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Patients who are bedridden are for a long-time prone to develop bedsores, especially in the hip and sacral areas and limbs, which causes eczema, ulcers, infection and other complications, resulting in pain and more medical costs. Therefore, the medical staff of the Second Affiliated Hospital of Zunyi Medical University designed and developed a kind of anti-bedsore turning pad, and has obtained the national utility model patent (ZL 2021 2 3004923.9), which is suitable for various long-term bedridden patients. The anti-bedsore turning pad includes the center axis of the turning pad, and ventilation pad 1 and ventilation pad 2 designed on the left and right of turning pad center axis. Under the ventilation pad 1 and the ventilation pad 2, the air pad 1 and the air pad 2 are respectively designed. There is a bedspread connected with ventilation pad 1 and ventilation pad 2 on the inflatable pad 1 and the inflatable pad 2. Through the design of inflatable pad 1 and inflatable pad 2, the left and right of the anti-bedsore turning pad can be lowered or raised independently, which is convenient for the patient's body to tilt and turn over, and can significantly reduce the number of nursing staff and the burden of nursing staff when turning over. In addition, it is convenient to replace the force site at any time and reduce the occurrence of pressure ulcers caused by long-term pressure on the force site. Through the design of ventilation cushion 1 and ventilation cushion 2, the internal gas flow of the turning pad can be made, and the ventilation between the patient and the turning pad can be kept dry, so as to reduce the occurrence of eczema, ulcers or infection and other complications, and ultimately reduce the occurrence of bedsores. In addition, through the design of the most superficial limb pad, the patient's limb can be appropriately elevated or massaged, which increases the comfort of the patient. The anti-bedsore turning pad is simple and effective, and can be widely used in long-term bedridden patients.
Assuntos
Humanos , Úlcera por Pressão/epidemiologia , Úlcera , Respiração , Fatores de Risco , EczemaRESUMO
AIM: To investigate the changes of small intestine villus and sublingual microcirculation perfusion in the rabbits during endotoxic shock by sidestream dark-field imaging (SDF) after resuscitation to a mean arterial pressure (MAP) level.METHODS: New Zealand white rabbits (n=60) were randomly divided into 2 groups (group of villus and group of sublingua).The fistula operation of ileum was performed.Lipopolysaccharide was injected to establish endotoxic shock model, and fluid resuscitation (lactated Ringer's solution, 30 mL·kg-1·h-1) was given to maitain the MAP of the animals to 80 mmHg.Continuous norepinephrine was intravenously injected at 0.5~1 μg·kg-1·min-1 only if fluid therapy did not maintain the MAP level.The changes of microcirculatory perfusion indexes in small intestine villus and sublingual tissues such as vessels per villus (VV), microvascular flow index (MFI), proportion of perfused villi (PPVi), villus border score, villus vessel score, total vessel density (TVD), perfused vessel density (PVD) and proportion of perfused vessels (PPVe) were continuously observed and recorded by SDF before shock, during shock and after fluid resuscitation.RESULTS: MFI and PPVi in small intestine villus, and MFI, PPVe, TVD and PVD in sublingual tissues were significantly decreased after shock (P<0.01).Compared with MFI in sublingual microcirculation, MFI in villus was significantly decreased (P<0.01).MFI and PPVi in small intestine villus, and MFI, PPVe, TVD and PVD in sublingual tissues were improved after recovered to the target MAP by fluid resuscitation (P<0.05).However, MFI in small intestine villus was significantly lower than that in sublingual tissues after fluid resuscitation (P<0.01).CONCLUSION: The difference between small intestine villus and sublingual microcirculation perfusion during endotoxic shock is observed.The descent degree of microcirculation perfusion in small intestine villus is larger than that in sublingual tissues after shock, and the recovery degree of small intestine villus microcirculation is lower than that of sublingual microcirculation afer fluid resuscitation.
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Objective Changes of small intestine villus microcirculation perfusion in sidestream dark-field (SDF) imaging in the rabbits during endotoxic shock after fluid resuscitation with different target mean arterial pressure (MAP), and evaluation of feasibility of monitoring small intestine villus microcirculation by SDF were studied. Methods Sixty standard New Zealand white rabbits were randomly divided into two groups: low target MAP group (group A, n = 30) and high target MAP group (group B,n = 30). Fistula operation of ileum was madein vitro, and lipopolysaccharide (LPS, 2 mg/kg) was injected to establish endotoxic shock model. Group A was administered with the lower dose fluid resuscitation (lactated Ringer solution, 20 mL·kg-1·h-1) for target MAP of 65 mmHg (1 mmHg =0.133 kPa); group B was administered with the higher dose fluid resuscitation (lactated Ringer solution, 30 mL·kg-1·h-1) for MAP of 80 mmHg. Continuous norepinephrine intravenous injection (0.5-1.0μg·kg-1·min-1) was administered only after fluid therapy couldn't reach the target MAP. The changes of small intestine villus microcirculation perfusion indexes such as vessels per villus (VV), proportion of perfused villi (PPV), microvascular flow index (MFI), borders of villus score (BVS), vessels villus score (VVS) were continuously observed and recorded before the shock, during the shock and after fluid resuscitation using SDF imaging. The differences of microcirculation perfusion were compared between two groups using the specific parameter evaluation system to determine severity of villi microcirculation and injury scores at different stages.Results VV and borders of villus were clear and contact before shock in two groups. After shock, VV, PPV were significantly decreased in both two groups, the borders of villus were destroyed, MFI, BVS, VVS and the total score of villi injury microcirculation were obviously and severely decreased. Partial blood flow of villous capillaries after fluid resuscitation was recovered in two groups, but the perfusion of some region was un-balanced with the outworn borders of villus. VV were rose as compared before and after fluid resuscitation in groups A and B (vessels: 1.21±0.22 vs. 0.81±0.12, 1.54±0.28 vs. 0.79±0.13), and PPV [(31±4)% vs. (12±2)%, (38±5)% vs. (13±3)%], MFI (1.55±0.09 vs. 1.09±0.03, 1.97±0.11 vs. 1.05±0.03), VVS (points: 1.22±0.08 vs. 0.89±0.02, 2.06±0.15 vs. 0.90±0.02) and the sum of MFI, BVS, VVS (3.70±0.19 vs. 2.85±0.07, 5.01±0.29 vs. 2.88±0.08) were significant rose (allP 0.05).Conclusions For the small intestine villus microcirculation perfusion, the higher target MAP (80 mmHg) after fluid resuscitation or/and vasoconstrictor drugs usage were probably better than the relatively lower target MAP (65 mmHg) during endotoxic shock. SDF imaging is a very promising technique for intestinal villi microcirculatory visualization and assessment.
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Objective To investigate the effects of heme oxygenase-1 (HO-1) preconditioning on oxidative damage in alveolar epithelial type Ⅱ (AE- Ⅱ) cells in rats. Methods The primarily cultured AE- Ⅱ cells isolated from male SD rats were randomly assigned to one of 6 groups (n = 8 each): control group (group C),H2O2 group and 4 different concentrations of HO-1 preconditioning group (group H1-4). The cells were continuously incubated for 5 h in group C. H2O2 0.5 mmol/L was added and the cells were incubated for3 h in group H2O2.In group H1-4, HO-1 0.01, 0.10, 1.00 and 10.00 μmol/L were added and the cells were incubated for2 h, then H2O2 0.5 mmol/L was added and the cells were incubated for 3 h. After the end of incubation, the cell morphology was observed under inverted phase contrast microscope, the AE- Ⅱ cells were counted, and the cell viability was determincd. Results The most AE- Ⅱ cells were adherent and round, had homogeneous cytoplasm, and the cytoplasm contains granular materials in group C and H2-4, while the vacuoles appeared in AE- Ⅱ cells and the cell debris appearecd in the supernatant in group H2 O2 and H1 . Compared with group C, the cell count and cell viability were significantly decreased in group H2 O2 and H1 (P ＜ 0.05). Compared with group H2 O2 and H1, the cell count and cell viability were significantly increased in group H2-4 (P ＜ 0.05). There was no significant difference in the cell count and cell viability between group H2O2 and H1, and among group H2～4(P ＞ 0.05) .Conclusion Preconditioning with 0.10-10.00 μmol/L HO-1 can reduce oxidative damage in rat AE- Ⅱ cells.