The Effect Of Gap Junction On Pulmonary Arteriospasm At The Early Stage Of Rabbit's Acute Pulmonary Embolism

PartⅠThe role of gap junction in pulmonary vasoconstrictionObjective:To investigate the role of gap junction in pulmonary vasoconstriction.Methods: Forty-eight pulmonary arterial rings(PARs) were divided into six groups randomly. (1) control group(n=8): PARs was contracted by adnephrin (1μmol/L for 15min), The tension curve was recorded. Then, after eluting thoroughly, equal dose of alcohol was added to treat or pretreat the PARs. The change of the maximal tension induced by adnephrin was observed. (2) experimental group(n=16):①group treated by heptanol: after the adnephrin or K+ induced contractile response had reached steady-state, heptanol was cumulatively added to the PARs bath (concentrations ranging from 0.1 to 5 mmol/L). The tension curve was recorded.②group pretreated by heptanol(n=24): The maximal adnephrin(1μmol/L) induced contractile responses were determined on every ring. after eluting thoroughly, the PARs was pretreated by distinct heptanol concentrations (0.2mmol/L,0.5mmol/L or 1mmol/L for 10 min), Then adnephrin(1μmol/L) was added to the PARs bath. The maximal contraction and the tension curve were observed.Result: Heptanol significantly inhibited the contraction of pulmonary arterial rings induced by 1μmol/L adnephrin. The magnitude of the heptanol-induced relaxation was does-dependent. In 1mmol/L heptanol, the magnitude of the adnephrin-induced contraction reduced 73%(P<0.01); while in 5mmol/L heptanol, it reduced 93%(P<0.001). After pretreated pulmonary arterial rings for ten minutes, 0.5 mmol/L and 1mmol/L heptanol diminished the maximal amplitude of adnephrin-induced contraction to 68±10%(P<0.05)and 33±8%(P<0.01). In contrast, there is no detectable effect on the magnitude of K+-induced contractile responses.Conclusion:Heptanol might significantly inhibited the adnephrin, but not K+, induced contraction of rabbit pulmonary artery in vitro. The gap junction might play an important role in pulmonary vasoconstriction. PartⅡThe creation of rabbit model of acute pulmonary embolism and the effect of Gap junction on pulmonary arteriospasm at the early stage of rabbit's acute pulmonary embolismObjective:To explore the feasibility of creating rabbit acute pulmonary embolism model by using autoblood clots and to observe the effect of heptanol on pulmonary arteriospasm at the early stage of rabbits acute pulmonary embolism.Methods:Forty New Zealand big ear rabbits were divided into two groups randomly(one group was 9 animals without pulmonary embolism; another group was 31 animals with pulmonary embolism); after the creation of rabbit model of acute pulmonary embolism, they were divided into 3 group randomly(control group, solvent group, heptanol group).(1)The creation of rabbit model of acute pulmonary embolism: Blood clots were made with blood(2ml) taken from auto-ear vein and poured into a sterile glass plate. After coagulation, it was bathed in 70℃water for ten minutes, then, the clot was cut into small particles (2×2×5mm). Clot particles were repeat injected into right ventricular cavity by a catheter. Pulmonary arteries were obstructed by emboli and rabbit model of acute pulmonary embolism was created.(2)experimental procedure: 1. control group: Using the method of right heart catheter, right ventricular pressure was detected before PTE or 0 min, 10min, 20min, 30min, 60min, 120min after PTE. 2. solvent group and heptanol group: The two group received 20% alcohol (1ml/kg) or heptanol (0.2mmol/ kg) which was injected from right heart catheter after pulmonary embolism. Right ventricular pressure was detected before PTE or 0 min, 10min, 20min, 30min, 60min, 120min after alcohol or heptanol was injected. 3. The group without pulmonary embolism: right ventricular pressure was detected at 0, 10min, 20min, 30min, 60min, 120min. The pulmonary tissue specimen fixation after the experiment ended, then pathological analysis was carried. Results: In three PTE groups, the difference of the changing tendency of right ventricular end systole pressure (RVESP) after PTE was significant (P<0.01). Among them, the changing tendency between control group and solvent group showed no difference(P>0.05). The difference in the changing tendency between heptanol group and control group or between heptanol group and solvent group was significant(P<0.01, P<0.01). In heptanol group, the RVESP got maximum instantly when pulmonary embolized. Then it decreased gradually. A significant decrease in RVESP after 30 min,60min,and 120min (P<0.01) . The difference in RVESP between 120min after PTE and before PTE was significant (P<0.01). Compared with control group, there is no difference in RVESP of heptanol group before pulmonary embolism or at the time of pulmonary embolism(P=0.78,P=0.76); A significant decrease in RVESP at the time of 30 min,60min,and 120min after pulmonary embolism was observed compared with those in control group (P<0.01,P<0.01,P<0.01).Conclusion: 1,The method of creating rabbits acute pulmonary embolism by auto- blood clot is simple and with high successful rate. The RVESP can keep stable in two hours after pulmonary embolism. 2,Heptanol , the gap junction blocker, can inhibit the pulmonary arteriospasm at the early stage of rabbits acute pulmonary embolism. The gap junction may play a pathophysiological role in the pulmonary arteriospasm at the early stage of pulmonary embolism.