Cardiovascular effects of intravenous anesthetic agents

1994 ◽  
pp. 193-233 ◽  
Author(s):  
David R. Gross
Keyword(s):  
Cardiovascular Effects ◽  
Intravenous Anesthetic ◽  
Anesthetic Agents

Effects of intravenous anesthetic agents on left ventricular function in dogs

1977 ◽  
Vol 232 (1) ◽  
pp. H44-H48
Author(s):  
L. D. Horwitz
Keyword(s):  
Left Ventricular Pressure ◽  
Cardiovascular Effects ◽  
Sympathetic Nerves ◽  
Left Ventricular ◽  
Intravenous Anesthetic ◽  
First Derivative ◽  
Anesthetic Agents ◽  
Thiopental Sodium ◽  
Stimulation Of ◽  
Mean Heart Rate

The cardiovascular effects of ketamine hydrochloride and thiopental sodium were studied in 11 dogs. During anesthesia, mean heart rate rose to 185 beats/min with ketamine and 147 beats/min with thiopental. Cardiac output was increased with ketamine but unchanged by thiopental. The maximum first derivative of the left ventricular pressure (dP/dt max) fell by 14% with thiopental but did not change significantly with ketamine. Propranolol resulted in attenuation of the tachycardia and a fall of 10% in dP/dt max with ketamine but had little effect on the response to thiopental. Phentolamine had no consistent effects on either drug. With pentolinium both drugs decreased dP/dt max. Intracoronary injection of ketamine decreased dP/dt max. Adrenalectomy had little effect on the responses to either anesthetic. The results lead to the conclusion that both ketamine and thiopental have myocardial depressant effects, but, whereas thiopental does not alter sympathetic tone, the depressive effects of ketamine are obscured by stimulation of cardiac sympathetic nerves.

scholarly journals Total Intravenous Anesthesia for Myocardial Protection and Preconditioning

2021 ◽  
Author(s):  
Minati Choudhury
Keyword(s):  
Protective Effect ◽  
Surgical Procedure ◽  
Myocardial Protection ◽  
Myocardial Injury ◽  
Volatile Anesthetic ◽  
Organ Protection ◽  
Intravenous Anesthesia ◽  
Intravenous Anesthetic ◽  
Anesthetic Agents ◽  
Anesthetic Preconditioning

AbstractPerioperative myocardial injury is common after any major surgical procedure even with best possible anesthesia and surgical management. Organ preservation during surgical procedure prevents morbidity and mortality. The effect of ischemic preconditioning on myocardial as well as other organ protection is well known. A variety of other agents also shown to have preconditioning thus protective effect on myocardium during anesthesia and surgery. The beneficial effect of volatile anesthetic preconditioning is well studied. However, the effect of intravenous anesthetic agents on this context is still way to go. This review is an attempt to look into the latest available research regarding the preconditioning and myocardial protective effect of intravenous anesthetic agents.

The Interaction of Intravenous Anesthetic Agents with Native and Recombinant GABAA Receptors

1997 ◽  
pp. 121-156 ◽  
Author(s):  
Jeremy J. Lambert ◽  
Delia Belelli ◽  
Marco Pistis ◽  
Claire Hill-Venning ◽  
John A. Peters
Keyword(s):  
Gabaa Receptors ◽  
Intravenous Anesthetic ◽  
Anesthetic Agents

scholarly journals General Anesthesia With Dexmedetomidine and Remifentanil in a Neonate During oracotomy and Resection of a Congenital Cystic Adenomatoid Malformation

2018 ◽  
Vol 23 (3) ◽  
pp. 215-218 ◽  
Author(s):  
Ellise Cappuccio ◽  
Arlyne K. Thung ◽  
Joseph D. Tobias
Keyword(s):  
General Anesthesia ◽  
Early Life ◽  
Neonatal Period ◽  
Congenital Cystic Adenomatoid Malformation ◽  
Unique Combination ◽  
Limited Data ◽  
Intravenous Anesthetic ◽  
Anesthetic Agents ◽  
Cystic Adenomatoid Malformation ◽  
Animal Data

Based on animal data, concern has been expressed regarding the potential deleterious neurocognitive effects of general anesthesia during infancy and early life. Although there are no definitive data to prove this effect, the neonatal period has been suggested to be the most vulnerable period. While various inhaled and intravenous anesthetic agents have been implicated, dexmedetomidine and the opioids may be devoid of such effects. However, there are limited data regarding the combination of these agents during neonatal surgery and anesthesia. We present the use of these agents in combination with epidural anesthesia for postoperative analgesia in a 1-day-old neonate during thoracotomy and excision of a congental cystic adenomatoid malformation. Previous reports of the use of this unique combination of agents are reviewed and their role in this scenario discussed.

Intravenous Anesthetic Agents

2020 ◽  
pp. 83-93
Author(s):  
Ankur Luthra ◽  
Rajeev Chauhan ◽  
Summit D. Bloria
Keyword(s):  
Intravenous Anesthetic ◽  
Anesthetic Agents

Effects of Intravenous Anesthetic Agents on Glutamate Release

2000 ◽  
Vol 92 (4) ◽  
pp. 1067-1073 ◽  
Author(s):  
Donal J. Buggy ◽  
Beverley Nicol ◽  
David J. Rowbotham ◽  
David G. Lambert
Keyword(s):  
Glutamate Release ◽  
Receptor Activation ◽  
Gamma Aminobutyric Acid ◽  
Half Maximum ◽  
Intravenous Anesthetic ◽  
Anesthetic Agents ◽  
Acid Type ◽  
Maximum Inhibition ◽  
Dependent Inhibition ◽  
Anesthetic Action

Background Many anesthetic agents are known to enhance the alpha1beta2gamma2S gamma-aminobutyric acid type A (GABAA) chloride current; however, they also depress excitatory neurotransmission. The authors evaluated two hypotheses: intravenous anesthetic agents inhibit glutamate release and any observed inhibition may be secondary to GABAA receptor activation. Methods Cerebrocortical slices were prepared from Wistar rats. After perfusion in oxygenated Krebs buffer for 60 min at 37 degrees C, samples for glutamate assay were obtained at 2-nmin intervals. After 6 min, a 2-min pulse of 46 mM K+ was applied to the slices (S1); this was repeated after 30 min (S2). Bicuculline (1-100 microM) was applied when the S1 response returned to basal level, and 10 min later, thiopental (1-300 micro/M), propofol (10 microM), or ketamine (30 microM) were also applied until the end of S2. Perfusate glutamate concentrations were measured fluorometrically, and the area under the glutamate release curves was expressed as a ratio (S2/S1). Results Potassium (46 mM) evoked a monophasic release of glutamate during S1 and S2, with a mean control S2/S1 ratio of 1.07 +/- 0.33 (mean +/- SD, n = 96). Ketamine and thiopental produced a concentration-dependent inhibition of K+-evoked glutamate release with half-maximum inhibition of release values of 18.2 and 10.9 /microM, respectively. Release was also inhibited by propofol. Bicuculline produced a concentration dependent reversal of thiopental inhibition of glutamate release with a half-maximum reversal of the agonist effect of 10.3 microM. Bicuculline also reversed the effects of propofol but not those of ketamine. Conclusions The authors' data indicate that thiopental, propofol, and ketamine inhibit K+-evoked glutamate release from rat cerebrocortical slices. The inhibition produced by thiopental and propofol is mediated by activation of GABAA receptors, revealing a subtle interplay between GABA-releasing (GABAergic) and glutamatergic transmission in anesthetic action.

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