Abstract
In acute experiments on isolated perfused rabbit’s Сhinchilla lungs changes of pulmonary microhemodynamics were studied in case of pulmonary embolization in the comparison group and after pretreatment with ethosuximide, mibefradil, chloroquine and nifedipine. In response to administration of T-type Ca2+-channel blockers ethosuximide and mibefradil, pulmonary artery pressure, precapillary and pulmonary vascular resistance decreased approximately to the same extent, postcapillary resistance did not change. After pretreatment with chloroquine pulmonary artery pressure, precapillary and pulmonary vascular resistance decreased more than in response to the administration of ethosuximide and mibefradil and the antagonist of L-type Ca2+-channels nifedipine; postcapillary resistance decreased. In the case of chloroquine administration combined with infusion of the KATP- channel blocker glibenclamide, most parameters of pulmonary microcirculation decreased almost to the same extent as in response to mibefradil administration, and postcapillary resistance did not change. After pretreatment with chloroquine in response to pulmonary embolization, pulmonary vascular resistance, pre- and postcapillary resistance increased less pronounced than with thromboembolism after pretreatment with ethosuximide, mibefradil and nifedipine. When modeling thromboembolism after pretreatment with chloroquine combined with KATP-channels blocker glibenclamide, the studied hemodynamics parameters increased to the same extent as after nifedipine pretreatment. Thus, chloroquine exhibits the properties of L- and T-type Ca2+-channels blocker, as well as an activator of KATP-channels, whereas ethosuximide has a blocking effect mainly on T-type Ca2+-channels of smooth muscle cells of pulmonary arterial vessels. Shifts of capillary filtration coefficient under these conditions depend more on changes of precapillary resistance than from the changes of permeability of endothelium of pulmonary vessels.
Published Version
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