| Pulmonary hypertension (PH) and right ventricular hypertrophy (RVH) and failure (RVF) play an important role in the development of pulmonary hypertension syndrome (PHS). Many studies focus on endothelial cells which induced the pulmonary vasoconstrition and remodeling of pulmonary blood vessels in hypoxia pulmonary hypertension , but some previous studies reported that mast cells (MC) also play an important role in those process. The purpose of this experiment was to study the relationship between mast cells and PHS induced by low ambient temperatures in broiler chickens.1 .The technique for catheterization of right ventricle was used for measuring the pulmonary artery pressure, right ventricular pressure and the maximum increasing rate of right ventricular (RV±dp/dtmax) was similar to that described by Qiao et al. MC was stained with Alcian blue staining method. Image analysis were measured for the area and the average grey of value of MC, and vessel wall area, vessel total area and mean medial thickness in pulmonary arterioles. The rate of degraunlation of MC was calculated. The result shows: (1) At 38 and 45 days of age, some birds of low ambient temperature group (LT) occured ascites (14.28%), it indicates the PHS was induced successfully. At 24, 31,38 days of age, the mean pulmonary artery pressure (mPAP) of LT (2.47 ± 0.40-3.59 ± 0.47 kPa) was significantly higher than that of normal temperature group(NTX 1.07±0.02-2.76±0.59 kPa). The right ventricular systolic and diastolic function decreased significantly ( p <0.05). The ascites heart index (AHI) of LT was significantly more than that of NT at 45 days of age (p<0.05). (2) The rate of degranuation of MC of pulmonary parenchyma (17.49±1.55%~35.14±3.66% vs 9.91±0.87%-18.61 ± 1.76%), peripheral pulmonary blood vessel walls (PPBVWX12.32±1.65%- 21.77±3.68 % vs 35.28 ±2.90%-44.77±2.78%) of lung in LT were more significantly than in NT(/t<0.05). The average grey of value of MC were decreased significantly in LT ( pulmonary parenchyma: 115.44±16.24%~128.48 ± 11.19 % vs 72.89±12.25%~83.33 ±11.85%, PPBVW: 115.68±12.97%~129.97±14.01% vs 67.15 ±10.62%~78.65±9.33%) than in NT. (3) the MC number of peripheral pulmonary blood vessel walls (6.40±1.29-15.67±2.56 cells/mm2 vs 27.56± 1.16-38.51±2.90 cells/mm2), pulmonary inner blood vessel (10.59 ± 0.58-19.06 ± 0.90 cells/mm2 vs 37.55 ± 6.39-62.95 ± 11.74 cells/mm2) , mucosal bronchus (105.21±28.74-186.48±18.86 cells/mm2 vs 230.18±6.49-291.73±30.25 cells/mm2) and right ventricle (7.47±1.95-10.39 ±1.99 cells/mm2 vs 22.08±2.57- 41.17 ± 3.45 cells/mm2) were decreased significantly ( p <0.05). The change of biological properties of MC may be caused by released the granule mediator during the development of PHS, it shows that the MC could be involved in the development of PHS.2. The transmembrane movement of Ca 2± was observed in MC degraunlated by LSCM. The result shows: (1) Degraunlated MC was increased significantly intracellular Ca2±. (2)The Ca2± channelblocking agent (verapamil) can decrease significantly the pulmonary artery systolic pressure (PASP) (2.52±0.84-3.91±0.62 kPa vs 3.89±0.34~5.17±0.42 kPa) and pulmonary artery diastolic pressure (PADP) (0.82±0.42-1.43±0.43 kPa vs 1.76±0.44-2.80 ±0.57 kPa), and promote the number of MC in peripheral pulmonary blood vessel walls (13.26±1.57~21.91±1.71 cells/mm2 vs 6.40±1.29~15.67±2.56 cells/mm2) and right ventricle (36.10±2.90~43.12±2.58 cells/mm2 vs 7.47±1.95~8.80±1.48 cells/mm2), and decrease markedly the rate of degranulation of MC. This result suggests that the degranulation of MC could be related to the development of PHS.3. This paper investigated the effect of two histamine receptor antagonists, chlorphenamine maleate (Hi-receptors antagonists) and cixnetidine (H2-receptors antagonists), on PHS induced by low ambient temperature in acute and chronic experiment in broiler chickens. The results were as follows: (1) In acute trial, chlorphenamine maleate decreased the PASP (2.7... |
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