation of hyperoxic lung injury in rabbits with superoxide dismutase: effects on inflammatory mediators.

BACKGROUND: Superoxide dismutase (SOD) has been shown to attenuate hyperoxic lung injury. This effect is thought to be exhibited by scavenging superoxide released from neutrophils and other aerobic cells. The aim of the current study was to investigate the effect of pre-treatment with SOD on the chemical mediators in hyperoxic lung injury. METHODS: Thirty male anesthetized rabbits were allocated to receive one of three treatments (n = 10 for each group): ventilated with 100% oxygen for 36 h with or without recombinant human SOD (rhSOD) treatment, and ventilated with air for 36 h without rhSOD. In the rhSOD-treated group, a single intravenous dose of rhSOD 10,000 U kg BW-1 was administered immediately after the start of exposure to 100% oxygen and thereafter infused at a rate of 340,000 U kg BW-1 day-1 for 36 h until the animals were sacrificed. The lungs of all rabbits were ventilated with 100% oxygen or air. Haemodynamics, PaO2, and lung mechanics were recorded during the ventilation period. After exposure to 100% oxygen, lung mechanics, cell fraction of bronchoalveolar lavage fluid (BALF), activated complements, cytokines, and arachidonic acid metabolite concentrations in BALF were measured and analyzed. The lung wet-to-dry (W/D) weight ratio and albumin concentrations in BALF were determined as indices of pulmonary oedema. RESULTS: Exposure to the high concentration of oxygen for 36 h caused no significant changes in haemodynamics but decreased compliance and increased A-aDo2. In the rhSOD-treated group, the decrease in compliance was not observed. At the end of the 36 hr-exposure period, however, hyperoxia significantly increased the lung W/D weight ratio, influx of neutrophils into the lung, BALF concentrations of C3a, C5a, tumor necrosis factor-alpha, interleukin (IL)-1 beta, IL-6, IL-8, thromboxane B2, and albumin. Pre-treatment with rhSOD attenuated these increases. Exposure to 100% oxygen caused extensive morphologic lung damage (alveolar haemorrhage and hyaline membrane formation), which was lessened by rhSOD. CONCLUSION: These results indicate that intravenous rhSOD prevented hyperoxic lung injury (decreases in PaO2 and compliance, increased pulmonary vascular permeability, histopathological damage) in rabbits. This prophylactic effect of rhSOD amy be due, in part, to decreased chemical mediators such as activated complements, cytokines, and arachidonic acid metabolites.

Animals↗
PubMed1995

The accuracy of reference lists in Acta Anaesthesiologica Scandinavica.

To determine the accuracy of bibliographic citation in Acta Anaesthesiologica Scandinavica, we reviewed all 1990 volumes and part of 1994 volumes of the journal and sequentially numbered all references appearing in those years (n = 2701 and 2158 in 1990 (No. 1-No. 8) and 1994 (No. 1-No.5), respectively). We randomly selected 100 references from each year. After citations of nonjournal articles were excluded, the remaining 195 citations were carefully scrutinized. Authors' names, article title, journal title, volume number, page numbers, and year were examined in each selected reference. A reference was deemed correct if each element of the citation was identical to its source. Of the examined references, 40% and 45% contained one or more errors in 1990 and 1994, respectively. The elements most likely to be inaccurate were, in descending order of frequency, article title, author, and page number. No significant differences existed in the error rate between the two years. We have found many citation errors in the reference lists of Acta Anaesthesiologica Scandinavica and no improvement in these latest four years. All contributors to Acta Anaesthesiologica Scandinavica should thoroughly check the accuracy of reference lists.

Anesthesiology↗
PubMed1995

Fentanyl attenuates cardiovascular responses to tracheal extubation.

We carried out a controlled, randomized, double-blind study to examine the effects of intravenous fentanyl (1 or 2 micrograms kg-1) on hemodynamic changes during tracheal extubation and emergence from anesthesia in 60 ASA physical status I or II patients undergoing elective gynecological surgery. Anesthesia was maintained with 0.5%-1.5% isoflurane and 60% nitrous oxide (N2O) in oxygen. Muscle relaxation was achieved with vecuronium. The patients were randomly assigned to three group (each, n = 20), and fentanyl (1 or 2 micrograms kg-1), or saline (as a control) was given at the time of peritoneal closure. Changes in heart rate (HR) and blood pressure (BP) were measured during and after tracheal extubation. Adverse effects, including postoperative sedation and respiratory depression, were also assessed. The HR, systolic BP, and diastolic BP increased significantly during tracheal extubation in the control group (P < 0.05). Fentanyl 2 micrograms kg-1 attenuated the increases in these variables more effectively than fentanyl 1 microgram kg-1. The time interval from the study drug to extubation was similar in each group. Postoperative somnolence and respiratory depression were not observed in any patients in any of the three groups. We concluded that a bolus dose of intravenous fentanyl 2 micrograms kg-1 given at the time of peritoneal closure was of value in attenuating the cardiovascular changes associated with tracheal extubation and emergence from anesthesia, and that this treatment did not prolong the recovery. However, further studies are required to assess this technique in patients with cardiovascular or cerebrovascular diseases.

Adult↗
PubMed1995

Role of G proteins and KCa channels in the muscarinic and beta-adrenergic regulation of airway smooth muscle.

We have examined the functional consequences of G protein coupling to calcium-activated potassium (KCa) channels using isometric tension records from guinea pig tracheal smooth muscle. After incubation with 1 microgram/ml pertussis toxin (PTX) for 6 h, the contraction response to 1 microM methacholine (MCh) was suppressed by 31.7 +/- 5.0% (n = 10). Similarly, the contraction was inhibited by 29.1 +/- 5.0% (n = 6) after application of 0.1 microM AF-DX 116, an M2-selective muscarinic receptor antagonist. Cholera toxin (CTX, 2.0 micrograms/ml for 6 h), which activates the stimulatory G protein of adenylyl cyclase (Gs), also suppressed contraction by 43.9 +/- 3.3% (n = 11). The inhibitory effects of PTX, AF-DX 116, or CTX were reversed in the presence of 100 nM charybdotoxin (ChTX), a selective KCa channel inhibitor. These findings suggest that disruption of inhibitory coupling between muscarinic receptor and KCa channels mediated by PTX-sensitive G proteins, or KCa channel activation induced by Gs/adenylyl cyclase-linked processes, antagonizes muscarinic contraction. The isoproterenol concentration-inhibition curves for precontracted trachea (1 microM MCh) were shifted to the left after perfusion with PTX or AF-DX 116, and the leftward shift of the curve was blocked by ChTX. Thus direct or indirect regulation of KCa channels mediated by the inhibitory guanine nucleotide binding protein (Gi) and Gs may play a functionally important role in the mechanical antagonism by the two receptor agonists.

Adenylate Cyclase Toxin↗