Ultrasound-accelerated catheter-assisted thrombolytic therapy applications in deep vein thrombosis.

BACKGROUND: Ultrasound-accelerated catheter-directed thrombolysis (UCT) increases the invasion of thrombolytic agent into the thrombus using ultrasonic energy, provides less infusion of thrombolytic agent, reduces complication, and post-thrombotic syndrome (PTS) development rates. For these reasons, this procedure is a promising method for the treatment of deep vein thrombosis (DVT). MATERIALS AND METHODS: Patients diagnosed with DVT by ultrasonography (USG) who underwent UCT between May 2013 and August 2014 at Gazi University Hospital Cardiovascular Surgery Clinic were included in the study. The demographic characteristics and postoperative acute and long-term patency rates and deep venous insufficiency rates were evaluated retrospectively to determine the efficacy of the UCT procedure. Patients were classified as acute, subacute, and chronical DVT according to the onset of complaints. The efficacy of the UCT procedure was assessed by Doppler USG performed 6 months and 2 years after the procedure, and patients were re-evaluated for deep venous insufficiency and thrombus findings to determine the relationship between UCT procedure and deep venous insufficiency. RESULTS: In acute phase, 57.1% (n = 8) complete and 35.7% (n = 5) partial openings were obtained. No complete patency was obtained in any of the subacute patients. However, partial openness rate was 60%. In patients admitted during the chronic period, complete patency was obtained in 20% (n = 8) and partial openings in 60% (n = 3). Although thrombolysis success was not considered as statistically significant, the success rate was numerically higher in the acute phase. CONCLUSION: As a result, UCT applications provide thrombolysis especially in acute deep vein thrombosis, preventing deep venous insufficiency and especially post-thrombotic syndrome formation. UCT prevents bleeding complications by keeping thrombolytic amount low and can be used as an endovascular method of high safety in patient population with high bleeding complications such as patients with malignancies.

The histopathological effects of levosimendan on liver injury induced by myocardial ischemia and reperfusion.

BACKGROUND: The aim of this study was to evaluate the histological and immunohistochemical effects of levosimendan on liver injury induced by myocardial ischemia and reperfusion (I/R) in a rat model. METHODS: Twenty-four male Wistar Albino rats were randomly divided into the four groups: Group C (Control, n = 6), Group I/R (n = 6), Group BI (I/R group treated with levosimendan before ischemia, n = 6), and Group AI (I/R group treated with levosimendan after ischemia, n = 6). Myocardial I/R was induced by ligation of the left anterior descending coronary artery for 30 min followed by two hours of reperfusion in I/R and I/R+Levosimendan groups. At the end of the study, liver tissue samples were obtained for histopathological and immunohistochemical examination. RESULTS: Masson Trichrome staining revealed significant hepatocyte degeneration and necrosis most marked in portal acinus Zone 3, especially around the central veins in Group I/R. Histopathological changes in Group AI were more similar to the changes in Group I/R. Milder hepatocellular degeneration was found in Group BI, when compared to groups I/R and AI. Immunohistochemical score was found to be significantly higher in Group I/R compared to groups C, BI and AI (p < 0.0001). The scores in groups BI and AI were found to be similar (p = 0.068). CONCLUSION: Levosimendan ameliorates liver injury induced by myocardial IR, especially when administered before induction of ischemia (Fig. 9, Ref. 37).

The effects of iloprost on lung injury induced by skeletal muscle ischemia-reperfusion.

PURPOSE: The aim of this study was to investigate the effects of iloprost (I) on lung injury as a remote organ following skeletal muscle ischemia-reperfusion injury in a rat model. MATERIALS AND METHODS: Twenty-four Wistar Albino rats were randomized into four groups (n = 6). Laparotomy was performed in all groups under general anesthesia. Only laparotomy was applied in Group S (Sham). Ischemia reperfusion group (Group I/R) underwent ischemia and reperfusion performed by clamping and declamping of the infrarenal abdominal aorta for 120 minutes. Group iloprost (Group I) received intravenous infusion of iloprost 0.5 ng/kg/min, without ischemia and reperfusion. Group I/R/I received intravenous infusion of iloprost 0.5 ng/kg/min immediately after 2 hours of ischemia. At the end of the study, lung tissue was obtained for determining total oxidant status (TOS) and total antioxidant status (TAS) levels, histochemical and immunohistochemical determination. RESULTS: Diffuse lymphocyte infiltration was detected in immunohistochemical examination of lung tissue in Group I/R. The connective tissue around bronchi, bronchioles and vessel walls was found to be increased. Although minimal local lymphocyte infiltration was detected in some fields in Group I/R/I, the overall tissue was found to be similar to Group S. iNOS expression was significantly higher in Group I/R, when compared with Group S and significantly lower in Group I/R/I compared to Group I/R.TOS levels were significantly higher in Group I/R, when compared with groups S and I (p = 0.028, p = 0.016, respectively) and significantly lower in group I/R/I, when compared with Group I/R (p = 0.048). TAS levels were significantly higher in Group I/R, when compared with groups S, I (p = 0.014, p = 0.027, respectively) and significantly lower in Group I/R/I, when compared with Group I/R (p = 0.032). CONCLUSION: These results indicate that administration of iloprost may have protective effects against ischemia reperfusion injury (Fig. 8, Tab. 1, Ref. 30)

The protective effects of dexmedetomidine on liver injury-induced myocardial ischemia reperfusion.

PURPOSE: The aim of this study was to evaluate the effect of dexmedetomidine (100 µg/kg-ip) on liver injury-induced myocardial ischemia and reperfusion (IR) in rats. MATERIALS AND METHODS: Twenty-four Wistar Albino rats were separated into four groups. There were four experimental groups (Group C (Control; n = 6), Group IR (ischemia-reperfusion, n = 6), Group D (Dexmedetomidine; n = 6) that underwent left thoracotomy and received ip dexmedetomidine without IR administered via 100 µg/kg ip route 30 minutes before ligating the left coronary artery, and Group IR-D (IR-Dexmedetomidine; n = 6). A small plastic snare was threaded through the ligature and placed in contact with the heart. To produce IR, a branch of the left coronary artery was occluded for 30 min followed by two hours of reperfusion. However, after the above procedure, the coronary artery was not occluded or reperfused in the control rats. At the end of the study, liver tissue was obtained for histochemical and immunohistochemical determination.Some part of tissue samples were stained with Masson-trichrome for the evaluation of ultrastructural changes and inducible nitric oxide synthase (iNOS) expression was evaluated in other part of samples for immunohistochemical examination. RESULTS: Histopathological changes were detected in Group IR when compared with Group C. iNOS expression was found to be increased and stronger particularly in the vascular wall, perisinusoidal space and hepatocytes around vena centralis in this group compared to the control group. Perivascular oedema was detected to be decreased in Group IR-D compared to Group IR. It was also observed that the impairment in the radial arrangement of hepatocytes significantly recovered in Group IR-D. The immunoreactivity was found to be significantly decreased in the assessment of iNOS expression in the same group when compared with Group IR. CONCLUSION: Administration of dexmedetomidine ameliorates liver injury induced by myocardial ischemia and reperfusion (Fig. 8, Ref. 33).

Antioxidative effects of adrenomedullin and vascular endothelial growth factor on lung injury induced by skeletal muscle ischemia-reperfusion.

PURPOSE: The aim of this study was to investigate the effects of adrenomedullin (AM) and vascular endothelial growth factor (VEGF) on lung injury as a remote organ following skeletal muscle ischemia-reperfusion injury in a rat model. MATERIALS AND METHODS: Thirty-six Wistar rats were randomized into six groups (n=6). Laparotomy was performed in all groups under general anesthesia. Nothing else was done in Group S (Sham). Ischemia reperfusion group (Group I/R) underwent ischemia and reperfusion performed by clamping and declamping of the infrarenal abdominal aorta for 120 minutes, respectively. Group VEGF and Group AM received intravenous infusion of VEGF (0.8 µg/kg) or AM (12 µg /kg) respectively, without ischemia and reperfusion. Group IR+VEGF and Group IR+AM received intravenous infusion of VEGF (0.8 µg/kg) or AM (12 µg /kg) respectively immediately after 2 hours period of ischemia. At the end of reperfusion period. Lung tissue samples were taken for biochemical examination. Total oxidant status (TOS) and total antioxidant status (TAS) levels in lung tissue were determined by using a novel automated method. p<0.05 was considered as statistically significant. RESULTS: TOS levels were significantly higher in Group I/R, when compared with groups S, AM and VEGF (p=0.004, p=0.011, p=0.017, respectively) and significantly lower in groups I/R+AM and I/R+VEGF, when compared with Group I/R (p=0.018, p=0.006, respectively). TAS levels were significantly higher in Group I/R, when compared with groups S, AM and VEGF (p=0.006 p=0.016, p=0.016, respectively) and significantly lower in Group I/R+AM, when compared with Group I/R (p=0.016). CONCLUSION: These findings indicate that AM and VEGF acted effectively on the prevention of lung injury induced by skeletal muscle ischemia-reperfusion injury in a rat model (Fig. 2, Ref. 30).

Comparison of the effects of pulsatile cardiopulmonary bypass, non-pulsatile cardiopulmonary bypass and off-pump coronary artery bypass grafting on the inflammatory response and S-100beta protein.

BACKGROUND: We aimed to investigate the effects of off-pump coronary artery bypass grafting, pulsatile cardiopulmonary bypass, and non-pulsatile cardiopulmonary bypass techniques on the inflammatory response and the central nervous system in the current study. METHODS: A total of 32 patients who were scheduled for elective coronary artery bypass graft surgery were included in the study. The patients were allocated into three different groups according to the perfusion techniques used during the cardiopulmonary bypass procedure as follows: off-pump coronary artery bypass grafting group (n=10); pulsatile cardiopulmonary bypass group (n=11); and non-pulsatile cardiopulmonary bypass group (n=11). Serum interleukin-6, interleukin-8, tumor necrosis factor-alpha and S-100beta levels were measured preoperatively, and at 0, 6, and 24 hours postoperatively. RESULTS: The postoperative increase in the levels of interleukin-6 and interleukin-8 was significantly lower in the off-pump group compared to the other two groups (p<0.05), while there was no significant difference in tumor necrosis factor-alpha levels between the groups. Postoperative S-100ß levels, an indicator of cerebral injury, was significantly lower in the off-pump CABG group compared to the other two groups (p<0.05). CONCLUSION: We found that off-pump coronary artery bypass grafting had less negative effects on inflammatory response and central nervous system compared to pulsatile cardiopulmonary bypass and non-pulsatile cardiopulmonary bypass techniques.