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T Yang

Publications and source records attributed to T Yang.

At least 91 records · Page 5Linked to original sources
PubMed2000

De novo deletions of SNRPN exon 1 in early human and mouse embryos result in a paternal to maternal imprint switch.

Prader-Willi syndrome (PWS) is a neurogenetic disease characterized by infantile hypotonia, gonadal hypoplasia, obsessive behaviour and neonatal feeding difficulties followed by hyperphagia, leading to profound obesity. PWS is due to a lack of paternal genetic information at 15q11-q13 (ref. 2). Five imprinted, paternally expressed genes map to the PWS region, MKRN3 (ref. 3), NDN (ref. 4), NDNL1 (ref. 5), SNRPN (refs 6-8 ) and IPW (ref. 9), as well as two poorly characterized framents designated PAR-1 and PAR-5 (ref. 10). Imprinting of this region involves a bipartite 'imprinting centre' (IC), which overlaps SNRPN (refs 10,11). Deletion of the SNRPN promoter/exon 1 region (the PWS IC element) appears to impair the establishment of the paternal imprint in the male germ line and leads to PWS. Here we report a PWS family in which the father is mosaic for an IC deletion on his paternal chromosome. The deletion chromosome has acquired a maternal methylation imprint in his somatic cells. We have made identical findings in chimaeric mice generated from two independent embryonic stem (ES) cell lines harbouring a similar deletion. Our studies demonstrate that the PWS IC element is not only required for the establishment of the paternal imprint, but also for its postzygotic maintenance.

Adult↗
PubMed2000

Serpins in the human hair follicle.

Proteinases and their inhibitors are very likely to function as mediators or regulators of the hair growth cycle. Very little information is currently available, however, regarding the specific inhibitors present in human hair follicles at defined stages of their growth cycle. In this study we have analyzed two proteinase inhibitors, plasminogen activator inhibitor type 2 and protease nexin 1, in human hair follicles using in situ hybridization and/or immunohistochemistry. Protease nexin 1 mRNA was found only in the mesenchymal population of the hair follicle, i.e., the follicular papilla cells, during the anagen but not the catagen phase. In contrast, plasminogen activator inhibitor type 2 was localized to several epithelial populations in the follicle: the more differentiated cells of the infundibulum; the companion layer in anagen follicles; and the single layer of outer root sheath cells directly abutting the club hair in telogen follicles. At least some of the plasminogen activator inhibitor type 2 in human follicles appears to be in the relaxed form, as evidenced by strong staining with an antibody that is specific for this form of the inhibitor. This suggests that plasminogen activator inhibitor type 2 interacts with and is cleaved by an endogenous follicular proteinase and supports a constitutive role for this inhibitor in human follicular epithelia.

Amyloid beta-Protein Precursor↗
PubMed2000

Down-regulation of TGF-beta1 production restores immunogenicity in prostate cancer cells.

The objective of this study is to determine if a non-immunogenic Dunning's rat prostate cancer cell line, MATLyLu, can become immunogenic by reducing the endogenous production of TGF-beta1. An expression construct containing a DNA sequence in an antisense orientation to TGF-beta1 (TGF-beta1 antisense) was stably transfected into MATLyLu cells. Following transfection, cellular content of TGF-beta1 reduced from 70 to 10 pg per 2x10(4) cells and the rate of in vitro 3H-thymidine incorporation increased 3-5-fold. After subcutaneous injection of tumour cells into syngeneic male hosts (Copenhagen rats), the tumour incidence was 100% (15/15) for the wild type MATLyLu cells and cells transfected with the control construct, but only 43% (9/21, P< or =0.05) for cells transfected with TGF-beta1 antisense. However, when cells were injected into immunodeficient hosts (athymic nude rats), the incidence of tumour development was 100% (10/10) for both the wild type MATLyLu cells and cells transfected with the control construct and 90% (9/10) for cells transfected with TGF-beta1 antisense. These observations support the concept that MATLyLu cells are immunogenic, when the endogenous production of TGF-beta1 is down-regulated.

Animals↗
PubMed2000

Leukocyte common-antigen-related tyrosine phosphatase receptor: altered expression of mRNA and protein in the New England Deaconess Hospital rat line exhibiting spontaneous pheochromocytoma.

Regulation of cell proliferation by protein tyrosine phosphatases (PTPs) suggests that PTPs are important tumor suppressor genes. The gene encoding the leukocyte common-antigen-related (LAR) PTP receptor maps to chromosome 1p32-33, a region in which loss of heterozygosity is associated with human pheochromocytoma and other neuroectodermal tumors. The rat pheochromocytoma PC12 cell line was originally derived from the transplantable P259 tumor originating from the New England Deaconess Hospital (NEDH) line of Wistar inbred rats. Compared with their Wistar counterparts, 1-2-year-old NEDH rats exhibit a high incidence of spontaneous pheochromocytomas. This study investigates whether levels of LAR transcripts and protein are altered in NEDH adrenal tissue prior to tumor onset. In addition, alternative splicing of an LAR extracellular domain [LAR alternatively spliced element-c (LASE-c)], regulating LAR interaction with extracellular matrix components, was examined. These changes in LAR expression and alternative splicing were hypothesized to be more pronounced in tumor tissue and PC12 cells. Northern blot analysis demonstrated the presence of the approximately 5 kb LAR transcript in all cell lines examined, except PC12. In adrenal medulla tissue harvested from 2-3-month-old rats, LAR approximately 8 and approximately 5 kb transcript expression was decreased in NEDH compared with Wistar samples. RT-PCR demonstrated increased splicing of the LASE-c 27 bp alternatively spliced insert in the LAR extracellular domain in NEDH adrenal medulla tissue. Even greater LASE-c splicing was detected in adrenal medulla tumor tissue derived from 12-month-old NEDH rats and in PC12 cells. Western blot analysis demonstrated decreased levels of LAR protein and increased levels of LASE-c containing LAR protein isoforms in NEDH adrenal medulla tissue. These studies demonstrate that patterns of altered LAR expression present in PC12 cells and in pheochromocytoma tumor tissue are also present in adrenal tissue predisposed to a high incidence of spontaneous pheochromocytoma.

Adrenal Cortex↗
PubMed2000

Time-dependent astroglial changes after gamma knife radiosurgery in the rat forebrain.

OBJECTIVE: Using an experimental rat model and a clinically relevant treatment dose, we performed gamma knife radiosurgery to define the hyperacute radiation effects in normal rat forebrain, the time dependence of the astrocytic reaction, and the participation of astrocytes in the healing process after single-dose gamma radiation injuries. METHODS: Seventy-one rats underwent radiosurgical treatment (4-mm collimator) of the caudate-putamen nucleus (single-fraction maximal dose of 100 Gy) and were killed at times ranging from 3 hours to 90 days. Serial cryostat brain sections were processed with the immunohistochemical avidin-biotin complex technique, using anti-glial fibrillary acidic protein as the primary antibody (to identify astrocytes). RESULTS: Vascular changes, including endothelial hyperplasia and vessel wall thickening, were identified as the earliest postradiation manifestations and continued throughout the observation period. Astrocytes reacted to the radiation injury with hyperplasia and hypertrophy. At earlier time points (3-24 h), proliferation was the predominant reaction. The expression of glial fibrillary acidic protein in the proliferating and hypertrophic astrocytes formed an initial peak in the adjacent corpus callosum 3 days after radiosurgery and peaked within the target site between 14 and 30 days. Astrocytic proliferation and hypertrophy were also observed in distant cortices (frontal, parietal, insular, and piriform cortices) and in the hippocampus. No necrosis was observed less than 30 days after irradiation. By Day 90, necrotic lesions with a mean diameter of 4 mm were identified, with glial scar at their peripheries. Astrocytic morphological features varied according to the distance from the necrosis. The irradiated side contained more glial fibrillary acidic protein-containing cells than did the nonirradiated contralateral side. CONCLUSION: During the early phase after radiation, vasculopathy was the first morphological change and may serve as the initiating factor for subsequent changes. Reactive astrocytes appeared not only at the target site but also in the surrounding regions; the severity of injury was determined by the distance from the target.

Animals↗
PubMed2000

Association between aminolevulinate dehydrogenase genotype and blood lead levels in Taiwan.

This study was designed to evaluate the association between the aminolevulinate dehydrogenase (ALAD) genotype and blood lead levels in a general population environmentally exposed to lead. This study population of 660 subjects was secondarily sampled from the 3000 random samples of Taiwanese general population to study the distribution of blood lead levels in the Taiwanese population. A simple assay based on the polymerase chain reaction-restriction fragment length polymorphism technique was used to determine the genotype of the ALAD gene. This study found that most of the Taiwanese population was ALAD 1-1 (95.4%). Only 4.6% (30 subjects) of population were found to be 1-2 or 2-2. It has been hypothesized that the ALAD2 allele is associated with increased absorption of lead. This study found that individuals with ALAD2 alleles had 20% higher blood lead levels than persons with ALAD1 alleles (7.83 +/- 5.95 vs 6.51 +/- 5.03 micrograms/dL). However, the difference was not statistically significant, even after adjustment for other risk factors of environmental exposure. The result supports the previous finding that individuals with ALAD2 allele had higher blood lead levels. The small sample size and large amount of variation in our study may account for the insignificant association.

Asian People↗
PubMed2000

Renin expression in COX-2-knockout mice on normal or low-salt diets.

Experiments were performed in mice to investigate whether cyclooxygenase-2 (COX-2) in epithelial cells near the tubulovascular contact point (macula densa and TAL cells) may regulate renin gene expression in juxtaglomerular granular cells. Renin activity, afferent arteriolar granularity, and renin mRNA were determined in wild-type mice and in COX-2-knockout mice on control and low-NaCl diets. Renin activity in microdissected glomeruli assessed as angiotensin I formation in the presence of excess substrate and afferent arteriolar granularity determined by direct visualization and immunostaining were significantly reduced in COX-2 -/- compared with wild-type animals. Similarly, renal cortical mRNA levels were lower in COX-2 -/- than in wild-type mice. Maintaining mice on a low-salt diet for 14 days induced an increase in renin mRNA, afferent arteriolar granularity, and renin activity in wild-type mice. In contrast, renin mRNA and renin granularity did not significantly increase in low-salt-treated COX-2 -/- mice, whereas the increase in juxtaglomerular renin enzyme activity was markedly attenuated, but not fully blocked. In additional experiments we found that COX-2 mRNA was increased in angiotensin type 1A receptor-knockout mice compared with wild-type mice. We conclude that COX-2 in the tubulovascular contact region is a critical determinant of renin synthesis in granular cells under resting conditions and that it participates in the stimulation of renin expression caused by a low-NaCl intake.

Animals↗
PubMed2000

Blunted respiratory responses to hypoxia in mutant mice deficient in nitric oxide synthase-3.

In the present study, the role of nitric oxide (NO) generated by endothelial nitric oxide synthase (NOS-3) in the control of respiration during hypoxia and hypercapnia was assessed using mutant mice deficient in NOS-3. Experiments were performed on awake and anesthetized mutant and wild-type (WT) control mice. Respiratory responses to 100, 21, and 12% O(2) and 3 and 5% CO(2)-balance O(2) were analyzed. In awake animals, respiration was monitored by body plethysmography along with O(2) consumption (VO(2)) and CO(2) production (VCO(2)). In anesthetized, spontaneously breathing mice, integrated efferent phrenic nerve activity was monitored as an index of neural respiration along with arterial blood pressure and blood gases. Under both experimental conditions, WT mice responded with greater increases in respiration during 12% O(2) than mutant mice. Respiratory responses to hyperoxic hypercapnia were comparable between both groups of mice. Arterial blood gases, changes in blood pressure, VO(2), and VCO(2) during hypoxia were comparable between both groups of mice. Respiratory responses to cyanide and brief hyperoxia were attenuated in mutant compared with WT mice, indicating reduced peripheral chemoreceptor sensitivity. cGMP levels in the brain stem during 12% O(2), taken as an index of NO production, were greater in mutant compared with WT mice. These observations demonstrate that NOS-3 mutant mice exhibit selective blunting of the respiratory responses to hypoxia but not to hypercapnia, which in part is due to reduced peripheral chemosensitivity. These results support the idea that NO generated by NOS-3 is an important physiological modulator of respiration during hypoxia.

Animals↗
PubMed2000

HERG-Like potassium current regulates the resting membrane potential in glomus cells of the rabbit carotid body.

Direct evidence for a specific K(+) channel underlying the resting membrane potential in glomus cells of the carotid body has been absent. The product of the human ether-a-go-go-related gene (HERG) produces inward rectifier currents that are known to contribute to the resting membrane potential in other neuronal cells. The goal of the present study was to determine whether carotid body glomus cells express HERG-like K(+) current, and if so, to determine whether a HERG-like current regulates the resting membrane potential. Freshly dissociated rabbit glomus cells under whole cell voltage clamp exhibited slowly decaying outward currents that activated 20-30 mV positive to the resting membrane potential. Raising extracellular K(+) revealed a slowly deactivating inward tail current indicative of HERG-like K(+) current. HERG-like currents were not found in cells resembling type II cells. The HERG-like current was blocked by dofetilide (DOF) in a concentration-dependent manner (IC(50) = 13 +/- 4 nM, mean +/- SE) and high concentrations of Ba(2+) (1 and 10 mM). The biophysical and pharmacological characteristics of this inward tail current suggest that it is conducted by a HERG-like channel. The steady-state activation properties of the HERG-like current (V(h) = -44 +/- 2 mV) suggest that it is active at the resting membrane potential in glomus cells. In whole cell, current-clamped glomus cells (average resting membrane potential, - 48 +/- 4 mV), DOF, but not tetraethylammonium, caused a significant (13 mV) depolarizing shift in the resting membrane potential. Using fluorescence imaging, DOF increased [Ca(2+)](i) in isolated glomus cells. In an in-vitro carotid body preparation, DOF increased basal sensory discharge in the carotid sinus nerve in a concentration-dependent manner. These results demonstrate that glomus cells express a HERG-like current that is active at, and responsible for controlling the resting membrane potential.

Animals↗
PubMed2000

Fifty-one kilobase HSV-1 plasmid vector can be packaged using a helper virus-free system and supports expression in the rat brain.

Herpes simplex virus type 1 (HSV-1) plasmid vectors have a number of attractive features for gene transfer into neurons. In particular, the large size of the HSV-1 genome suggests that HSV-1 vectors might be designed to accommodate large inserts. We now report the construction and characterization of a 51 kb HSV-1 plasmid vector. This vector was efficiently packaged into HSV-1 particles using a helper virus-free packaging system. The structure of the packaged vector DNA was verified by both Southern blot and PCR analyses. A vector stock was microinjected into the rat striatum, the rats were sacrificed at 4 days after gene transfer, and numerous X-gal positive striatal cells were observed. This 51 kb vector was constructed using general principles that may support the routine construction of large vectors. Potential applications of such HSV-1 vectors include characterizing large promoter fragments or genomic clones and co-expressing multiple genes.

Animals↗
PubMed2000

Co-administration of aprotinin and epsilon-aminocaproic acid during cardiopulmonary bypass in a swine model.

Despite the beneficial effects of pharmacological interventions to prevent bleeding and to reduce the need for autogeneic blood, there are concerns that these agents induce a prothrombotic state. The purpose of this study was to examine the coagulation phenomena influenced by the coadministration of epsilon-aminocaproic acid (EACA) and aprotinin during cardiopulmonary bypass (CPB). A swine model of CPB was utilized in this study. During 120 min of CPB, treatment animals (N = 5) received 6 x 10(6) Kiu of aprotinin and 30 grams of EACA; whereas, control animals (N = 3) received an equal volume of 0.9% saline. Indices of thrombogenicity included hematological variables, gross pathology, and circuit examination for the presence of thrombus. The application of both antifibrinolytics resulted in an increase use of heparin. Total heparin requirements were significantly different between treatment group (58,800 +/- 3493 iu) versus control group (51,000 +/- 3464 iu). D-dimer concentration was also significantly higher in the control group (500-1000 ng mL-1) than in the treatment group (250-500 ng mL-1) at 5 and 30 min postprotamine. Other coagulation markers tested were not observed to be statistically significant between groups. Thromboelastographic (TEG) index decreased in the treatment group during the surgical procedure and bypass from 2.74 +/- 2.9 to -1.36 +/- 4.1 as compared to an increase from 2.62 +/- 2.9 to 4.05 +/- 0.4 in the control group. Pathologic analysis revealed occurrences of thrombus formation in small vessels in the lung and kidney glomeruli of treatment animals. The concurrent use of both aprotinin and EACA may induce a prothrombotic or coagulant state as determined by histological assessment.

Aminocaproic Acid↗
PubMed2000

A cardiopulmonary bypass perfusion technique for the surgical repair of aortic type I dissections requiring the elephant trunk procedure.

The effect of cerebral and spinal cord protection by a modified perfusion technique during the elephant trunk procedure was assessed. Between 1997 and 1998, six patients underwent selective cerebral perfusion (SCP) and lower half of the body perfusion (LBP), in which the right subclavian and left femoral arteries were separately cannulated and perfused by individual pump heads. Moderate systemic cooling was used (nasal temp. 20-30 degrees C; rectal temp. 23-26 degrees C). The open distal aortic repair was performed using only the selective cerebral perfusion; while the aortic arch reconstruction was performed using both selective cerebral and lower half of the body simultaneous perfusion. Blood oxygen saturation of the left jugular vein (SjO2) and regional oxygen saturation cerebral (rSO2) in the front region of the brain, was monitored along with the pressure of the left temporal superficial and femoral artery. The mean cardiopulmonary bypass time was 136 minutes, with a mean arrest time of 92 minutes. Mean duration of isolated selective cerebral perfusion was 23 minutes, with flow rates of 5-8 mL/kg/min; a left temporal superficial artery pressure of 50 mmHg; SjO2 65-80%, and rSO2 58-72%. Mean duration of simultaneous selective cerebral and lower half of the body perfusion was 27 minutes; cerebral flow rates 5-8 mL/kg/min; the left temporal superficial artery pressure of 45-50 mmHg; SjO2 70-85% and rSO2 55-76%. At the same time, lower half of the body flow rates were maintained within 30-50 mL/kg/min; with a femoral artery pressure 50-80 mmHg. Mean extubation time was 28 hours; mean ICU time was 4.5 days. There were no neurologic complications in any patient. All patients survived the operation and were discharged from the hospital. This modified perfusion technique of SCP and LBP worked well and provided satisfactory cerebral and spinal cord protection.

Adult↗
PubMed2000

Effect of anti-digoxin antiserum on endoxin and membrane ATPase activity in hypoxia-reoxygenation induced myocardial injury.

AIM: To evaluate the protective effect of anti-digoxin antiserum on hypoxia-reoxygenation induced injured myocardium and its mechanism. METHODS: Anti-digoxin antiserum of different concentrations was used, its effect on endoxin and ATPase activity in cell membrane in hypoxia-reoxygenation myocardium model was observed. RESULTS: The level of endoxin was remarkably higher, ATPase activities in cell membrane were remarkably lower in hypoxic group and hypoxia-reoxygenation injury group than those of normal group; anti-digoxin antiserum could resume ATPase activity in a concentration-dependent manner. CONCLUSION: Rise of endoxin was the molecular biological basis of myocardial damage during myocardial hypoxia-reoxygenation. Anti-digoxin antiserum had lessened myocardial injury and had a protective effect on hypoxia-reoxygenation myocardium by antagonizing effect of endoxin.

Animals↗
PubMed2000

Effect of combination of valsartan with benazepril on blood pressure and left ventricular hypertrophy in SHR.

AIM: To evaluate the antihypertensive efficacy of angiotensin converting enzyme inhibitor (ACEI) benazepril in combination with AT1 receptor antagonist valsartan and their effect on left ventricular hypertrophy, renin angiotensin aldosterone system (RAAS) and endoxin in spontaneously hypertensive rat (SHR). METHODS: WKY control group (n = 6) and other 4 groups consisted of 24 SHR (14-week-old, male, n = 6): SHR control group, benazepril group, valsartan group, and combination drug therapy group. Systolic blood pressure (SBP) of SHR was measured at the beginning and at the end of 2, 4, 6, and 8 wk of drug intervention. Morphometric determination, renin activities, angiotensin II (Ang II), endoxin, and ATPase activity analysis were performed at the end of 8 week of drug intervention. RESULTS: SBP, ratio of left ventricular mass (LVM), body weight (BW) (LVM/BW), and transverse diameter of myocardial cell (TDM) of SHR were remarkably decreased after drug intervention, and this decrease was most remarkable in the combination drug therapy group. Renin activities of plasma and myocardium were remarkably increased in drug intervention groups. The levels of Ang II in plasma and myocardium were remarkably increased in valsartan group, decreased in benazepril group and combination drug therapy group. Na(+)-K(+)-ATPase activities in myocardium were remarkably increased and the level of endoxin in myocardium were remarkably decreased as SBP decreased after drug intervention. CONCLUSION: Both benazepril and valsartan can decrease SBP of SHR, and cause regression of ventricular hypertrophy. The efficacy of combination drug therapy group is most remarkable among all groups and avoids the side effects of induction of high Ang II levels in plasma and myocardium caused by long-term use of valsartan alone.

Angiotensin II↗
PubMed2000

p53 mutation, EGFR gene amplification and loss of heterozygosity on chromosome 10, 17 p in human gliomas.

OBJECTIVE: To further illustrate the roles of p53 gene, epidermal growth factor receptor (EGFR) gene and loss of heterozygosity (LOH) on chromosome 10 and 17 p in human glioma progression. METHODS: p53 mutations were scanned in 50 gliomas with various malignant grades using the polymerase chain reaction single strand conformation polymorphism (PCR-SSCP) assay, and were confirmed by direct sequencing. LOH for chromosome 10, 17 p and amplification of the EGFR gene were also assessed using Southern blot analysis. RESULTS: p53 mutations were found in 9 of 17 high-grade astrocytomas (53%), 1 of 15 low-grade astrocytomas (7%), and the only subject of eppendymoblastoma but in none of the 10 medulloblastomas and 7 eppendymomas. The majority of gliomas (38/50) analyzed here retained both 17 p alleles. The frequency of p53 mutations was 13% in this group of tumors and increased to 50% (6/12) in tumors with one 17 p allele (P < 0.025). LOH on chromosome 10 was found in 35% (6/17) of high-grade astrocytomas, in 10% (1/10) of medulloblastomas, but in 0% of low-grade gliomas. EGFR gene amplification was found in 9 high-grade gliomas, 60% (6/9) of which also presented LOH for chromosome 10. CONCLUSIONS: These results indicate that p53 inactivation is a common genetic event in astrocytoma progression that may be more strongly associated with the progression of astrocytomas than with their origin. Absence of p53 mutations in 50% of the tumors with one 17 p allele suggests that a tumor suppressor gene other than p53 may be located on chromosome 17 p and involved in progression to malignancy of some gliomas. The loss of alleles on chromosome 10 and the amplification of the EGFR gene appear to be restricted to high-grade tumors, suggesting that these events may be related to tumor progression rather than initiation.

Brain Neoplasms↗
PubMed2000

Transcatheter closure of secundum atrial septal defects using Amplatzer device.

OBJECTIVE: To evaluate the feasibility and short term results of transcatheter closure of secundum atrial septal defects (TCSASDs) using Amplatzer occluder device. A new self-centering device, the Amplatzer atrial septal occluder, has recently been evaluated in an animal model with excellent results. This paper reports our clinical research with this device. METHODS: 30 patients underwent an attempt at TCSASDs at an average age of 35.6 +/- 15.9 y (range, 5-62 y) and average weight of 63.6 +/- 14.5 kg (range, 17-78 kg) using the Amplatzer atrial septal occluder. The average ASD diameter measured by transesophageal echocardiography (TEE) was 23.6 +/- 4.0 mm (range, 16-31 mm), and the average atrial septal defects (ASD) balloon stretched diameter was 25.2 +/- 5.8 mm (range, 9-34 mm). All patients had right atrial and ventricular volume overload with a Qp/Qs of 3.4 +/- 1.2 (1.4-5.2). A F8-12 catheter was used for delivery of the device in all patients. RESULTS: The device was placed correctly in all patients. There was immediate and complete closure in 30 patients. The average device waist size used to close the defect was 25.6 +/- 5.9 mm (range, 9-34 mm). There was no episode of device embolization or any other complication. Follow-up was performed using transthoracic echocardiography (TTE) 1 day, 1 month, 3 months, 6 months and 1 year after the procedure. The first day after operation; there was complete closure of the ASD in all patients; there have been no episodes of endocarditis, thromboembolism, or wire fracture. CONCLUSION: TCSASDs using the Amplatzer occluder device was an efficient nonsurgical method which had a very high technical success rate and satisfactory short term and follow-up results.

Adult↗
PubMed2000

[The inhibitory effects of chloroquine and dexamethasone on the formation of pulmonary edema in the early stage of smoke inhalation injury in rats].

OBJECTIVE: To explore the inhibitory effects of chloroquine and dexamethasone on the formation of pulmonary edema in the early stage of smoke inhalation injury in rats. METHODS: Wistar rats were used and randomly divided into 10 groups, i.e. normal control, 1 PBH (postburn hour), 3 PBH, 6 PBH, 12 PBH and 24 PBH groups of smoke inhalation injury, 6 PBH and 12 PBH groups with dexamethasone treatment, and 6 PBH and 12 PBH groups with chloroquine treatment. The lung water content (LWC), pulmonary vascular permeability (PVP) and hemorrhagic amount (PHA) were measured. RESULTS: The LWC and PVP (measured by the pulmonary exudation amount of (131)I -- labelled albumin) increased obviously, peaked at 6 PBH and lasted to 24 PBH (P < 0.01) in rats injured by smoke inhalation. In groups treated with chloroquine or dexamethasone, the LWC and PVP were significantly lower at 6 PBH (P < 0.05). Similarly, the PHA in injured group exhibited remarkable, especially at 1 PBH and up to 24 PBH when the value was still higher than that in normal control group (P < 0.01). In groups treated with chloroquine or dexamethasone, PHA abated evidently at 6 PBH (P < 0.01). But there were no significant difference of the indices among groups at 12 PBH. CONCLUSION: Both chloroquine and dexamethasone be effective in preventing and treating pulmonary edema in rats in the early stage of smoke inhalation injury.

Animals↗