Follow up of neonata hypoxic ischemic encephalopathy and ventricular dilatation / 实用儿科临床杂志

Objective To investigate the prognostic sequelae in neontes with hypoxic-ischemic encephalopathy (HIE) and ven-tricnlar dilatation.Methods Seventy-six full term newborns infants with HIE were followed up at the age from 3 to 19 months after therapy. Twenty-five infants among them were followed up by telephone in the epidemic period of SARS.Results Among 76 infants of 88 newborn infants with HIE(84.6%), 73 infants were normal (96.1% ). 1 infant had cerebral palsy (1.3%), 2 infants died (2.6 %).Among 39 cases with mild HIE, none of them had cerebral sequelae; among moderate HIE. 1 infant had cerebral palsy (2.9%) 1 infant died (2. 9 %), interlenkin-4 among severe HIE 50 % died (P00.5 The poor outcome of HIE in those infants were related to intrauterine growth retardation,severe birth asphyxia;and inadequate treatment.Cranial ultra-sonography of 49 infants were done on follow-up,and 12 of them (24.5 % ) had ventricular dilatations, which appeared after birth with 6 infants. Others occurred on follow-up with 1 infant had cerobral palsy,all ventricular dilatations recovered to normal at 12- 19 months except the cerebral palsy.Conclusions The poor outcome of HIE depends on the infants with intranterine growth relarda-tion,severe birth asphyxia and inadequate treatment.The prognosis of transient ventrealar ddatation are good except cerebral palsy.J Appl Clin pediatr,2004,19(12) : 1045- 1047

Effects and mechanisms of endotoxin pretreatment on lung of rat in endotoxemia / 中华外科杂志

<p><b>OBJECTIVE</b>To observe the effects and mechanisms of endotoxin pretreatment on the rat lung in endotoxemia.</p><p><b>METHODS</b>Eighty-four male Wistar rats were divided into seven groups (each group containing 12 rats): saline control and lipopolysaccharide (LPS)-treated 2 h, 4 h, 6 h groups and LPS-pretreated 2 h, 4 h, 6 h groups. LPS-pretreated rats were administrated with intraperitoneal injection of 0.25 mg/kg LPS. After 24 hours, they were injected with 0.5 mg/kg of LPS. Saline control and LPS-treated rats received an equivalent amount of saline. After 72 hours, LPS-treated and LPS-pretreated rats were intravenously injected with 10 mg/kg of LPS. An equivalent amount of saline was injected in the control rats. Blood was drawn from the carotid artery in LPS-treated and LPS-pretreated rats and sacrificed after intravenous injection of LPS 2, 4, 6 hours. Following saline injection of control rats, blood was drawn from the carotid artery after 6 hours. Arterial blood was drawn for blood gas analysis. The lungs were removed for detecting the mRNA levels of intercellular adhesion molecule-1 (ICAM-1) by reverse transcription polymerase chain reaction and the protein levels of inhibitor kappa B-alpha (I kappa B-alpha) by immunohistochemical staining. Bronchoalveolar lavage was performed in the right lung. Cell counts were evaluated with a light microscopy. The supernatant of bronchoalveolar lavage fluid (BALF) was assayed for the level of protein. The whole lung was weighed and the value was used to determine the lung-body index. The tissue was homogenized and centrifuged for the determination of myeloperoxidase enzyme (MPO) activity.</p><p><b>RESULTS</b>The rats exposed to LPS alone demonstrated an increase in lung-body index, protein in BALF, and MPO activity in the lung tissue. In contrast, the rats exposed to LPS pretreatment exhibited a significant decrease in lung-body index, protein in BALF, and MPO activity. There was a significant decrease in the level of arterial bicarbonate in the LPS-treated rats in comparison with saline-treated and LPS-pretreated animals at 2 hours to 6 hours after LPS administration. The decrease of arterial bicarbonate was compensated by alveolar hyperventilation in LPS-treated animals, with a significant decrease in partial pressure of carbon dioxide. At the same time, partial pressure of oxygen decreased significantly compared with saline control animals and LPS-pretreated animals. LPS-treated rats showed a significant gradually increase in ICAM-1mRNA in the lung in comparison with the saline group. In contrast, ICAM-1mRNA levels in rats pretreated with LPS was lower than that in LPS-treated rats. In LPS-treated animals, LPS caused a decrease of I kappa B-alpha protein expression at 2 hours, returned to control level at 4 hours, and remained at 6 hours. There was no decrease of I kappa B-alpha protein expression in LPS-pretreated animals.</p><p><b>CONCLUSION</b>The results in this study showed that administration of a small dose of LPS 72 hours before endotoxemia caused a attenuation effect on lung injury, which may be correlated to I kappa B-alpha expression induced by LPS pretreatment.</p>

The roles of carbon monoxide on hypoxic pulmonary vasoconstriction / 中国应用生理学杂志

<p><b>AIM AND METHODS</b>To study the roles of carbon monoxide on hypoxic pulmonary vasoconstriction (HPV) by investigating the effects of exogenous carbon monoxide and heme oxygenase inhibitor ZnPPIX on hypoxic vasoconstriction reaction of isolated rat pulmonary arterial rings (PAR).</p><p><b>RESULTS</b>Hypoxia caused constriction in PAR preconstricted by PE. Both ZnPPIX and carbon monoxide inhibited hypoxic pulmonary constriction significantly by increasing the cGMP level after hypoxia.</p><p><b>CONCLUSION</b>ZnPPIX and exogenous carbon monoxide can inhibit HPV. The reduction of cGMP induced by the decreased of CO may be one of reasons of HPV.</p>

Vasodilative action of carbon monoxide on rat pulmonary artery in vitro / 生理学报

The present study investigates the vasodilative action of carbon monoxide on rat pulmonary artery in vitro. After isolation of the pulmonary artery rings (PAR) from Wistar rats, an ACh concentration-response curve was generated; the PARs were incubated with the NOS inhibitor L-NAME (30 micromol/L, n=10) or the heme oxygenase inhibitor ZnPPIX (10 micromol/L)+L-NAME (30 micromol/L, n=10) for 30 min. After that, a second ACh concentration-response curve was elicited. Other isolated PARs were randomly divided into two groups: endothelium-intact group (n=8) and endothelium-denuded group (n=8). The effect of exogenous carbon monoxide (CO) on pulmonary arterial vessel tone was observed. The results showed that ACh induced a concentration-dependent pulmonary vasorelaxation. This relaxation disappeared after endothelium was denuded. The ACh induced relaxation was attenuated after pretreatment with 30 micromol/L L-NAME, and attenuated further after pretreatment with 10 micromol/L ZnPPIX+30 micromol/L L-NAME. Exogenous carbon monoxide relaxed pulmonary artery in both the endothelium-intact group and the endothelium-denuded group. These data suggest that ZnPPIX inhibits ACh induced endothelium-dependent pulmonary artery relaxation and that CO is an endothelium-derived relaxation factor, and exogenous CO can relax pulmonary artery.

Study of bone marrow T-lymphocyte activation in patients with systemic lupus erythematosus / 中华风湿病学杂志

0.05). In active SLE, the CD3~+HLA-DR~+, CD4~+HLA-DR~+ and CD8~+ HLA-DR~+ cells of BM were all higher than those of peripheral blood in the control group(P

Effects of pretreatment with small dose of lipopolysaccharide on cardiac function in endotoxemic rats / 中华麻醉学杂志

Objective It was reported that pretreatment with small dose of lipopolysaccharide (LPS) could protect the animal from lethal dose endotoxin. The purpose of this study was to investigate the effects of pretreatment with small dose of LPS on cardiac function in endotoxemic rats and the possible mechanism. Methods Sixty male Wistar rats weighing 200-280 g were randomly divided into 3 groups: group I normal saline(NS) ( n = 12); group Ⅱ LPS (n = 24) and group Ⅲ LPS-pretreatment ( n = 24). Group Ⅱ and group Ⅲ were further divided into 3 groups: 2 h,4 h and 6 h subgroups based the time when blood sample was taken and the animal was sacrificed. The table shows the LPS given in the 3 groups:groupⅠⅡ Ⅲ0hNSNSLPS 0.25 mg?kg-1ip24 hNSNSLPS0.5mg?kg-1ip96 hNSLPS 10 mg?kg-1 Ⅳ LPS 10 mg?kg-1 TVThe animals were anesthetized with 3 % pentobarbital 30 mg?kg ip and intubated. Right femoral artery and vein were cannulated for MAP monitoring and fluid infusion. Cardiac catheter was placed in the left ventricle for measurement of left ventricular systolic pressure (LVSP) and?dp/dt max. Blood samples were taken 2 h,4 h and 6 h after intravenous LPS (10 mg?kg-1) for determination of plasma levels of L-lactate-dehydrogenase (LDH) and creatine kinase (CK) . The animals were sacrificed right after blood sampling and the heart was removed for determination of myocardial HSP 70 expression using immuno-histochemical staining. Results LVSP and?dp/dt max gradually decreased 1h after intravenous administration of LPS in group Ⅱ (LPS group); while in group DI (pretreatment group) the cardiac contractility was maintained and LVSP,?dp/dt max did not decrease as compared with the baseline value. Plasma LDH concentration and CK activity increased significantly 4 h and 6 h after intravenous IPS in group Ⅱ . The plasma LDH and CK levels were significantly lower in groupⅢthan those in group Ⅱ ( P