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.

scholarly journals Newer Volatile Anesthetic Agents in Cardiac Anesthesia: Review of Literature

2021 ◽  
Author(s):  
Alka Mandke ◽  
Manjula Sarkar ◽  
Charulata Deshpande ◽  
Arun Maheshwari ◽  
Bhupesh Kumar ◽  
...  
Keyword(s):  
Volatile Anesthetic ◽  
Cochrane Library ◽  
Cochrane Central Register ◽  
Cardiac Anesthesia ◽  
Medical Subject Headings ◽  
Holistic View ◽  
Anesthetic Agents ◽  
Cardiac Anaesthesia ◽  
Mesh Terms ◽  
Inhalational Anaesthesia

AbstractMyocardial protection with volatile anesthetic agents have been suggested by multiple studies. These studies, however, are scattered and are often limited to a particular aspect of cardiac anesthesia. Older inhalational agents like halothane is known to cause significant hepatic damage in patients undergoing long duration surgeries while isoflurane is known to have marked vasodilating properties that also affects the coronary arteries leading to coronary “steal” phenomenon. Additionally, newer agents, like sevoflurane and desflurane, have shown more prominent cardioprotective effects than older agents. We searched ScholarOne, Medline, Embase, and the Cochrane Central Register of Controlled Trials (CENTRAL) in the Cochrane Library. The medical subject headings (MeSH) terms “anaesthesia, inhalational,” “anaesthesia, intravenous, or TIVA,” and “Cardiac anaesthesia or Cardiac Surgery” were used. Additional studies were identified by review of the reference sections of all eligible studies. The aim of this review article is to bring together the evidences with newer inhalational agents and provide a holistic view of their benefits and shortcomings in cardiac anesthesia.

scholarly journals Molecular Aspects of Volatile Anesthetic-Induced Organ Protection and Its Potential in Kidney Transplantation

2021 ◽  
Vol 22 (5) ◽  
pp. 2727
Author(s):  
Gertrude J. Nieuwenhuijs-Moeke ◽  
Dirk J. Bosch ◽  
Henri G.D. Leuvenink
Keyword(s):  
Kidney Transplantation ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Animal Experiments ◽  
Volatile Anesthetic ◽  
Organ Protection ◽  
Graft Outcome ◽  
Molecular Aspects

Ischemia reperfusion injury (IRI) is inevitable in kidney transplantation and negatively impacts graft and patient outcome. Reperfusion takes place in the recipient and most of the injury following ischemia and reperfusion occurs during this reperfusion phase; therefore, the intra-operative period seems an attractive window of opportunity to modulate IRI and improve short- and potentially long-term graft outcome. Commonly used volatile anesthetics such as sevoflurane and isoflurane have been shown to interfere with many of the pathophysiological processes involved in the injurious cascade of IRI. Therefore, volatile anesthetic (VA) agents might be the preferred anesthetics used during the transplantation procedure. This review highlights the molecular and cellular protective points of engagement of VA shown in in vitro studies and in vivo animal experiments, and the potential translation of these results to the clinical setting of kidney transplantation.

scholarly journals Effects of the volatile anesthetic agents on sinus node function and atrioventricular conduction in dogs: A comparison with chloralose anesthesia

1988 ◽  
Vol 2 (2) ◽  
pp. 188-193 ◽  
Author(s):  
Niall C.T. Wilton ◽  
Charles B. Hantler ◽  
Steven N. Landau ◽  
Lawrence O. Larson ◽  
Paul R. Knight
Keyword(s):  
Sinus Node ◽  
Volatile Anesthetic ◽  
Atrioventricular Conduction ◽  
Anesthetic Agents

Protective Effect ofAdansonia digitataagainst Isoproterenol-Induced Myocardial Injury in Rats

2016 ◽  
Vol 27 (2) ◽  
pp. 84-95 ◽  
Author(s):  
Mona A. M. Ghoneim ◽  
Amal I. Hassan ◽  
Manal G. Mahmoud ◽  
Mohsen S. Asker
Keyword(s):  
Protective Effect ◽  
Myocardial Injury

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

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 Diabetic Inhibition of Preconditioning- and Postconditioning-Mediated Myocardial Protection against Ischemia/Reperfusion Injury

2012 ◽  
Vol 2012 ◽  
pp. 1-9 ◽  
Author(s):  
Xia Yin ◽  
Yang Zheng ◽  
Xujie Zhai ◽  
Xin Zhao ◽  
Lu Cai
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Protective Effect ◽  
Myocardial Protection ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Diabetic Patients ◽  
Protective Mechanisms ◽  
Gsk 3Β ◽  
Pathogenic Effects

Ischemic preconditioning (IPC) or postconditioning (Ipost) is proved to efficiently prevent ischemia/reperfusion injuries. Mortality of diabetic patients with acute myocardial infarction was found to be 2–6 folds higher than that of non-diabetic patients with same myocardial infarction, which may be in part due to diabetic inhibition of IPC- and Ipost-mediated protective mechanisms. Both IPC- and Ipost-mediated myocardial protection is predominantly mediated by stimulating PI3K/Akt and associated GSK-3β pathway while diabetes-mediated pathogenic effects are found to be mediated by inhibiting PI3K/Akt and associated GSK-3β pathway. Therefore, this review briefly introduced the general features of IPC- and Ipost-mediated myocardial protection and the general pathogenic effects of diabetes on the myocardium. We have collected experimental evidence that indicates the diabetic inhibition of IPC- and Ipost-mediated myocardial protection. Increasing evidence implies that diabetic inhibition of IPC- and Ipost-mediated myocardial protection may be mediated by inhibiting PI3K/Akt and associated GSK-3β pathway. Therefore any strategy to activate PI3K/Akt and associated GSK-3β pathway to release the diabetic inhibition of both IPC and Ipost-mediated myocardial protection may provide the protective effect against ischemia/reperfusion injuries.

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