Hypoxic pulmonary vasoconstriction (HPV) is a beneficial mechanism that diverts blood from hypoxic alveoli to better ventilated areas of the lung, but breathing hypoxic air causes the pulmonary circulation to become hypertensive. Responses to airway hypoxia are associated with depolarization of smooth muscle cells in the pulmonary arteries and reduced activity of K+ channels. As Kv7 channels have been proposed to play a key role in regulating the smooth muscle membrane potential, we investigated their involvement in the development of HPV and hypoxia-induced pulmonary hypertension. Vascular effects of the selective Kv7 blocker, linopirdine, and Kv7 activator, flupirtine, were investigated in isolated, saline-perfused lungs from rats maintained for 3–5 days in an isobaric hypoxic chamber (FiO2 = 0.1) or room air. Linopirdine increased vascular resistance in lungs from normoxic, but not hypoxic rats. This effect was associated with reduced mRNA expression of the Kv7.4 channel α-subunit in hypoxic arteries, whereas Kv7.1 and Kv7.5 were unaffected. Flupirtine had no effect in normoxic lungs but reduced vascular resistance in hypoxic lungs. Moreover, oral dosing with flupirtine (30 mg/kg/day) prevented short-term in vivo hypoxia from increasing pulmonary vascular resistance and sensitizing the arteries to acute hypoxia. These findings suggest a protective role for Kv7.4 channels in the pulmonary circulation, limiting its reactivity to pressor agents and preventing hypoxia-induced pulmonary hypertension. They also provide further support for the therapeutic potential of Kv7 activators in pulmonary vascular disease.

Two mechanisms contribute in the development of pulmonary hypertension in pulmonary embolism (PE) -obstruction of pulmonary blood vessels and vasoconstriction. We hypothesize that hypoxia, increased shear stress and/or activation of gathered leukocytes in the PE may cause a release of reactive oxygen species (ROS). Therefore our aim was to determine the influence of the ROS scavenger Tempol on pulmonary hypertension and to describe NO synthase activity and production of NO oxidative products (NOx) after PE. In general anesthesia sephadex microspheres suspended in PSS were applied in right jugular vein as the pulmonary microembolism.Than we measured in isolated salt solution-perfused lungs the changes in perfusion pressure, activity of NO synthase and NOx plasma concentration in 7 groups of rats: C: control group (n=5), CN: C + sodium nitroprusside (SN) (n=5), EN: PE + SN (n=5), ETN: Tempol + PE + SN (n=5), CL: C + L-NAME (n=5), EL: PE + L-NAME (n=5), ETL: Tempol + PE + L-NAME (n=5). Tempol was applied intraperitoneally before PE. Animals that received Tempol (groups TN, TL) had significantly lower basal perfusion pressure than those which did not receive Tempol (EN, EL). Overall we measured a higher decrease of perfusion pressure than in the control group (C) after application of SN. Administration of L-NAME after PE (EL) increased the pressure more than in the control group (NL). NOx concentration was higher after PE. We found that preventive administration of Tempol decreases the increase in perfusion pressure after PE. PE increased NO release and concentration of NOx. Key words ROS scavenger • Pulmonary hypertension • Pulmonary embolism• Nitric oxide • Free radicals Corresponding authorR. Mizera, Traumatologicko-ortopedické centrum KNL a.s.,

Proximal hamstring avulsion is an uncommon muscle injury with a lack of consensus on indications and the timing and technique of surgery. Poor clinical symptoms and difficulties in the diagnostic process can lead to a false diagnosis. The authors present three cases of proximal hamstring avulsion, two complete and one partial ruptures of the biceps femoris muscle. MRI and ultrasound scans were used for optimal treatment alignment. Acute surgery reconstruction (< 4 weeks) was done in two patients. Re-attachment of the full thickness ruptures was performed to the original place and secured by suture anchors, the partial rupture was fixed by a simple suture. Two patients were free of any symptoms at 6 months after surgery, the last one had pain in the subgluteal area and a mild deficit in hamstring strength. Two interesting systematic reviews published on the treatment of proximal hamstring avulsion are discussed in the final part of the paper.

Pulmonary vasoconstriction is an important mechanism contributing to the development of pulmonary hypertension after pulmonary embolism (PE) probably due to increased production of reactive oxygen species (ROS). Our aim was to investigate the change of NO production and to determine the effect of ROS scavenger, Tempol, on pulmonary hypertension after PE.Using the model of in vivo pulmonary embolism and isolated, perfused rat lungs we measured the perfusion pressure and its changes after sodium nitroprusside administration and after NO synthase inhibition by L‐NAME.We used 6 groups of Wistar male rats:NN: control group + sodium nitroprusside (SN) (n=5), EN: PE + SN (n=5), TN: Tempol + PE + SN (n=5), NL: control group + L‐Name (n=5), EL: PE + L‐Name (n=5), TL: Tempol + PE + L‐name (n=5). Tempol was administered before PE.PE caused higher pulmonary pressure. Tempol‐treated rats (TN, TL) had significantly lower perfusion pressure than the animals without Tempol (EN, EL). The decrease of perfusion pressure after application of SN was higher in EN than in NN. Administration of L‐Name after PE (EL) increased the pressure more than in the controls (NL). PE also caused increased NOx production.ROS‐induced vasoconstriction contributed to the pulmonary hypertension after PE. Also, PE caused increased production of NO and NOx. Tempol decreased pulmonary hypertension after PE by inhibiting the free radicals production.

Background Two mechanisms that contribute to pulmonary hypertension after acute pulmonary embolism (PE) are vascular obstruction and vasoconstriction. Vasoconstriction is influenced by NO release. We focused on NO synthase activity, production of NO oxidative products (NOx) and effect of phosphodiesterase‐5 (PDE‐5) blockade by sildenafil on pulmonary hypertension after PE. Methods Using the model of in vivo pulmonary embolism we measured changes of perfusion pressure in isolated rat lungs after blockade of NO‐synthase by L‐NAME and of PDE‐5 by Sildenafil. The NOx concentration was measured before and after PE in venous blood. Results The increase in pulmonary perfusion pressure after L‐NAME administration was higher in rats after PE. NOx plasma concentration was higher after PE than before. Perfusion pressure after PE in rats treated with sildenafil was lower (12.9 ± 0,79 mmHg) than after PE in control group (21.4 ± 3,20 mmHg). Conclusion Experimental PE in rats increases NO‐synthase activity and production of NOx. Administration of sildenafil inhibits pulmonary hypertension after PE. Our study indicates that similarly as in other forms of pulmonary hypertension sildenafil may be beneficial in the treatment of acute pulmonary embolism. Grant Funding Source: Supported by GAUK n. 634112/2012