The effect of post-reperfusion levosimendan in an experimental intestinal ischemia-reperfusion model.

BACKGROUND: Levosimendan has been reported to have a positive effect on ischemia-reperfusion injury. Herein, we aimed to evaluate the effects of levosimendan applied after reperfusion in an experimental intestinal injury-reperfusion (IR) model. METHODS: Twenty-one Wistar-albino male rats were separated into three groups: Sham group (n = 7): solely superior mesenteric artery (SMA) was dissected after laparotomy; intestinal ischemia-reperfusion group (IIR, n = 7): SMA was clamped for 60 min and unclamped for 120 min to cause ischemia-reperfusion; IIR + levosimendan group (IIR + L, n = 7): levosimendan was administered in ischemia-reperfusion model. The mean arterial pressures (MAP) were measured in all groups. MAP measurements were performed at the end of stabilization, at the 15th, 30th, and 60th minute of ischemia; at the 15th, 30th, 60th, and 120th minute of reperfusion; and at the end of levosimendan bolus application and when levosimendan infusion concluded. Reperfusion injury was evaluated with tissue malondialdehyde (MDA) and by Chiu score. RESULTS: MAP at 15 min, 30 min, and 60 min of reperfusion was lower in IIR and IIR + L groups compared with basal inter-group measurements. Decline in MAP at 30 min after reperfusion was statistically significant in IIR and IIR + L groups when compared with the sham group. There was no significant difference between MDA levels in the groups. Chiu score was significantly lower in the sham group when compared to IIR and IIR + L groups and higher in IIR when compared to the IIR + L group. CONCLUSION: Levosimendan leads to a decrease in intestinal damage although it did not affect lipid peroxidation and MAP when administered after reperfusion in an experimental intestinal IR model.

Evaluation of bronchoscopic lung volume reduction coil treatment results in patients with severe emphysema.

INTRODUCTION: Bronchoscopic lung volume reduction coil (BLVR-C) implantation is an alternative therapeutic approach that can be applied together with medical treatment for patients with severe emphysema. BLVR-C is both easier and safer in terms of complications than volume reduction surgery. This study aimed to evaluate medium-term outcomes following BLVR-C treatment. METHODS: Forty patients who underwent BLVR-C between September 2013 and March 2014 were reviewed retrospectively. We compared changes between the baseline and 6-month post-procedural results with respect to pulmonary function tests, a 6-min walk test (6MWT), chronic obstructive pulmonary disease (COPD) assessment test (CAT), St. George's Respiratory Questionnaire (SGRQ), and pulmonary artery pressure (PAP) and arterial blood gas analyses. Secondary outcomes included procedure-related and follow-up complications. RESULTS: An average of 9.5 (range: 5-11) coils were placed per lung in an average procedural duration of 20.8 ± 7.0 min (range: 9-45) min. Six months after BLVR-C treatment, significant improvements were observed in patients' pulmonary function tests and quality of life. Changes were observed in the forced exhalation volume in 1 s (+150 mL), residual volume (-14.5%), 6MWT (+48 m), SGRQ (-10.5) and CAT Score (-7.5). Changes in the PAP and partial pressure of carbon dioxide values were not significant, and pneumothorax did not occur. In a 6-month follow-up, 11 cases of COPD exacerbation (41.4%), 7 cases of pneumonia (16.9%) and 1 death (2%) occurred. Treatment in 1 case was postponed because of hypotension and bradycardia during the process. CONCLUSION: BLVR-C treatment appears to be effective over the medium-term and safe for patients with severe emphysema.

Ischemic preconditioning attenuates lipid peroxidation and apoptosis in the cecal ligation and puncture model of sepsis.

Sepsis and septic shock are are among the major causes of mortality in intensive care units. The lung and kidney are the organs most affected by sepsis. Evidence exists that lipid peroxidation and apoptosis may be responsible for the high mortality due to sepsis. Ischemic preconditioning (IP) is a method for the protection of tissues and organs against ischemia/reperfusion injury by reducing reactive oxygen species levels, lipid peroxidation and apoptosis. In the present study, the effects of IP were investigated in cecal ligation and puncture (CLP)-induced sepsis in rats. The three groups of animals used in the present controlled study were the sham-operated group (sham, n=7), which only underwent a laparotomy; the sepsis group (sepsis, n=7), which underwent cecal ligation and perforation; and the IP + sepsis group (IP+sepsis, n=7), which underwent CLP immediately prior to the application of three cycles of IP to the hind limb. The study was terminated at 6 h after the induction of CLP. Blood, kidney and lung tissue samples were collected for the determination of serum creatinine, blood urea nitrogen (BUN), neutrophil gelatinase-associated lipocalin (NGAL) and lung tissue malondialdehyde (MDA) levels, as well as histological examination. The serum creatinine, plasma NGAL and lung tissue MDA levels in the sepsis group were significantly increased compared with those in the sham and the IP+sepsis groups (P<0.05). Alveolar macrophage counts, histological kidney and lung injury scores, kidney (caspase 3) and lung tissue immuonreactivity (M30) scores in the sepsis group were also significantly increased compared with those in the sham and IP+sepsis groups (P<0.05). The alveolar macrophage count in the IP+sepsis group was increased compared with that in the sham group (P<0.05). In conclusion, IP inhibits lipid peroxidation and attenuates histological injury and apoptosis in the lung and kidney during sepsis.

The effects of dexmedetomidine on secondary acute lung and kidney injuries in the rat model of intra-abdominal sepsis.

In the present study, the effects of dexmedetomidine on secondary lung and kidney injuries were studied in the rat model of intra-abdominal sepsis by immunohistological and biochemical examinations. We measured serum creatinine, kidney tissue malondialdehide and plasma neutrophil gelatinase-associated lipocalin levels. In order to evaluate tissue injury we determined kidney tissue mononuclear cell infiltration score, alveolar macrophage count, histological kidney and lung injury scores and kidney and lung tissue immunoreactivity scores. We demonstrated that dexmedetomidine attenuates sepsis-induced lung and kidney injuries and apoptosis in the rat model of sepsis. There is still need for comparative studies in order to determine the effects of dexmedetomidine on organ functions in early human sepsis.