General anesthetic agents in relation to analgesia

Pain Forum ◽  
1998 ◽  
Vol 7 (1) ◽  
pp. 29-36 ◽  
Author(s):  
Joan J. Kendig
Keyword(s):  
General Anesthetic ◽  
Anesthetic Agents

Proton Hopping In Living Systems.

2020 ◽  
Vol 16 ◽  
Author(s):  
Lemont Kier
Keyword(s):  
Living Systems ◽  
Specific Information ◽  
General Anesthetic ◽  
Memory Functions ◽  
Anesthetic Agents ◽  
Drug Receptor

: This review focuses on the two-century old concept of proton hopping. Introduced in 1806 by Grottus, it has evolved into an explanation of great diversity in describing many functions in living systems. It is a process involving water, which expands on the belief that life exists only in the presence of water. This review describes the mechanism of the process as it carries information through water. A focus is initially made on the process in water in the nerve systems. The nature of the process in these systems is described as the passage of proton hopping in living systems. In drug-receptor encounters, proton hopping is initiated, carrying specific information from these specialized encounters. The review continues with an explanation of sleep, arising from an alteration in proton hopping. A similar phenomenon of the effect of general anesthetic agents is described, as they interfere with by proton hopping. Finally, memory functions are addressed in the realm of events carried by proton hopping.

scholarly journals General anesthesia with remimazolam in a patient with mitochondrial encephalomyopathy: a case report

2021 ◽  
Vol 7 (1) ◽  
Author(s):  
Yuji Suzuki ◽  
Matsuyuki Doi ◽  
Yoshiki Nakajima
Keyword(s):  
Lactic Acidosis ◽  
General Anesthesia ◽  
Mitochondrial Disease ◽  
Muscle Relaxation ◽  
Anesthetic Management ◽  
Perioperative Period ◽  
Mitochondrial Encephalomyopathy ◽  
Anesthesia Induction ◽  
General Anesthetic ◽  
Anesthetic Agents

Abstract Background Systemic anesthetic management of patients with mitochondrial disease requires careful preoperative preparation to administer adequate anesthesia and address potential disease-related complications. The appropriate general anesthetic agents to use in these patients remain controversial. Case presentation A 54-year-old woman (height, 145 cm; weight, 43 kg) diagnosed with mitochondrial encephalomyopathy with lactic acidosis and stroke-like episodes underwent elective cochlear implantation. Infusions of intravenous remimazolam and remifentanil guided by patient state index monitoring were used for anesthesia induction and maintenance. Neither lactic acidosis nor prolonged muscle relaxation occurred in the perioperative period. At the end of surgery, flumazenil was administered to antagonize sedation, which rapidly resulted in consciousness. Conclusions Remimazolam administration and reversal with flumazenil were successfully used for general anesthesia in a patient with mitochondrial disease.

scholarly journals Isoflurane and Propofol Block Neurotoxicity Caused by MK-801 in the Rat Posterior Cingulate/Retrosplenial Cortex

1997 ◽  
Vol 17 (2) ◽  
pp. 168-174 ◽  
Author(s):  
Vesna Jevtović-Todorović ◽  
Charity O. Kirby ◽  
John W. Olney
Keyword(s):  
Brain Injury ◽  
Neuronal Degeneration ◽  
Nmda Antagonist ◽  
Retrosplenial Cortex ◽  
Acute Brain Injury ◽  
Nmda Antagonists ◽  
General Anesthetics ◽  
General Anesthetic ◽  
Mk 801 ◽  
Anesthetic Agents

In acute brain injury syndromes, the potent N-methyl-D-aspartate (NMDA) antagonist, MK-801, can prevent neuronal degeneration, and the general anesthetics, isoflurane and propofol, may also provide neuroprotective benefits. An obstacle to the use of NMDA antagonists for neuroprotective purposes is that they can cause a neurotoxic vacuole reaction in cerebrocortical neurons. This study demonstrates the ability of isoflurane and propofol to prevent the neurotoxic vacuole reaction induced by MK-801. Low sedative doses of inhaled isoflurane (1%) or intravenous (i.v.) propofol (7.5 mg/kg/h) were as effective as higher general anesthetic doses. Thus, in the clinical management of acute brain injury conditions such as stroke and brain trauma, administration of one of these anesthetic agents together with an NMDA antagonist may be an excellent formula for obtaining optimal neuroprotection while eliminating serious side effects.

The Role of Intercostal Block and Three General Anesthetic Agents as Predisposing Factors to Postoperative Pulmonary Problems

1972 ◽  
Vol 51 (4) ◽  
pp. 638???644 ◽  
Author(s):  
PHILLIP O. BRIDENBAUGH ◽  
L. DONALD BRIDENBAUGH ◽  
DANIEL C. MOORE ◽  
GALE E. THOMPSON
Keyword(s):  
Predisposing Factors ◽  
General Anesthetic ◽  
Anesthetic Agents ◽  
Intercostal Block

scholarly journals Sedation in the intensive care unit

2019 ◽  
Vol 72 (3-4) ◽  
pp. 123-130
Author(s):  
Milanka Tatic ◽  
Skeledzija Miskovic ◽  
Ranko Zdravkovic ◽  
Milica Gojkovic ◽  
Aleksandra Kovac ◽  
...  
Keyword(s):  
Intensive Care ◽  
Prolonged Mechanical Ventilation ◽  
Diagnostic Procedures ◽  
General Anesthetic ◽  
Richmond Agitation Sedation Scale ◽  
Vein Thrombosis ◽  
Anesthetic Agents ◽  
Increased Risk ◽  
Prolonged Recovery ◽  
Deep Vein

Introduction. Sedation is the reduction of irritability or agitation by the use of certain drugs mostly to facilitate therapeutic or diagnostic procedures. Scales for evaluation of the depth of sedation. Riker Sedation-Agitation Scale and Richmond Agitation-Sedation Scale are the most commonly used scales. Drugs. Sedation is generally produced by using medications from the group of opioids, benzodiazepines, intravenous and inhalation general anesthetic agents, neuroleptics, phenothiazines, ?-agonists and barbiturates. Adverse effects of sedatives. Sedation is often associated with hypotension, prolonged mechanical ventilation and longer time on respiratory support, higher frequency of delirium, immunosuppression, deep vein thrombosis, increased risk for development of nosocomial pneumonia, all of which leads to the prolonged recovery time. Conclusion. Sedatives currently used in intensive care units are widely used, but they have limitations. The goal is to get the desired level of sedation with as few side effects as possible.

scholarly journals Early Developmental Exposure to General Anesthetic Agents in Primary Neuron Culture Disrupts Synapse Formation via Actions on the mTOR Pathway

2018 ◽  
Author(s):  
Jing Xu ◽  
R. Paige Mathena ◽  
Michael Xu ◽  
YuChia Wang ◽  
CheJui Chang ◽  
...  
Keyword(s):  
Neuronal Development ◽  
Synapse Formation ◽  
Epidemiologic Studies ◽  
Mtor Pathway ◽  
General Anesthetic ◽  
Neuron Culture ◽  
Neurodevelopmental Disease ◽  
Anesthetic Agents ◽  
Pharmacologic Inhibition

Human epidemiologic studies and laboratory investigations in animal models suggest that exposure to general anesthetic agents (GAs) have harmful effects on brain development. The mechanism underlying this putative iatrogenic condition is not clear and there are currently no accepted strategies for prophylaxis or treatment. Recent evidence suggests that anesthetics might cause persistent deficits in synaptogenesis by disrupting key events in neurodevelopment. Using an in vitro model consisting of dissociated primary cultured mouse neurons we demonstrate abnormal pre- and post-synaptic marker expression after a clinically relevant isoflurane anesthesia exposure conducted during neuron development. We find that pharmacologic inhibition of the mechanistic target of rapamycin (mTOR) pathway can reverse the observed changes. Isoflurane exposure increases expression of phospho-S6, a marker of mTOR pathway activity, in a concentration-dependent fashion and this effect occurs throughout neuronal development. The mTOR 1 complex (mTORC1) and the mTOR 2 complex (mTORC2) branches of the pathway are both activated by isoflurane exposure and this is reversible with branch-specific inhibitors. Upregulation of mTOR is also seen with sevoflurane and propofol exposure, suggesting that this mechanism of developmental anesthetic neurotoxicity may occur with all the commonly used GAs in pediatric practice. We conclude that GAs disrupt the development of neurons during development by activating a well-defined neurodevelopmental disease pathway and that this phenotype can be reversed by pharmacologic inhibition.

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