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PubMed1998

[Pain management from the viewpoint of the anesthetist].

In a pain clinic team the anesthetist has the knowledge and experience concerning the peripheral and central neural blockades. The value of the diagnostic, prognostic and therapeutic blockades is today under discussion. Patients with a chronic regional pain syndrome (CRPS) can find some relief with a series of somatic and sympatholytic blockades, which allow an aggressive physiotherapy. Epidural steroid injections are helpful in radiculopathic pain. In other types of pain (neuropathic, postherpetic, failed back surgery syndrome, abdominal, cervico-cephalgic, phantom limb pain und tumor pain) the spinal cord stimulation (SCS) and the intrathecal morphine pump are approved methods for intactable pain.

Analgesia, Epidural↗

PubMed1976

Adrenergic neuronal degeneration induced in portal vein and caudal artery by 6-hydroxydopamine in vitro.

Fluorescence histochemistry and electron microscopy were used to study the structural consequences of in vitro exposure to the sympatholytic agent 6-hydroxydopamine on two blood vessels, the portal mesenteric vein and caudal artery of the rat. The results showed depletion of catecholamines to indetectable levels associated with clear signs of adrenergic nerve degeneration, such as cytoplasmic shrinking, virtual absence of dense core vesicles and swelling of mitochondria. All of the changes observed occurred within 2 hours in the caudal arteries and 3.5 hours in the portal veins. Comparison of electron and fluorescence micrographs of incubated control specimens with those of unincubated, fresh specimens showed that the nerve endings of the incubated controls were well preserved for at least 3.5 hours. With destruction of nerve endings in such a short period of time, the processes of specific neuronal degeneration could be clearly demonstrated in isolated blood vessels.

Animals↗

PubMed1998

Clonidine improves recovery from myocardial stunning in conscious chronically instrumented dogs.

UNLABELLED: Clonidine, an alpha2-adrenergic agonist, has been widely used in anesthesia because of its sedative, analgesic, sympatholytic, and specific hemodynamic effects. The use of clonidine in myocardial ischemia is controversial because of its bradycardic and hypotensive effects. In the present study, we tested the hypothesis that clonidine improves recovery from myocardial stunning in conscious dogs. Seven dogs were chronically instrumented to allow measurement of left atrial pressure (LAP), aortic blood pressure (ABP), left ventricular pressure (LVP), maximal rate of increase of LVP (LVdP/dtmax), and myocardial wall thickening fraction (WTF). The myocardial blood flow was measured using colored microspheres. To compensate for any potential interaction between the two ischemic episodes, experiments were performed on separate days in a cross-over fashion (four animals underwent Condition 1, and three underwent Condition 2 as their first experiment). The ischemic episodes involved 1) 10 min of ischemia of the left anterior descending (LAD) coronary artery without any intervention, and 2) 10 min of LAD ischemia 30 min after 10 microg/kg iv clonidine. WTF was measured before the induction of ischemia or the application of clonidine (baseline) and at predetermined time points until complete recovery of myocardial function. WTF recovered faster during the first 2 h of reperfusion when clonidine was administered. The increase in plasma epinephrine was attenuated by clonidine during ischemia, but there was no change during reperfusion. The increase of plasma norepinephrine levels was attenuated during ischemia and reperfusion. The hemodynamic effects of clonidine did not depress myocardial perfusion or impair myocardial function. IMPLICATIONS: In this study, we investigated the effects of IV clonidine on myocardial stunning in chronically instrumented dogs. Clonidine improved the recovery from myocardial stunning and attenuated increases in catecholamine plasma levels.

Adrenergic alpha-Agonists↗

PubMed1999

Identification of a novel, inhibitory action of amiodarone on vesicular monoamine transport.

The benzofuran antiarrhythmic drug, amiodarone, exhibits a wide range of pharmacological properties. Recent in vivo biochemical studies suggest that amiodarone may exert an antiadrenergic action in the heart, which resembles the effects of reserpine. To investigate the cellular basis for this apparent presynaptic, sympatholytic action we used Chinese hamster ovary (CHO) cells expressing the type 2 vesicular monoamine transporter (VMAT2) as a synaptic vesicular model. Amiodarone inhibited the uptake of [3H]norepinephrine in VMAT2-transfected CHO cells in a concentration-dependent manner, with a -log EC50 of 6.44 +/- 0.32. To further identify the site at which amiodarone suppressed vesicular monoamine transport, we examined the ability of amiodarone to displace [3H]reserpine from its binding site in membrane fractions prepared from CHO cells expressing VMAT2. [3H]Reserpine binding was inhibited in a concentration-dependent manner by amiodarone, with an -log EC50 of 6.76 +/- 0.03, reaching 84 +/- 5% inhibition of reserpine binding at 10 microM. A pH-dependent mechanism for this action of amiodarone was excluded in studies using the pH-sensitive fluorescent indicator 2',7'-bis (carboxyethyl)-5,6-carboxyfluorescein (BCECF). These data indicate that amiodarone inhibits the uptake of monoamine into the axoplasmic storage vesicle by inhibiting VMAT. Furthermore, amiodarone competes specifically with reserpine for binding to VMAT. These findings suggest a novel presynaptic site of action for amiodarone.

Adrenergic Uptake Inhibitors↗

PubMed1953