There is a lack of information on critical care in Korea. The aim of this study was to determine the current status of Korean intensive care units (ICUs), focusing on the organization, characteristics of admitted patients, and nurse and physician staffing. Critical care specialists in charge of all 105 critical care specialty training hospitals nationwide completed a questionnaire survey. Among the ICUs, 56.4% were located in or near the capital city. Only 38 ICUs (17.3%) had intensive care specialists with a 5-day work week. The average daytime nurse-to-patient ratio was 1:2.7. Elderly people ≥ 65 yr of age comprised 53% of the adult patients. The most common reasons for admission to adult ICUs were respiratory insufficiency and postoperative management. Nurse and physician staffing was insufficient for the appropriate critical care in many ICUs. Staffing was worse in areas outside the capital city. Much effort, including enhanced reimbursement of critical care costs, must be made to improve the quality of critical care at the national level.Graphical Abstract
This study was performed to evaluate the effects of epigallocatechin 3 gallate (EGCG) on lipopolysaccharide (LPS)-induced acute lung injury in a murine model. In the present study, production of TNF-alpha and MIP-2 and activation of extracellular signal-regulated kinases (ERK)1/2, c-Jun amino terminal kinases (JNK) and p38 in RAW264.7 cells were measured. EGCG inhibited the production of TNF-alpha and MIP-2, and attenuated phosphorylation levels of ERK1/2 and JNK, but not p38 in RAW264.7 cells stimulated with LPS. Also, EGCG attenuated the production of TNF-alpha and MIP-2, and the phosphorylation of ERK1/2 and JNK in the lungs of mice administered with LPS intratracheally. It reduced wet/dry weight ratio, histological severities, and neutrophil accumulation in the lungs in mice given LPS. Our results showed that EGCG attenuated LPS-induced lung injury by suppression of the MIP-2 and TNF-alpha production, and ERK1/2 and JNK activation in macrophage stimulated with LPS.
Critical (or intensive) care medicine (CCM) is a branch of medicine concerned with the care of patients with potentially reversible life-threatening conditions. Numerous studies have demonstrated that adequate staffing is of crucial importance for patient outcome. Adequate staffing also showed favorable cost-effectiveness in terms of ICU stay, decreased use of resources, and lower re-admission rates. The current status of CCM of our contry is not comparable to that of advanced countries. The global pandemic episodes in the past decade showed that our society is not well prepared for severe illnesses or mass casualty. To improve CCM in Korea, reimbursement of the government must be amended such that referral hospitals can hire sufficient number of qualified intensivists and nurses. For the government to address these urgent issues, public awareness of the role of CCM is also required.
This study was undertaken to clarify the effects of urinary trypsin inhibitor (UTI) on lipopolysaccharide (LPS)-induced acute lung injury. Rabbits were randomly assigned to one of seven groups: saline only, UTI, LPS, pre- or post-UTI-high (infusion of UTI of 25,000 U/kg followed by 25,000 U/kg over 2 h), pre- or post-UTI-low (infusion of UTI of 2,500 U/kg followed by 2,500 U/kg over 2 h). UTI was administered 30 min before (pre-groups) or 15 min after (post-groups) LPS administration. Rabbits were mechanically ventilated with 40% oxygen for 6 h. LPS decreased peripheral blood leukocyte counts and increased wet/dry weight ratio of lung, lung injury score, neutrophil infiltration in lung, and IL-8 production in systemic blood and bronchoalveolar lavage fluid (BALF). Rabbits treated by UTI were protected from LPS-induced lung injury, as determined by wet/dry weight ratio, neutrophil infiltration in lung, lung injury score, and IL-8 in BALF levels. UTI attenuated LPS-induced acute lung injury in rabbits mainly by inhibiting neutrophil and IL-8 responses, which may play a central role in sepsis-related lung injury.
The purpose of the present study was to investigate the effect of various opioids including remifentanil, sufentanil, alfentanil and fentanyl on human neutrophil activation induced by lipopolysaccharide (LPS) and to reveal the correlation involving the activation of cytokines and mitogen-activated protein kinases (MAPKs). Neutrophils from human blood were incubated with various concentrations of opioids with LPS. We measured protein levels for tumor necrosis factor-alpha (TNF-α), interleukin (IL)-6 and IL-8 after 4 h incubation period. To clarify the intracellular signaling pathway, we measured the levels of phosphorylation of p38, extracellular signal-regulated protein kinases 1 and 2 (ERK1/2) and c-Jun N-terminal kinase. We also measured the levels for cytokines and MAPKs to reveal the effects of several opioid receptor subtype antagonists on remifentanil with LPS. In the present experiment, only remifentanil could attenuate activation of human neutrophils exposed to LPS. In particular, remifentanil decreased activation of intracellular signaling pathways, including p38 and ERK1/2, and expression of pro-inflammatory cytokines, including TNF-α, IL-6 and IL-8. Especially the decreased activation of cytokines and MAPKs was significantly reverted by a kappa-opioid receptor antagonist on remifentanil with LPS. These results demonstrate that remifentanil can attenuate human neutrophils activations induced by LPS and a kappa-opioid receptor be probably involved in these anti-inflammatory effects mediated by remifentanil.
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