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Objective:To screen risk factors for delirium and its duration in intensive care unit (ICU)patients.Methods:1 200 patients admitted to ICU of the Second Hospital of Shanxi Medical University from May 2017 to May 2019 were enrolled. The gender, age, anesthesia mode, duration of mechanical ventilation and hypoxia, acute physiology and chronic health evaluation Ⅱ (APACHE Ⅱ) score, sedative drug use, and length of ICU stay were recorded. The occurrence and duration of ICU delirium were recorded. Multivariate Logistic regression analysis and multiple linear regression analysis were used to analyze the factors with statistical significance differences between the groups for screening the risk factors for delirium and its duration in ICU patients.Results:397 of 1 200 patients developed delirium, the incidence of ICU delirium was 33.1%. The duration of delirium in 189 patients (47.6%) was 1.0 day, and the duration of delirium in 397 delirium patients was 2.0 (1.5, 2.5) days. ① Analysis of risk factors for delirium: univariate analysis showed that there was no significant difference in the incidence of ICU delirium among patients with different genders or ages. The incidence of ICU delirium in patients with duration of mechanical ventilation or hypoxia 4-9 days and ≥ 10 days was higher than that in patients with ≤ 3 days. The incidence of ICU delirium of general anesthesia and internal medicine patients was higher than that of patients with lumbar anesthesia. The incidence of ICU delirium in patients with APACHEⅡ score ≥ 20 was higher than that in patients with ≤ 10 and 11-19. The patients with length of ICU stay > 9 days had a higher ICU delirium incidence than those ≤ 8 days. Increased incidence of ICU delirium in sedative patients was found as compared with those who did not use sedatives. Multivariate Logistic regression analysis showed that APACHEⅡ score [odds ratio ( OR) = 5.491, 95% confidence interval (95% CI) was 4.361-6.913, P < 0.001], the length of ICU stay ( OR = 2.679, 95% CI was 1.822-3.941, P < 0.001) and the use of sedatives ( OR = 2.479, 95% CI was 1.821-3.374, P < 0.001) were risk factors for ICU delirium. ② Analysis of risk factors of ICU delirium duration: univariate analysis showed that there was no significant difference in ICU delirium duration in patients with different genders or ages. The duration of ICU delirium in patients with duration of mechanical ventilation or hypoxia ≥ 10 days was longer than that in patients with ≤ 3 days and 4-9 days. The duration of ICU delirium in general anesthesia and non-surgical patients was higher than that in patients with spinal anesthesia. The ICU delirium duration in patients with APACHEⅡ score ≥ 20 was longer than that in patients with ≤ 10 and 11-19. The duration of ICU delirium in patients with the length of ICU stay > 9 days was longer than that in patients with ≤ 8 days. The duration of ICU delirium in patients on sedatives was longer than those not taking sedatives. Multiple linear regression analysis showed that the duration of ICU delirium increased by an average of 0.061 days (β = 0.061, 95% CI was 0.032-0.090, P < 0.001) for each additional day of hypoxia (hypoxia duration was divided into three grades of ≤ 3, 4-9 and ≥ 10 days). For every one increase in APACHE Ⅱ score (APACHE Ⅱ score was divided into three grades of ≤ 10, 11-19 and ≥ 20), duration of ICU delirium extended an average of 0.058 days (β = 0.058, 95% CI was 0.048-0.068, P < 0.001). ICU delirium duration increased by an average of 0.065 days in patients with length of ICU stay > 9 days as compared with those ≤ 8 days (β = 0.065, 95% CI was 0.056-0.075, P < 0.001). On average, the duration of ICU delirium was prolonged by 0.362 days in patients on sedatives as compared with those who did not use sedatives (β = 0.362, 95% CI was 0.234-0.490, P < 0.001). Conclusions:APACHEⅡ score, the length of ICU stay and the use of sedatives were common risk factors for ICU delirium and its duration. The hypoxic duration was risk factors for ICU delirium duration.
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Objective To evaluate the role of the mitochondrial ATP-sensitive potassium (mitoKATP) channel in reduction of myocardial ischemia-reperfusion (I/R) injury by calcitonin gene-related peptide (CGRP) in rats in an in vitro experiment.Methods Healthy adult male Sprague-Dawley rats,weighing 250-300 g,were used in this study.After the animals were anesthetized,their hearts were immediately removed and retrogradely perfused with oxygenated K-H solution at 37 ℃ in a Langendorff apparatus.Twenty-four isolated rat hearts were assigned into 4 groups (n =6 each) using a random number table:control group (C group),I/R group,CGRP group and 5-hydroxydecanoate (5-HD) group.The hearts were first perfused with K-H solution for 30 min in the three groups.The hearts were continuously perfused with K-H solution for 150 min in group C.The hearts were subjected to ischemia for 30 min followed by 120 min of reperfusion to establish the model of myocardial I/R injury.In group CGRP,after the hearts were perfused with K-H solution for 10 min,10-8 mol/L CGRP was infused for 20 min at a rate of 0.5 ml/min via the aorta,and then the model of myocardial I/R injury was established.In 5-HD group,specific mito-KATP channel blocker 5-HD 100 μmol/L was infused for 10 min at a rate of 0.5 ml/nin via the aorta,and the other treatments were similar to those previously described in CGRP group.At the end of equilibration and 30,60,90 and 120 min of reperfusion,heart rate (HR),left ventricular systolic pressure (LVSP),left ventricular end-diastolic pressure (LVEDP) and the maximum rate of increase or decrease in left ventricular pressure (±dp/dtmax) were recorded.The myocardial infarct size was measured by 2,3,5-triphenyltetrazolium chloride staining at 120 min of reperfusion.Results Compared with C group,HR,LVSP and ±dp/dtmax were significantly decreased and LVEDP was increased during reperfusion,and the percentage of myocardial infarct size was increased at 120 min of reperfusion in the other three groups (P＜0.05).Compared with I/R group,HR,LVSP and ±dp/dtmax were significantly increased and LVEDP was decreased during reperfusion,and the percentage of nyocardial infarct size was decreased at 120 min of reperfusion in CGRP group (P＜0.05).Compared with CGRP group,HR,LVSP and ±dp/dtmax were significantly decreased and LVEDP was increased during reperfusion,and the percentage of myocardial infarct size was increased at 120 min of reperfusion in 5-HD group (P＜0.05).Conclusion Opening of mito-KATP channels is involved in CGRP-iuduced reduction of myocardial I/R injury in rats in an in vitro experiment.
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Objective To investigate the effects of calcitonin gene-related peptide (CGRP) combined with norepinephrine (NE) on L-type calcium current (LCa-l) in rat ventricular myocytes. Methods Ventricular myocytes were isolated from SD rats (weighing 260-280 g) by retrograde perfusion of the heart via the aorta with an enzyme-containing solution as previously described. Whole-cell patch-clamp recording was made using Axopatch 200B amplifier. The cells were perfused for 1 min with Tyrode solution containing CGRP 1 × 10-7 mol/L (group CGRP) , NE 1 × 10-6 mol/L (group NE), or CGRP 1 × 10-7 mol/L + NE 1 × 10-6 mol/L (group CN) and again washed with Tyrode solution. ICa-L was recorded 1 min before and 1 min after the cells were perfused and 1 min after the cells were washed. I-V curve of ICa-L was made after the cells were perfused with solution containing CGRP or NE alone. Results CGRP significantly inhibited the peak of ICa-L, while NE significantly promoted the peak of ICa-L(P < 0.05) . The peak of ICa-L was significantly decreased 1 min after the cells were perfused in group CGRP,while increased 1 min after the cells were perfused in group NE compared with group CN ( P < 0.05). CGRP made the I-V curve of ICa-L move up-ward, while NE made the I-V curve of ICa-L move down-ward. Conclusion CGRP can weaken the promotion of ICa-L induced by NE in rat ventricular myocytes.