Psycho-Babble Medication Thread 982158

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orth. hypotension + tachycardia

Posted by desolationrower on April 7, 2011, at 1:01:37

have you read this: http://www.dr-bob.org/babble/20091001/msgs/919606.html

tachycardia - don't worry about it, do long slow ærobic work, meditate. You have to increase vagal tone.

if you want something off the wall, an ACHEi:

Pressor and bradycardic effects of tacrine and other acetylcholinesterase inhibitors in the rat
Abstract

The cardiovascular effects of three different acetylcholinesterase inhibitors: physostigmine, tacrine and rivastigmine injected by intravenous (i.v.) route were compared in freely moving Wistar rats. The three drugs significantly increased both systolic and diastolic blood pressure and decreased heart rate. Compared to physostigmine, a 20-fold higher dose of tacrine and a 40-fold higher dose of rivastigmine was necessary to induce a comparable pressor effect. Tacrine was chosen as a model to study the mechanisms underlying the cardiovascular effects of i.v. cholinesterase inhibitors. Atropine totally abolished while methylatropine did not affect tacrine pressor effects. Conversely, both drugs abolished tacrine-induced bradycardia. The α1-adrenoceptor antagonist prazosin or the vasopressin V1 receptor antagonist, [β-mercapto-β,β-cyclopenta-methylenepropionyl1, O-Me-Tyr2, Arg8] vasopressin partially but significantly reduced tacrine pressor effect and mostly abolished it when administered concomitantly. The tacrine pressor response was inhibited in a dose-dependent manner by the i.c.v. administration of the non-selective muscarinic receptor antagonist atropine (ID50=1.45 μg), the muscarinic M1 receptor antagonist pirenzepine (ID50=4.33 μg), the muscarinic M2 receptor antagonist methoctramine (ID50=1.39 μg) and the muscarinic M3 receptor antagonist para-fluoro-hexahydro-sila-difenidol (ID50=31.19 μg). Central injection of such muscarinic receptor antagonists did not affect tacrine-induced bradycardia. Our results show that acetylcholinesterase inhibitors induce significant cardiovascular effects with a pressor response mediated mainly by the stimulation of central muscarinic M2 receptors inducing a secondary increase in sympathetic outflow and vasopressin release. Conversely, acetylcholinesterase inhibitor-induced bradycardia appears to be mediated by peripheral muscarinic mechanisms.

-d/r

Re: orth. hypotension + tachycardia » desolationrower

Posted by SLS on April 7, 2011, at 8:03:10

In reply to orth. hypotension + tachycardia, posted by desolationrower on April 7, 2011, at 1:01:37

You might want to research the possibility that this kind of tachycardia is accompanied by a reduction of ejection fraction. The heart would beat faster, but with less effort.

- Scott

> tachycardia - don't worry about it, do long slow ærobic work, meditate. You have to increase vagal tone.
>
> if you want something off the wall, an ACHEi:
>
> Pressor and bradycardic effects of tacrine and other acetylcholinesterase inhibitors in the rat
> Abstract
>
> The cardiovascular effects of three different acetylcholinesterase inhibitors: physostigmine, tacrine and rivastigmine injected by intravenous (i.v.) route were compared in freely moving Wistar rats. The three drugs significantly increased both systolic and diastolic blood pressure and decreased heart rate. Compared to physostigmine, a 20-fold higher dose of tacrine and a 40-fold higher dose of rivastigmine was necessary to induce a comparable pressor effect. Tacrine was chosen as a model to study the mechanisms underlying the cardiovascular effects of i.v. cholinesterase inhibitors. Atropine totally abolished while methylatropine did not affect tacrine pressor effects. Conversely, both drugs abolished tacrine-induced bradycardia. The α1-adrenoceptor antagonist prazosin or the vasopressin V1 receptor antagonist, [β-mercapto-β,β-cyclopenta-methylenepropionyl1, O-Me-Tyr2, Arg8] vasopressin partially but significantly reduced tacrine pressor effect and mostly abolished it when administered concomitantly. The tacrine pressor response was inhibited in a dose-dependent manner by the i.c.v. administration of the non-selective muscarinic receptor antagonist atropine (ID50=1.45 μg), the muscarinic M1 receptor antagonist pirenzepine (ID50=4.33 μg), the muscarinic M2 receptor antagonist methoctramine (ID50=1.39 μg) and the muscarinic M3 receptor antagonist para-fluoro-hexahydro-sila-difenidol (ID50=31.19 μg). Central injection of such muscarinic receptor antagonists did not affect tacrine-induced bradycardia. Our results show that acetylcholinesterase inhibitors induce significant cardiovascular effects with a pressor response mediated mainly by the stimulation of central muscarinic M2 receptors inducing a secondary increase in sympathetic outflow and vasopressin release. Conversely, acetylcholinesterase inhibitor-induced bradycardia appears to be mediated by peripheral muscarinic mechanisms.
>
> -d/r
>

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