Journal of Anesthesiology and Pain Research

First and foremost, we'd want to express our profound gratitude to every one of the Open Access Journal's editors who serve on the editorial board. The Journal of Anaesthesiology and Pain Research engaged with 18 editorial board members and it  publishes high-quality publications in the fields of anaesthesiology and pain research. An Editorial Tracking System, which is an online manuscript submission, review, and tracking device, is used for quality control in the peer-review process. Each citable manuscript must be authorised by at least two independent reviewers before being accepted by the publisher; review processing is handled by members of the Journal's editorial board or outside experts. Authors will send manuscripts and use the tracking system to track their development. As everyone is aware, reviewers play a critical role in promoting the Editors' need to maintain high standards of informative excellence in the work we distribute. We are grateful to our board members for their significant contributions to both our rigorous companion audit system and the Journal's critical advancement. Global experts in similar logical distributions are part of the Journal community. All submitted papers go through various processes to ensure uniformity in delivery. The compositions are audited using the standard companion audit procedure. Preliminary scanning is done using an endless amount of paper. After that, fitting papers are given out, along with two free references. The remarks of the arbitrators are taken into account by the Editor in Chief, who is in responsibility of making a final decision.

Acute respiratory distress syndrome (ARDS) is a life-threatening lung disease that results in low blood oxygen levels. People who acquire acute respiratory distress syndrome can develop over several days or abruptly worsen. Shortness of breath is frequently the first symptom of acute respiratory distress syndrome. Low blood oxygen, fast breathing, and clicking, bubbling, or rattling noises in the lungs are also signs and symptoms of acute respiratory distress syndrome. Acute respiratory distress syndromes are usually sick as a result of another illness or a significant accident. Surfactant breaks degraded as fluid builds up inside the small air sacs of the lungs in acute respiratory distress syndrome can develop over several days or abruptly worsen. Shortness of breath is frequently the first symptom of ARDS. Low blood oxygen, fast breathing, and clicking, bubbling, or rattling noises in the lungs are also signs and symptoms of acute respiratory distress syndrome. Surfactant is a frothy substance that helps people breathe by keeping their lungs fully extended. These alterations make it difficult for the lungs to fill with air and transport adequate oxygen into the circulation and throughout the body. Scarring and stiffening of the lung tissue is a possibility. Acute respiratory distress syndrome can develop over several days or abruptly worsen. Shortness of breath is frequently the first symptom of acute respiratory distress syndrome can develop over several days or abruptly worsen. Shortness of breath is frequently the first symptom of acute respiratory distress syndrome.

Humans can only survive for a few minutes without oxygen, which is why it is such an important element for life. In order to sustain homeostasis in the body, there must be a balance between oxygen demand and delivery. The respiratory and cardiovascular systems are the two main organ systems responsible for oxygen supply in the body and maintaining homeostasis. Hypoxemia and its negative repercussions would result if any of these two functions abnormally. Hypoxemia can be caused by a variety of factors, but the most common underlying cause is a ventilation/perfusion mismatch. The current review will concentrate on the definition, aetiology, mechanisms, and treatment of hypoxemia in humans. Hypoxemia is characterised by a drop in the partial pressure of oxygen in the blood, whereas hypoxia is characterised by a reduction in tissue oxygenation. It could be caused by either a lack of oxygen delivery or a lack of oxygen use by the tissues. Hypoxia and hypoxemia do not necessarily go hand in hand. If there is a compensatory rise in haemoglobin level and cardiac output, patients can develop hypoxemia without hypoxia (CO). 

Methylprednisolone is a synthetic glucocorticoid steroid that was created to have better anti-inflammatory and mineralocorticoid activity than cortisol, the prototype glucocorticoid steroid (hydrocortisone). As a glucocorticoid or antiinflammatory medication, methylprednisolone is about four times as effective as hydrocortisone, with around 0.8 times the amount of mineralocorticoid. Methylprednisolone also has a longer action time than hydrocortisone, with a plasma half-life of 2.5 hours compared to 1.5 hours for hydrocortisone. In the current treatment of MS, methylprednisolone is particularly crucial in the acute phase of recurrence. It reduces the inflammatory cycle in a variety of ways, including dampening the inflammatory cytokine cascade, inhibiting T cell activation, decreasing immune cell extravasation into the central nervous system, facilitating apoptosis of activated immune cells, and indirectly decreasing the cytotoxic effects of nitric oxide and TNF-a. As more information about these systems becomes available, it may become possible to develop therapy regimens that are better tailored to the individual as well as the disease state. The only effective neuroprotective drug studied in controlled multicentre clinical trials is high-dose methylprednisolone, as suggested by the National Acute Spinal Cord Injury Studies (NASCIS-2 and NASCIS-3). Methylprednisolone was studied as a lipid peroxidation inhibitor, with the goal of reducing posttraumatic degenerative alterations in the damaged spinal cord. However, several researchers and physicians have questioned the usefulness of methylprednisolone for the treatment of acute traumatic SCI due to inconsistent experimental data and the relatively tiny neurological benefits shown in humans

Dexmedetomidine is a strong 2-adrenoceptor agonist with an affinity for the receptor that is 8 times greater than clonidine. After intravenous treatment to healthy volunteers or postsurgical patients in the intensive care unit, dexmedetomidine exerts sedative, analgesic, and anxiolytic effects. In postsurgical patients, dexmedetomidine caused a predicted haemodynamic drop (dose-dependently lower arterial blood pressure and heart rate), which coincided with lower plasma catecholamin levels. Dexmedetomidine 0.2 to 0.7 g/kg/h generated clinically effective sedation and greatly reduced analgesic requirements in postsurgical ventilated critical care unit patients in phase III clinical trials. After the assisted ventilator was turned off, there was no clinically noticeable respiratory depression. Dexmedetomidine (Precedex) is a selective a2-adrenergic receptor agonist that is a pharmacologically active dextroisomer of medetomidine. In the United States, it is approved for the sedation of mechanically ventilated adult patients in an intensive care unit, as well as non-intubated adult patients before to and/or during surgical and other procedures.