Tricyclic Antidepressant

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Robin Rasmussen - One of the best experts on this subject based on the ideXlab platform.

  • reversal of severe Tricyclic Antidepressant induced cardiotoxicity with intravenous hypertonic saline solution
    Annals of Emergency Medicine, 2003
    Co-Authors: Patrick E Mckinney, Robin Rasmussen
    Abstract:

    Abstract A 29-year-old woman ingested 8 g of nortriptyline and presented to the emergency department with coma, hypotension, and widened QRS interval. After intubation, gastric lavage, hyperventilation, and therapy with intravenous normal saline solution, sodium bicarbonate boluses (rapid intravenous push), and high doses of norepinephrine and dopamine, she transiently improved, only to deteriorate on arrival to the ICU. Because her arterial pH was alkalemic at 7.5 at this point, she was given additional sodium in the form of 200 mL of 7.5% NaCl by means of rapid intravenous infusion (intravenous push) to treat hypotension and widening QRS interval with ventricular ectopy. A continuous 12-lead ECG documented narrowing of her QRS interval with concomitant improvement of hypotension within 3 minutes of hypertonic saline solution infusion. Hypertonic saline solution should be considered for wide complex QRS and hypotension caused by Tricyclic Antidepressant-induced cardiotoxicity that is unresponsive to standard therapies. [ Ann Emerg Med. 2003;42:20-24.]

Artur H Swiergiel - One of the best experts on this subject based on the ideXlab platform.

John Fata - One of the best experts on this subject based on the ideXlab platform.

  • experimental Tricyclic Antidepressant toxicity a randomized controlled comparison of hypertonic saline solution sodium bicarbonate and hyperventilation
    Annals of Emergency Medicine, 1998
    Co-Authors: James L Mccabe, Daniel J Cobaugh, James J Menegazzi, John Fata
    Abstract:

    Abstract Study objective: We sought to compare the effects of hypertonic sodium chloride solution (HTS), sodium bicarbonate solution, and hyperventilation (HV) on severe Tricyclic Antidepressant (TCA) toxicity in a swine model. Methods: Twenty-four mixed-breed, domestic swine of either sex were given an intravenous infusion of nortriptyline (NT) until development of both a QRS duration longer than 120 ms and a systolic blood pressure (SBP) less than or equal to 50 mm Hg. Animals were randomly assigned to 1 of 4 groups. On reaching toxicity, the control group received 10 mL/kg of 5% dextrose in water (D5W); the HTS group received 10 mL/kg of 7.5% NaCl solution (15 mEq Na + /kg); the NaHCO 3 group received 3 mEq/kg of 8.4% sodium bicarbonate solution followed by enough D5W solution to equal 10 mL/kg of total volume; and the HV group was mechanically hyperventilated to maintain arterial pH between 7.50 and 7.60 and given 10 mL/kg of D5W. Results: The mean SBP 10 minutes after treatment was 54±18 mm Hg in the control group, 134±21 mm Hg in the HTS group, 85±19 mm Hg in the NaHCO 3 group, and 60±12 mm Hg in the HV group ( P <.05). Mean QRS duration 10 minutes after treatment was 144±38 ms in the control group, 80±14 ms in the HTS group, 105±38 ms in the NaHCO 3 group, and 125±46 ms in the HV group ( P Conclusion: In this model of TCA, toxicity HTS was more effective than sodium bicarbonate. Hyperventilation had little effect. Sodium loading may be the most important factor in reversing TCA toxicity. [McCabe JL, Cobaugh DJ, Menegazzi JJ, Fata J: Experimental Tricyclic Antidepressant toxicity: A randomzed, controlled comparison of hypertonic saline solution, sodium bicarbonate, and hyperventilation. Ann Emerg Med September 1998;32:329-333.]

Patrick E Mckinney - One of the best experts on this subject based on the ideXlab platform.

  • reversal of severe Tricyclic Antidepressant induced cardiotoxicity with intravenous hypertonic saline solution
    Annals of Emergency Medicine, 2003
    Co-Authors: Patrick E Mckinney, Robin Rasmussen
    Abstract:

    Abstract A 29-year-old woman ingested 8 g of nortriptyline and presented to the emergency department with coma, hypotension, and widened QRS interval. After intubation, gastric lavage, hyperventilation, and therapy with intravenous normal saline solution, sodium bicarbonate boluses (rapid intravenous push), and high doses of norepinephrine and dopamine, she transiently improved, only to deteriorate on arrival to the ICU. Because her arterial pH was alkalemic at 7.5 at this point, she was given additional sodium in the form of 200 mL of 7.5% NaCl by means of rapid intravenous infusion (intravenous push) to treat hypotension and widening QRS interval with ventricular ectopy. A continuous 12-lead ECG documented narrowing of her QRS interval with concomitant improvement of hypotension within 3 minutes of hypertonic saline solution infusion. Hypertonic saline solution should be considered for wide complex QRS and hypotension caused by Tricyclic Antidepressant-induced cardiotoxicity that is unresponsive to standard therapies. [ Ann Emerg Med. 2003;42:20-24.]

Amy L Firth - One of the best experts on this subject based on the ideXlab platform.

  • inhibitory effect of the Tricyclic Antidepressant amitriptyline on voltage dependent k channels in rabbit coronary arterial smooth muscle cells
    Clinical and Experimental Pharmacology and Physiology, 2018
    Co-Authors: Sung Eun Shin, Mi Seon Seo, Euntaek Han, Seokho Hong, Ilwhan Choi, Dae Sung Lee, Mijin Yim, Jeong Min Lee, In Duk Jung, Amy L Firth
    Abstract:

    Amitriptyline, a Tricyclic Antidepressant (TCA) drug, is widely used in treatment of psychiatric disorders. However, the side effects of amitriptyline on vascular K+ channels remain to be determined. Therefore, we investigated the effect of the Tricyclic Antidepressant and serotonin reuptake inhibitor amitriptyline on voltage-dependent K+ (Kv) channels in freshly isolated rabbit coronary arterial smooth muscle cells, using the whole-cell patch clamp technique. The Kv current amplitudes were inhibited by amitriptyline in a concentration-dependent manner, with an apparent IC50 value of 2.2 ± 0.14 μmol/L and a Hill coefficient of 0.87 ± 0.03. Amitriptyline shifted the activation curve to a more positive potential, but had no significant effect on the inactivation curve, suggesting that amitriptyline altered the voltage sensitivity of Kv channels. Pretreatment with Kv1.5 and Kv1.2 channel inhibitors did not alter the inhibitory effect of amitriptyline on Kv channels. Additionally, application of train pulses (1 and 2 Hz) did not affect amitriptyline-induced inhibition of Kv currents, which suggested that the action of amitriptyline on Kv channels was not use (state)-dependent. From these results, we concluded that amitriptyline inhibited the channels in a concentration-dependent, but state-independent manner.

  • nortriptyline a Tricyclic Antidepressant inhibits voltage dependent k channels in coronary arterial smooth muscle cells
    The Korean Journal of Physiology and Pharmacology, 2017
    Co-Authors: Sung Eun Shin, Mi Seon Seo, Euntaek Han, Seokho Hong, Ilwhan Choi, Amy L Firth, Han Sol Kim, Hye Won Kim, Young Min Bae, Won Sun Park
    Abstract:

    We demonstrated the effect of nortriptyline, a Tricyclic Antidepressant drug and serotonin reuptake inhibitor, on voltage-dependent K+ (Kv) channels in freshly isolated rabbit coronary arterial smooth muscle cells using a whole-cell patch clamp technique. Nortriptyline inhibited Kv currents in a concentration-dependent manner, with an apparent IC50 value of 2.86±0.52 µM and a Hill coefficient of 0.77±0.1. Although application of nortriptyline did not change the activation curve, nortriptyline shifted the inactivation current toward a more negative potential. Application of train pulses (1 or 2 Hz) did not change the nortriptyline-induced Kv channel inhibition, suggesting that the effects of nortiprtyline were not use-dependent. Preincubation with the Kv1.5 and Kv2.1/2.2 inhibitors, DPO-1 and guangxitoxin did not affect nortriptyline inhibition of Kv channels. From these results, we concluded that nortriptyline inhibited Kv channels in a concentration-dependent and state-independent manner independently of serotonin reuptake.