ABSTRACT
Objective:To observe the relationship between inducible carbon monoxide synthase (iNOS) and delayed encephalopathy after acute carbon monoxide poisoning (DEACMP), and explore its mechanism of action in DEACMP.Methods:This study was designed as prospective cohort study. Patients with acute carbon monoxide poisoning who met the diagnostic criteria and were admitted to Emergency Intensive Care Unit(EICU) of our hospital from June 2019 to June 2021 were selected as subjects. Patients were divided into the DEACMP group and non-DEACMP group according to the occurrence of DEACMP. Serum samples were collected on the first 24 h after admission and on day 7 and 14 after admission, and the serum nitric oxide (NO), neuronal nitric oxide synthase (nNOS), inducible carbon monoxide synthase (iNOS), and endothelial nitric oxide synthase (eNOS) level were measured by enzyme-linked immunosorbent assay. The generalized estimating equation was used to estimate the difference of NO, nNOS, iNOS and eNOS between DEACMP and non-DEACMP patients.Results:A total of 78 patients with carbon monoxide poisoning were included in our study finally, including 49 (62.82%) males and 29 (37.18%) females, with an average age of (53.96±14.95) years, 20 (25.64%) patients with DEACMP, and 1 (1.28%) death. Univariate analysis showed that patients with DEACMP had an average increase of 3 h (95% CI: 1.00, 5.00) in carbon monoxide exposure time and a 5-point decrease in GCS score (95% CI: 1.00, 6.00) than the patients without DEACMP, and the proportion of patients with severe carbon monoxide poisoning in the DEACMP group was higher than that of the non-DEACMP group (90.00% vs. 32.76%). According to the analysis of generalized estimation equation, on day 7 and 14 after admission, Compared with non-DEACMP patients, neither by performing unadjusted nor adjusted analysis with the iNOS of DEACMP patients was significantly higher than that in non-DEACMP patients regardless of whether exposure time, GCS score, coma time or severity of carbon monoxide poisoning were adjusted or not ( P <0.01 or P <0.05). Except for the level of nNOS in the GEE model adjusted with carbon monoxide exposure time, the levels of NO, nNOS and eNOS showed no significant difference between DEACMP and non-DEACMP patients ( P >0.05). Conclusions:The expression of iNOS level is increased in DEACMP patients, and its continuous expression may be involved in the pathogenesis of DEACMP.
ABSTRACT
Objective:To clarify the anatomical characteristics and adjacent relationship of the superior segment of the inferior vena cava during laparoscopic surgery.Methods:In December 2018, two frozen and two fresh adult cadavers were dissected. The chest of the frozen cadavers was opened along the bilateral midline of the clavicle, the anterior pericardial wall was opened, and the superior vena cava and the inferior vena cava was dissected. The abdominal cavity was opened along the midline of the abdomen, the left and right hepatic lobes were turned over, the inferior vena cava and the second hilum of the posterior segment of the liver were exposed, and the hiatus of the inferior vena cava was opened and entered the pericardium.The anatomical characteristics and adjacent relationship of the superior segment of the inferior vena cava were observed, and the length of the superior segment of the inferior vena cava was measured. The fresh frozen cadaver patients underwent laparoscopic surgery.Five 12 mm trocars were placed at the side of umbilicus, right rectus abdominis about 4 cm from umbilicus, midline of abdomen about 6 cm above umbilicus, right axillary front about 2 cm below inferior edge of liver, left midline of clavicle about 2 cm below inferior edge of liver. Laparoscopic-assisted turning of the left and right hepatic lobes, exposing the posterior inferior vena cava and the second hilum of the liver, opening of the vena cava hiatus into the pericardium.The anatomical characteristics and adjacent relationship of the upper diaphragmatic segment of the inferior vena cava were observed.Results:In two autopsies, the inferior vena cava entered the chest through the cava sulcus of the liver and the phrenic foramen cava, and then through the fibrous pericardium into the right atrium. The length from the diaphragm of inferior vena cava to the right atrium was 1.67 cm, 2.57 cm. In laparoscopic operation, the diaphragm entrance of the posterior segment of the liver inferior vena cava, the second hepatic portal and the inferior vena cava could be well exposed.The diaphragm could be opened along the hole of the vena cava with a relatively non vascular anatomical layer of adipose tissue.There was a large anatomical gap between the pericardium and the right atrium, and the inferior vena cava, the superior vena cava and the right atrium could be well exposed, and the whole diaphragm could be completely and continuously exposed from the bottom to the inferior vena cava at the entrance segment of the right atrium.Conclusions:There was a relatively avascular anatomical layer beside the inferior vena cava. During laparoscopic operation, opening the diaphragm through the abdominal cavity could safely enter the pericardium and expose the inferior vena cava, the superior vena cava and the right atrium, which provides a possibility for the removal of Mayo Ⅳ grade inferior vena cava tumor thrombus through this approach.