Macroshock

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Kenneth J. Broadley - One of the best experts on this subject based on the ideXlab platform.

  • Airway Hyperresponsiveness in Anaesthetised Guinea‐Pigs 18–24 Hours after Antigen Inhalation Does Not Occur with All Intravenously Administered Spasmogens
    Pharmacology & toxicology, 1999
    Co-Authors: Alexia Johnson, Kenneth J. Broadley
    Abstract:

    : Actively sensitised guinea-pigs were exposed to inhalation challenges with ovalbumin aerosol (macro- and microshock) and airway responsiveness to six intravenously administered spasmogens was evaluated 18 to 24 hr later in the anaesthetised animal. An increase in airway sensitivity was defined as a significant leftward shift of the dose-response curve when compared with saline-challenged control sensitized animals. After ovalbumin-Macroshock (1% ovalbumin for 2 min. with mepyramine cover against fatal anaphylaxis), airway hyperresponsiveness was seen to 5-HT, the thromboxane A2-mimetic, U-46619, and bradykinin but not to methacholine, histamine or substance P. A similar pattern was seen after ovalbumin-microshock (0.01% ovalbumin for 60 min.), with induction of airway hyperreactivity to 5-HT and U-46619 but not methacholine or histamine. When the U-46619 dose-response curve was constructed following treatment of the animals with atropine (1 mg/kg, intravenously), airway hyperresponsiveness was no longer significant. As an index of airway inflammation, lung weights were significantly heavier in ovalbumin-challenged animals, than in saline-challenged controls. The results of this study with intravenously administered spasmogens does not support claims that ovalbumin-induced airway hyperreactivity in the guinea-pig is a ‘non-specific’phenomenon.

  • Early and late phase bronchoconstrictions in conscious sensitized guinea-pigs after macro- and microshock inhalation of allergen and associated airway accumulation of leukocytes.
    International journal of immunopharmacology, 1996
    Co-Authors: Christine A. Lewis, Alexander W. Johnson, Kenneth J. Broadley
    Abstract:

    Guinea-pigs were sensitized by i.p. injection of 10 μg OA and 100 mg aluminium hydroxide in 1 ml normal saline. Fourteen to twenty-one days after sensitization, animals were exposed to Macroshock (1% OA for 2 min) or microshock (0.01% for 60 min) inhalation challenges with OA. Animals were protected against fatal anaphylaxis in the case of Macroshocks with mepyramine (30mg/kg i.p.) 30 min before exposure. Specific airway conductance (sGaw) was measured in conscious animals by whole body plethysmography at intervals up to 72h after challenge. An early phase bronchoconstriction peaked significantly (P < 0.05) at 15 min after both Macroshock and microshock OA exposures, with maximum falls in sGaw of 70.8 ± 3.8 and −40.0 ± 5.9%, respectively. These had resolved after 5 h. A late phase bronchoconstriction peaked variably between 17 and 24 h: the mean peak falls in sGaw after the macro- and microshock challenges were significantly different from baseline (P < 0.05), at −21.6 ± 3.7 and −38.0 ± 3.9%, respectively. Control exposures of OA-sensitized guinea-pigs to saline for either 2 or 60 min, in place of OA, produced no significant variation in sGaw values over the predicted early and late phases. Bronchoalveolar lavage (BAL) performed at 5 or 24h after OA challenge revealed significant increases in total cell numbers (P < 0.05) at 5 and 24 h after the OA Macroshock challenge and at 24 h after the microshock, compared with saline challenges. Differential cell counts showed a significant (P < 0.05) increase in the proportion of neutrophils at 5 h and of neutrophils and eosinophils at 24 h after the Macroshock exposure to OA, compared with saline controls. A significant (P < 0.05) increase in the proportion of eosinophils also occurred in BAL fluid at 24 h after microshock OA challenge. Neutrophils, however, did not alter at 24 h, yet a late phase bronchoconstriction was recorded. Thus, Macroshock (with mepyramine cover) and microshock (without mepyramine cover) OA challenges result in both early and late phase bronchoconstrictions. The late phase is associated with influx of eosinophils in both models but neutrophils only appear after the Macroshock, indicating that late phase responses may not involve neutrophil infiltration to the airways.

  • Airway hyper‐ or hyporeactivity to inhaled spasmogens 24 h after ovalbumin challenge of sensitized guinea‐pigs
    British journal of pharmacology, 1995
    Co-Authors: Christine A. Lewis, Kenneth J. Broadley
    Abstract:

    1. The aim of this study was to determine whether an inhalation of ovalbumin (OA, 10 or 20 mg ml-1) by conscious OA-sensitized guinea-pigs leads to airway hyperreactivity to spasmogens 24 h later. In contrast to most previous studies, the spasmogens (5-HT, methacholine (MCh), U-46619 and adenosine) were administered by inhalation and airway function was measured in conscious guinea-pigs. 2. Guinea-pigs were sensitized by i.p. injection of 10 micrograms OA and 100 mg aluminium hydroxide in 1 ml normal saline; 14-21 days later they were exposed to an inhalation of 5-HT, MCh, U-46619 or adenosine. Specific airway conductance (sGaw) was measured in conscious animals by whole body plethysmography. The spasmogens caused bronchoconstriction, measured as a reduction in sGaw from the pre-inhalation basal values. Dose-related bronchoconstrictions were observed with 5-HT, MCh and U-46619. 3. The effect of an ovalbumin Macroshock challenge upon the responses to each spasmogen were examined by giving an inhalation of aerosolized OA at 24 h (or 7 days in the cause of adenosine) after an initial spasmogen challenge. Eighteen to twenty-four hours after the OA Macroshock, the same guinea-pigs were exposed to a repeated inhalation of 5-HT, MCh, U-46619 or adenosine. 4. U-46619 was the only spasmogen to demonstrate hyperresponsiveness, the peak change in sGaw being increased from -12.3 +/- 9.9 to -38.8 +/- 5.0% by 10 mg ml-1 OA challenge. In contrast, the ovalbumin challenge (20 mg ml-1) inhibited the bronchoconstrictions to 5-HT (50 micrograms ml-1) and MCh (100 micrograms ml-1). Adenosine demonstrated bronchoconstriction in sensitized guinea-pigs but no significant change in the response was observed after an OA challenge. 5. All results were compared with a control group of sensitized guinea-pigs receiving a NaCl challenge. The bronchoconstrictor responses to 5-HT, MCh, U-46619 or adenosine did not differ significantly before and after the saline challenge, indicating reproducibility of the responses. 6. In further experiments, guinea-pigs were exposed to inhalation of 5-HT (50 micrograms ml-1) or MCh (300 micrograms ml-1) 24 h before atropine (10 micrograms, 100 micrograms or 1 mg ml-1) and again at 0.5 to 1.5 h afterwards. Atropine, antagonized the 5-HT- and MCh-induced bronchoconstrictions over the same antagonist dose-range. This suggests that the bronchoconstriction induced in the conscious guinea-pig by 5-HT is mediated primarily via muscarinic receptors, possibly by a vagal reflex. The inhibition of the responses to 5-HT and MCh by OA challenge would therefore appear to be related to interference with a common cholinergic pathway for these spasmogens. 7. In summary, airway hyperresponsiveness was evident at 24 h after OA challenge as measured by an enhanced bronchoconstrictor response to inhaled U-46619. When 5-HT or MCh were used as the spasmogens, an opposing decrease in responsiveness was observed. This was presumed to be due to an inhibition of cholinergic pathways by the OA challenge. Adenosine caused a bronchoconstriction in the sensitized animals but this was not enhanced by the OA challenge.

Christine A. Lewis - One of the best experts on this subject based on the ideXlab platform.

  • Early and late phase bronchoconstrictions in conscious sensitized guinea-pigs after macro- and microshock inhalation of allergen and associated airway accumulation of leukocytes.
    International journal of immunopharmacology, 1996
    Co-Authors: Christine A. Lewis, Alexander W. Johnson, Kenneth J. Broadley
    Abstract:

    Guinea-pigs were sensitized by i.p. injection of 10 μg OA and 100 mg aluminium hydroxide in 1 ml normal saline. Fourteen to twenty-one days after sensitization, animals were exposed to Macroshock (1% OA for 2 min) or microshock (0.01% for 60 min) inhalation challenges with OA. Animals were protected against fatal anaphylaxis in the case of Macroshocks with mepyramine (30mg/kg i.p.) 30 min before exposure. Specific airway conductance (sGaw) was measured in conscious animals by whole body plethysmography at intervals up to 72h after challenge. An early phase bronchoconstriction peaked significantly (P < 0.05) at 15 min after both Macroshock and microshock OA exposures, with maximum falls in sGaw of 70.8 ± 3.8 and −40.0 ± 5.9%, respectively. These had resolved after 5 h. A late phase bronchoconstriction peaked variably between 17 and 24 h: the mean peak falls in sGaw after the macro- and microshock challenges were significantly different from baseline (P < 0.05), at −21.6 ± 3.7 and −38.0 ± 3.9%, respectively. Control exposures of OA-sensitized guinea-pigs to saline for either 2 or 60 min, in place of OA, produced no significant variation in sGaw values over the predicted early and late phases. Bronchoalveolar lavage (BAL) performed at 5 or 24h after OA challenge revealed significant increases in total cell numbers (P < 0.05) at 5 and 24 h after the OA Macroshock challenge and at 24 h after the microshock, compared with saline challenges. Differential cell counts showed a significant (P < 0.05) increase in the proportion of neutrophils at 5 h and of neutrophils and eosinophils at 24 h after the Macroshock exposure to OA, compared with saline controls. A significant (P < 0.05) increase in the proportion of eosinophils also occurred in BAL fluid at 24 h after microshock OA challenge. Neutrophils, however, did not alter at 24 h, yet a late phase bronchoconstriction was recorded. Thus, Macroshock (with mepyramine cover) and microshock (without mepyramine cover) OA challenges result in both early and late phase bronchoconstrictions. The late phase is associated with influx of eosinophils in both models but neutrophils only appear after the Macroshock, indicating that late phase responses may not involve neutrophil infiltration to the airways.

  • Airway hyper‐ or hyporeactivity to inhaled spasmogens 24 h after ovalbumin challenge of sensitized guinea‐pigs
    British journal of pharmacology, 1995
    Co-Authors: Christine A. Lewis, Kenneth J. Broadley
    Abstract:

    1. The aim of this study was to determine whether an inhalation of ovalbumin (OA, 10 or 20 mg ml-1) by conscious OA-sensitized guinea-pigs leads to airway hyperreactivity to spasmogens 24 h later. In contrast to most previous studies, the spasmogens (5-HT, methacholine (MCh), U-46619 and adenosine) were administered by inhalation and airway function was measured in conscious guinea-pigs. 2. Guinea-pigs were sensitized by i.p. injection of 10 micrograms OA and 100 mg aluminium hydroxide in 1 ml normal saline; 14-21 days later they were exposed to an inhalation of 5-HT, MCh, U-46619 or adenosine. Specific airway conductance (sGaw) was measured in conscious animals by whole body plethysmography. The spasmogens caused bronchoconstriction, measured as a reduction in sGaw from the pre-inhalation basal values. Dose-related bronchoconstrictions were observed with 5-HT, MCh and U-46619. 3. The effect of an ovalbumin Macroshock challenge upon the responses to each spasmogen were examined by giving an inhalation of aerosolized OA at 24 h (or 7 days in the cause of adenosine) after an initial spasmogen challenge. Eighteen to twenty-four hours after the OA Macroshock, the same guinea-pigs were exposed to a repeated inhalation of 5-HT, MCh, U-46619 or adenosine. 4. U-46619 was the only spasmogen to demonstrate hyperresponsiveness, the peak change in sGaw being increased from -12.3 +/- 9.9 to -38.8 +/- 5.0% by 10 mg ml-1 OA challenge. In contrast, the ovalbumin challenge (20 mg ml-1) inhibited the bronchoconstrictions to 5-HT (50 micrograms ml-1) and MCh (100 micrograms ml-1). Adenosine demonstrated bronchoconstriction in sensitized guinea-pigs but no significant change in the response was observed after an OA challenge. 5. All results were compared with a control group of sensitized guinea-pigs receiving a NaCl challenge. The bronchoconstrictor responses to 5-HT, MCh, U-46619 or adenosine did not differ significantly before and after the saline challenge, indicating reproducibility of the responses. 6. In further experiments, guinea-pigs were exposed to inhalation of 5-HT (50 micrograms ml-1) or MCh (300 micrograms ml-1) 24 h before atropine (10 micrograms, 100 micrograms or 1 mg ml-1) and again at 0.5 to 1.5 h afterwards. Atropine, antagonized the 5-HT- and MCh-induced bronchoconstrictions over the same antagonist dose-range. This suggests that the bronchoconstriction induced in the conscious guinea-pig by 5-HT is mediated primarily via muscarinic receptors, possibly by a vagal reflex. The inhibition of the responses to 5-HT and MCh by OA challenge would therefore appear to be related to interference with a common cholinergic pathway for these spasmogens. 7. In summary, airway hyperresponsiveness was evident at 24 h after OA challenge as measured by an enhanced bronchoconstrictor response to inhaled U-46619. When 5-HT or MCh were used as the spasmogens, an opposing decrease in responsiveness was observed. This was presumed to be due to an inhibition of cholinergic pathways by the OA challenge. Adenosine caused a bronchoconstriction in the sensitized animals but this was not enhanced by the OA challenge.

Mohammed S. Dhamee - One of the best experts on this subject based on the ideXlab platform.

  • Electrosurgery-induced ventricular fibrillation during pacemaker replacement : A unique mechanism
    Journal of Clinical Monitoring and Computing, 1996
    Co-Authors: Anil Aggarwal, Neil E. Farber, G. S. Kotter, Mohammed S. Dhamee
    Abstract:

    Arrhythmias and pacemaker malfunction are known to occur from the use of an electrosurgical device. The present case report describes a patient with sick sinus syndrome who experienced ventricular fibrillation while undergoing surgery. During replacement of his non-functioning cardiac pacemaker under general anesthesia, electrosurgery was used to ensure hemostasis. Electric current may have stimulated myocardial leads present in the surrounding tissue, leading to ventricular fibrillation. The patient was resuscitated from the episode without any residual sequelae. Microshock and possible mechanisms that can lead to ventricular arrhythmias in patients with pacemakers during electrosurgery are discussed.

  • Electrosurgery-induced ventricular fibrillation during pacemaker replacement — a unique mechanism
    Journal of Clinical Monitoring, 1996
    Co-Authors: Anil Aggarwal, Neil E. Farber, G. S. Kotter, Mohammed S. Dhamee
    Abstract:

    Arrhythmias and pacemaker malfunction are known to occur from the use of an electrosurgical device. The present case report describes a patient with sick sinus syndrome who experienced ventricular fibrillation while undergoing surgery. During replacement of his non-functioning cardiac pacemaker under general anesthesia, electrosurgery was used to ensure hemostasis. Electric current may have stimulated myocardial leads present in the surrounding tissue, leading to ventricular fibrillation. The patient was resuscitated from the episode without any residual sequelae. Microshock and possible mechanisms that can lead to ventricular arrhythmias in patients with pacemakers during electrosurgery are discussed.

Jan Ehrenwerth - One of the best experts on this subject based on the ideXlab platform.

  • Electrical and Fire Safety
    Anesthesia Equipment, 2021
    Co-Authors: Jan Ehrenwerth
    Abstract:

    Abstract A basic principle of electricity is known as Ohm's law (Voltage = current × resistance). To have the completed circuit necessary for current flow, a closed loop must exist and a voltage source must drive the current through the impedance. To receive a shock, one must contact the electrical circuit at two points, and there must be a voltage source that causes the current to flow through an individual. In electrical terminology, grounding is applied to two separate concepts: the grounding of electrical power and the grounding of electrical equipment. To provide an extra measure of safety from gross electrical shock (Macroshock), the power supplied to most operating rooms (ORs) is ungrounded. The line isolation monitor is a device that continuously monitors the integrity of an isolated power system. The ground fault circuit interrupter is a popular device used to prevent individuals from receiving an electrical shock in a grounded power system. An electrically susceptible patient (i.e., one who has a direct, external connection to the heart) may be at risk from very small currents; this is called microshock. Problems can arise if the electrosurgical return plate is improperly applied to the patient or if the cord connecting the return plate to the electrosurgical unit is damaged or broken. Fires in the OR are just as much a danger today as they were 100 years ago when patients were anesthetized with flammable anesthetic agents. The necessary components for a fire consist of the triad of heat or an ignition source, a fuel, and an oxidizer. The two major ignition sources for OR fires are the electrosurgical unit and the laser. It is known that desiccated carbon dioxide absorbent can, in rare circumstances, react with sevoflurane to produce a fire. All OR personnel should be familiar with the location and operation of fire extinguishers.

  • electrical injury to a nurse due to conductive fluid in an operating room designated as a dry location
    Anesthesia & Analgesia, 2009
    Co-Authors: John Wills, Jan Ehrenwerth, Dan Rogers
    Abstract:

    The National Fire Protection Association regulates electrical codes in health care facilities. Because the discontinuation of flammable anesthetic use, isolated power systems (IPSs) have not been required in dry locations. The National Fire Protection Association delegates responsibility of designating dry and wet locations to health care facilities. Our hospital has designated our operating rooms as dry locations, and they have neither IPSs nor ground fault circuit interrupters. We describe a Macroshock electrical injury to a nurse when she plugged in equipment to an extension cord. Designating the operating room as a wet location and installing an IPS would have prevented her injury. Language: en

Anil Aggarwal - One of the best experts on this subject based on the ideXlab platform.

  • Electrosurgery-induced ventricular fibrillation during pacemaker replacement : A unique mechanism
    Journal of Clinical Monitoring and Computing, 1996
    Co-Authors: Anil Aggarwal, Neil E. Farber, G. S. Kotter, Mohammed S. Dhamee
    Abstract:

    Arrhythmias and pacemaker malfunction are known to occur from the use of an electrosurgical device. The present case report describes a patient with sick sinus syndrome who experienced ventricular fibrillation while undergoing surgery. During replacement of his non-functioning cardiac pacemaker under general anesthesia, electrosurgery was used to ensure hemostasis. Electric current may have stimulated myocardial leads present in the surrounding tissue, leading to ventricular fibrillation. The patient was resuscitated from the episode without any residual sequelae. Microshock and possible mechanisms that can lead to ventricular arrhythmias in patients with pacemakers during electrosurgery are discussed.

  • Electrosurgery-induced ventricular fibrillation during pacemaker replacement — a unique mechanism
    Journal of Clinical Monitoring, 1996
    Co-Authors: Anil Aggarwal, Neil E. Farber, G. S. Kotter, Mohammed S. Dhamee
    Abstract:

    Arrhythmias and pacemaker malfunction are known to occur from the use of an electrosurgical device. The present case report describes a patient with sick sinus syndrome who experienced ventricular fibrillation while undergoing surgery. During replacement of his non-functioning cardiac pacemaker under general anesthesia, electrosurgery was used to ensure hemostasis. Electric current may have stimulated myocardial leads present in the surrounding tissue, leading to ventricular fibrillation. The patient was resuscitated from the episode without any residual sequelae. Microshock and possible mechanisms that can lead to ventricular arrhythmias in patients with pacemakers during electrosurgery are discussed.