Effects of Ranolazine and Ivabradine on Pulmonary Microhemodynamics in Experimental Model of Pulmonary Thromboembolism.

We studied changes of pulmonary microhemodynamics when modeling pulmonary artery thromboembolism on perfused isolated rabbit lungs after pretreatment with ranolazine and ivabradine. The increase in pulmonary artery pressure, pulmonary vascular resistance, and pre- and postcapillary resistance was less pronounced than in control animals, but was close to that in case of pulmonary thromboembolism after pretreatment with voltage-gated Na channel blockers lidocaine and ropivacaine. The increase of capillary filtration coefficient inversely correlated with values of capillary hydrostatic pressure.

Pulmonary Microcirculation in Experimental Model of Pulmonary Thromboembolism after Pretreatment with Chloroquine.

Changes of pulmonary microcirculation in response to pulmonary artery embolization after pretreatment with chloroquine were studied on the model of isolated perfused rabbit lungs. The increase in the pulmonary vascular resistance and pre- and postcapillary resistance was less pronounced than after pulmonary thromboembolism after pretreatment with mibefradil (T-type Ca channels blocker) or nifedipine (L-type Ca channels blocker). The shifts of capillary filtration coefficient correlated with changes in the precapillary resistance.

Changes of Pulmonary Microhemodynamics in Experimental Pulmonary Thromboembolism after Pretreatment with K-Channel Activators.

Changes in pulmonary microhemodynamics in response to pulmonary embolism under conditions of activation of K channels with nicorandil, Kv channels with dapagliflozin, and BK channels with Evans blue were studied on isolated rabbit lungs. Under conditions of activation of K and BK channels, the constrictor reactions of the pulmonary arterial vessels during embolization of the pulmonary artery were less pronounced than in the control. Activation of BK channels reduced constrictor reactions of the pulmonary venous vessels, while activation of K and Kv channels eliminates them.

[Pulmonary artery denervation in pulmonary hypertension: physiological and clinical aspects].

This article is a review of the findings of experimental and clinical studies of a new method of treatment of pulmonary hypertension - pulmonary artery denervation with the help of radiofrequency ablation, cryodenervation and ultrasonic impact. Pulmonary artery denervation results in decreased neurogenic tonic sympathetic and, probably, increased parasympathetic effects on pulmonary vessels. On models of experimental monocrotaline-induced pulmonary hypertension in various-species animals, it was determined that pulmonary artery denervation is followed by decreased activity of local pulmonary renin-angiotensin system, slowed processes of remodeling of pulmonary vessels, hypertrophy and fibrosis of the right ventricle, with inhibition of progression of pulmonary hypertension by means of suppression of extracellular signal-regulated kinase 1/2 (ERK 1/2) which regulates differentiation, proliferation and migration of smooth muscle cells.

Pulmonary Microcirculation during Experimental Pulmonary Thromboembolism under Conditions of Activation and Blockade of Muscarinic Acetylcholine Receptors.

Changes in pulmonary microcirculation were studied in isolated perfused rabbit lungs during modelling pulmonary thromboembolism under conditions of acetylcholine infusion against the background of treatment with M1 acetylcholine receptor blocker pirenzepine or blockade of muscarinic acetylcholine receptors with atropine. In the first case, the increase in pulmonary artery pressure was less pronounced than in case of atropine treatment. In response to pulmonary embolism after acetylcholine infusion against the background of pirenzepine pretreatment, the capillary hydrostatic pressure and postcapillary resistance did not change, while after atropine treatment, these parameters increased.