Sympathoneuronal and sympathoadrenal activation during ketamine anesthesia

Appel, E; Dudziak, R.; Palm, D.; Wnuk, A.

doi:10.1007/bf00563113

Cited by 43 publications

(26 citation statements)

References 28 publications

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“…In man, this cardiovascular stimulating effect of ketamine was mainly attributable to sympathetic stimulation via a central mechanism resulting in increased circulating levels of norepinephrine and epinephrine (APPEL et al, 1979). Despite the expected cardiovascular stimulating effects of ketamine, bradycardia was observed in 23 to 30% of dogs and hypotension was observed in 70 to 77% of dogs in the present study.…”

Section: Bressan Et Alcontrasting

confidence: 53%

Minimum alveolar concentration of isoflurane in dogs administered a single intramuscular injection of racemic or S (+)-ketamine after premedication with acepromazine-morphine

et al. 2017

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The present study evaluated the minimum alveolar concentration of isoflurane (ISOMAC) in twenty three dogs premedicated with acepromazine (0.02mgkg-1) and morphine (0.5mgkg-1) and administered racemic (RK) or S(+)-ketamine (SK). Dogs randomly received a single dose (3mgkg-1, IM) of either RK or SK 15minutes after anesthetic induction with propofol. The ISOMAC was determined by the up-and-down method. Approximately 20 minutes after administration of RK or SK, a surgical noxious stimulus was applied and the response evaluated. The ISOMAC was 0.50±0.01% in the RK group (n=10) and 0.31±0.04% in the SK group (n=13). The ISOMAC was 38% lower in the SK group compared to the RK group. Results of the present study revealed that in dogs premedicated with acepromazine and morphine, IM administration of 3mgkg-1 ketamine approximately 20 minutes before the noxious stimulus produced clinically important reduction in the ISOMAC and the MAC-sparing effect was significantly greater with SK compared to RK.

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Section: Bressan Et Alcontrasting

confidence: 53%

Minimum alveolar concentration of isoflurane in dogs administered a single intramuscular injection of racemic or S (+)-ketamine after premedication with acepromazine-morphine

et al. 2017

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“…It was been shown that ketamine releases epinephrine and norepinephrine. [45][46][47][48] It is interesting to note that a substantial vasoconstriction in the intestines was observed for at least 45 minutes after ketamine injection. It has been shown that an increase in blood pressure, cardiac output, and heart rate with a concomitant increase in epinephrine and norepinephrine plasma concentrations usually do not last more than 10 to 20 minutes after ketamine injection.…”

Section: Discussionmentioning

confidence: 99%

Effects of anaesthesia induction drugs on circulation in denervated intestinal loop preparation

et al. 1985

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“…Ketamin besitzt einen zentralen sympathikomimetischen Effekt [32], der zu gesteigerten Serumspiegeln von Adrenalin und Noradrenalin führt [4,9,18] [39]. Obwohl in In-vitro-Untersuchungen nachgewiesen wurde, dass Ketamin einen dosisabhängigen direkten negativ inotropen Effekt ausübt [22,38], überwiegt in vivo offenbar die sympathische Stimulation, sodass Ketamin Anstiege von HF, MAD, SV und HZV bewirkt [4,9,19].…”

Section: Stimulation Des Sympathischen Nervensystemsunclassified

Einsatz von Ketamin bei Sepsis und systemischen Entzündungsreaktionen

Lange¹,

Bröking²,

Aken³

et al. 2006

Anaesthesist

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Ketamine is the only intravenous anesthetic that causes an increase in mean arterial pressure without compromising cardiac output. These beneficial effects are basically linked to stimulation of the sympathetic nervous system, inhibition of adenosine triphosphate-sensitive potassium channels and interactions with the nitric oxide pathway. Experimental and clinical studies have shown that ketamine exerts antiinflammatory properties by inhibiting the release of proinflammatory cytokines, such as tumor necrosis factor-alpha and interleukin-6. In addition, there is increasing evidence that early ketamine administration reduces mortality in experimental sepsis models. In view of the current literature ketamine appears to represent a beneficial therapeutic option for long-term sedation of patients with arterial hypotension resulting from sepsis and systemic inflammatory response syndrome (SIRS). However, it has to be taken into account that ketamine inhibits endothelial nitric oxide synthase, thereby potentially aggravating impaired (micro) regional blood flow in sepsis. Future studies are required to investigate the role of ketamine in the treatment of patients with sepsis and SIRS.

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Sympathoneuronal and sympathoadrenal activation during ketamine anesthesia

Cited by 43 publications

References 28 publications

Minimum alveolar concentration of isoflurane in dogs administered a single intramuscular injection of racemic or S (+)-ketamine after premedication with acepromazine-morphine

Minimum alveolar concentration of isoflurane in dogs administered a single intramuscular injection of racemic or S (+)-ketamine after premedication with acepromazine-morphine

Effects of anaesthesia induction drugs on circulation in denervated intestinal loop preparation

Einsatz von Ketamin bei Sepsis und systemischen Entzündungsreaktionen

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