Effect of Music Intervention on Lung Expansion Exercises after Cardiothoracic Surgery.

Background: Music intervention can reduce anxiety. This study analyzed the physiological changes from using music intervention after cardiothoracic surgery. Methods: Subjects were randomly assigned to the music group or the control group. The maximal inspiratory pressure/maximal expiratory pressure (MIP/MEP), pulse oximeter oxygen saturation (SpO2), visual analogue scale (VAS) for pain, and State-Trait Anxiety Inventory (STAI) were compared. Results: Compared to the control group (n = 9), the music group (n = 9) had higher MIP and MEP during the overall test (p < 0.05), with significant differences in the changes and time (p < 0.001). However, only MEP was significant in terms of the interaction between music intervention and time (p < 0.001). In terms of the groups, SpO2 and VAS were significant (p < 0.05). SBP, SpO2, and VAS over time showed significant differences between the two groups (p < 0.05). In terms of the interaction between music intervention and time, only SpO2 was significant (p < 0.05). The STAI-S scale decreased by −5.7 ± 5.8 in the music group vs. −0.47 ± 9.37 in control group and the STAI-T scale increased by 4.17 ± 12.31 in the music group vs. 1.9 ± 9.29 in the control group, but showed no significance. Conclusions: Music intervention with nature sounds has a positive physiological impact and can reduce postoperative pain and anxiety in cardiothoracic surgery patients.

Release of endogenous heat shock protein 72 on the survival of sepsis in rats.

BACKGROUND: This study was undertaken to clarify the role of extracellular heat shock protein 72 on the survival of sepsis and to determine possible factor(s) that may be responsible for it. MATERIALS AND METHODS: Sepsis was induced by cecal ligation and puncture. Changes in serum levels of heat shock protein (Hsp72) and cytokines were determined during sepsis, and the results were correlated with the survival. Effects of heat pretreatment on Hsp72 expression in septic rat leukocytes and those of septic rat serum, lipopolysaccharide (LPS), and certain cytokines on the release of Hsp72 in macrophage NR8383 cells were determined. RESULTS: Circulating Hsp72 levels were increased during the progress of sepsis (0, 5.5, 6.5, 10, and 6.5 ng/mL at 0, 3, 6, 9, and 18 h after cecal ligation and puncture, respectively) and the increases were correlated positively with survival rates. LPS triggered the release of Hsp72 in heat pretreated animals. Heat pretreatment increased Hsp72 expression in nonsepsis (+535%, P < 0.01) and sepsis (+116%, P<0.01%) rat leukocytes. Incubation of sepsis rat serum with NR8383 cells increased levels of extracellular heat shock protein 72 in cultured medium. Cytokine profiling revealed that among the 19 cytokines screened, four of them were increased as follows: cytokine-induced neutrophil chemoattractant 3 (+211.3%, P < 0.05), interleukin 10 (+147%, P < 0.05), MCP-1 (+49.6%, P < 0.05), and tumor necrosis factor alpha (+51.8%, P < 0.05). MCP-1 and LPS were capable of releasing Hsp72 from NR8383 cells. CONCLUSIONS: These results demonstrate that the increases in the levels of circulating Hsp72 had a beneficial effect in improving animal survival during the progress of sepsis. The increases in circulating Hsp72 may be mediated via MCP-1 and/or LPS.

Attenuation of mitochondrial unfolded protein response is associated with hepatic dysfunction in septic rats.

This study was conducted to reveal if the mitochondrial unfolded protein response (mtUPR), a conserved mitochondrial-nuclear communication mechanism, plays a critical role in the protein quality control system to cope with damaged protein during sepsis. Sepsis was induced by cecal ligation and puncture (CLP) in Sprague-Dawley rats. The efficiency of mtUPR was evaluated by measuring the transcriptional factors (CCAAT/enhancer-binder protein homologous protein [CHOP] and CCAAT/enhancer-binder protein-ß) and chaperones (heat shock protein 60 [Hsp60] and Hsp10) expression in response to hepatic mitochondrial oxidized proteins (carbonylated proteins, car-proteins) and multi-ubiquitinated proteins (ub-proteins). The results showed that car-proteins and ub-proteins were significantly increased at 9 and 18 h after CLP. In addition, serum glutamic-oxaloacetic transaminase and glutamic-pyruvic transaminase were significantly positively correlated with mitochondrial car-proteins and ub-proteins and negatively with intramitochondrial adenosine triphosphate. The expression of mitochondrial Hsp60 and Hsp10 decreased notably during the progression of sepsis, implying that failure of mtUPR occurred in the late septic liver. Interestingly, we evaluated the ratio of mitochondrial Hsp60/Hsp10 to the ub-proteins and found that both ratios were statistically lowered at the time points of 9 and 18 h in comparison with 3 and 6 h after CLP. These ratios were also significantly negatively correlated with glutamic-oxaloacetic transaminase and glutamic-pyruvic transaminase levels, suggesting that the ratios could act as an index of mtUPR failure and be a useful tool in estimating the ability of mitochondrial-nuclear communication in sepsis. In conclusion, the results indicated that mtUPR failure occurred during sepsis, and that the index of mtUPR may be a valuable measurement in assessing the severity of organ dysfunction in the clinical setting.

Comparison of needlescopic and conventional video-assisted thoracic surgery for primary spontaneous pneumothorax.

Whether the outcome of primary spontaneous pneumothorax (PSP) when treated with needlescopic video-assisted thoracic surgery is positive is still under scrutiny. The present study was conducted to compare the needlescopic approach with the conventional approach. One-hundred and six patients with primary spontaneous pneumothorax who had undergone needlescopic video-assisted thoracic surgery (NVATS) between May 2006 and August 2008 were reviewed. Their age, gender, smoking status, BMI, side of attack, operative indications, operative time, intraoperative blood loss, postoperative length of stay, postoperative pain in visual analog scale (VAS), postoperative recurrence and follow-up period were recorded. These data were compared with those of 89 patients with PSP who had undergone conventional video-assisted thoracic surgery (CVATS) between June 2002 and April 2006. The operative time was shorter (NVATS: 82.36 ± 35.58 min, CVATS: 99.78 ± 35.74 min; p = 0.008) and intraoperative blood loss was less (NVATS: 16.67 ± 25.90 ml, CVATS: 24.36 ± 26.86 ml; p = 0.04) for the NVATS group. The postoperative pain in VAS was significantly less in NVATS. No major complication or mortality was found in either group. For treatment of primary spontaneous pneumothorax, NVATS is a safe and effective option. Further, it has the added benefit of less pain and improved cosmetics.

Effect of carbon dioxide inhalation on pulmonary hypertension induced by increased blood flow and hypoxia.

There is now increasing evidence from the experimental and clinical setting that therapeutic hypercapnia from intentionally inspired carbon dioxide (CO(2)) or lower tidal volume might be a beneficial adjunct to the strategies of mechanical ventilation in critical illness. Although previous reports indicate that CO(2) exerts a beneficial effect in the lungs, the pulmonary vascular response to hypercapnia under various conditions remains to be clarified. The purpose of the present study is to characterize the pulmonary vascular response to CO(2) under the different conditions of pulmonary hypertension secondary to increased pulmonary blood flow and secondary to hypoxic pulmonary vasoconstriction. Isolated rat lung (n = 32) was used to study (1) the vasoactive action of 5% CO(2) in either N(2) (hypoxic-hypercapnia) or air (normoxic-hypercapnia) at different pulmonary arterial pressure levels induced by graded speed of perfusion flow and (2) the role of nitric oxide (NO) in mediating the pulmonary vascular response to hypercapnia, hypoxia, and flow-associated pulmonary hypertension. The results indicated that inhaled CO(2) reversed pulmonary hypertension induced by hypoxia but not by flow alteration. Endogenous NO attenuates hypoxic pulmonary vasoconstriction but does not augment the CO(2)-induced vasodilatation. Acute change in blood flow does not alter the endogenous NO production.

Hypoxia-inducible factor 1α regulates the expression of the mitochondrial ATPase inhibitor protein (IF1) in rat liver.

A growing number of reports indicate that bioenergetic failure plays a crucial role in the development of multiple organ failure during sepsis. Our previous results showed that the suppression of IF1 (mitochondrial ATPase inhibitor protein) expression and subsequent elevated mitochondrial F(o)F1-ATPase activity might contribute to the bioenergetic failure in the liver during sepsis, and the influence of the decreased transcriptional level of IF1 might be an important factor. In this study, we investigated the interaction of IF1 protein expression and hypoxia-inducible factor 1 (HIF-1), a transcription factor that is correlated with the inflammatory status in sepsis. The results showed that nuclear HIF-1α protein, a subunit of HIF-1, and IF1 mRNA expression were coincidently reduced in late septic liver of rats. Furthermore, in vitro, overexpression of HIF-1α by hypoxia or CoCl2 (HIF-1α activator) treatment augmented IF1 protein levels. On the contrary, HIF-1α antisense oligonucleotide and siRNA were used to specifically downregulate HIF-1α expression, and then IF1 protein levels were significantly decreased in clone 9 cells. Meanwhile, downregulation of HIF-1α expression led to elevate the mitochondrial F(o)F1-ATPase activity in the presence of Bis-Tris buffer (pH 6.5). In conclusion, these results suggested for the first time that the HIF-1 might play a crucial role in regulating IF1 protein expression in late septic liver.

Outcome of physical therapy intervention on ventilator weaning and functional status.

Our study aimed to understand the characteristics of ventilator dependence in patients at a respiratory care center and the potential effects of physical therapy on ventilator weaning and patients' functional status. Prospective data collection consisted of the following: (1) demographic data, including name, gender, age, diagnosis, the Acute Physiology and Chronic Health Evaluation as a severity of the disease, modified Glasgow Coma Scale, mobility at the time of admission, and days of hospitalization; (2) Rapid shallow breathing index (RSBI) as a predictive indicator of ventilator weaning, including indicators of ventilator weaning were collected from the respiratory flow sheet; and (3) Barthel index. Between July 1 and December 31, 2007, 126 patients were admitted to the respiratory care center, and those who required mechanical ventilation for more than 14 days were enrolled. Fifty-five subjects received physical therapy. The RSBI in patients who received physical therapy was 75.7 +/- 37.9 before therapy and 80.0 +/- 48.5 afterwards, while the Barthel index increased from 0.8 +/- 1.4 to 1.9 +/- 2.5 (p < 0.05). The RSBI decreased as time of physical therapy lengthened, but not significantly (r = 0.12, p = 0.44). The success rate of ventilator weaning in patients receiving physical therapy intervention versus non-physical therapy intervention was 58.2% and 40.9%, respectively. The results indicated that lengthening the physical therapy intervention time enhanced the ventilator weaning success rate while mobility was not affected (r = -0.11, p = 0.41). Physical therapy may be offered to ventilator-dependent patients in line with their individual needs to improve or maintain basic mobility.

Effect of carbon dioxide on pulmonary vascular tone at various pulmonary arterial pressure levels induced by endothelin-1.

There have been contradictory reports suggesting that CO(2) may constrict, dilate, or have no effect on pulmonary vessels. Permissive hypercapnia has become a widely adopted ventilatory technique used to avoid ventilator-induced lung injury, particularly in patients with acute respiratory distress syndrome (ARDS). On the other hand, respiratory alkalosis produced by mechanically induced hyperventilation is the mainstay of treatment for newborn infants with persistent pulmonary hypertension. It is important to clarify the vasomotor effect of CO(2) on pulmonary circulation in order to better evaluate the strategies of mechanical ventilation in intensive care. In the present study, pulmonary vascular responses to CO(2) were observed in isolated rat lungs (n = 32) under different levels of pulmonary arterial pressure (PAP) induced by various doses of endothelin-1 (ET-1). The purposes of this study were to investigate (1) the vasodilatory effect of 5% CO(2) in either N(2) (hypoxic-hypercapnia) or air (normoxic-hypercapnia) at different PAP levels induced by various doses of endothelin-1, and (2) the role of nitric oxide (NO) in mediating the pulmonary vascular response to hypercapnia, hypoxia, and ET-1. The results indicated that (1) CO(2) produces pulmonary vasodilatation at high PAP under ET-1 and hypoxic vasoconstriction; (2) the vasodilatory effect of CO(2) at different pressure levels varies in accordance with the levels of PAP, the dilatory effect tends to be more evident at higher PAP; and (3) endogenous NO attenuates ET-1 and hypoxic pulmonary vasoconstriction but does not augment the CO(2)-induced vasodilatation.

Nitric oxide modulates air embolism-induced lung injury in rats with normotension and hypertension.

1. Air embolism the in lungs induces microvascular obstruction, mediator release and acute lung injury (ALI). Nitrite oxide (NO) plays protective and pathological roles in ALI produced by various causes, but its role in air embolism-induced ALI has not been fully investigated. 2. The purpose of the present investigation was to elucidate the involvement of NO and pro-inflammatory cytokines in the pathogenesis of ALI following air infusion into isolated perfused lungs from spontaneously hypertensive rats (SHR) and normotensive Wistar Kyoto (WKY) rats. 3. The extent of ALI was evaluated by changes in lung weight, Evans blue dye leakage, the protein concentration in the bronchoalveolar lavage and pathological examination. We also measured nitrite/nitrate (NO(x)), tumour necrosis factor (TNF)-alpha and interleukin (IL)-1beta concentrations in lung perfusate and determined cGMP in lung tissue. 4. The NO synthase (NOS) inhibitors N(G)-nitro-l-arginine methyl ester (l-NAME) and l-N(6)-(1-iminoethyl)-lysine (l-Nil), as well as the NO donors sodium nitroprusside (SNP) and s-nitroso-N-acetylpenicillamine (SNAP), were administered 30 min before air embolism at a concentration of 10(-3) mol/L in the lung perfusate. 5. Air embolism-induced ALI was enhanced by pretreatment with l-NAME or l-Nil, but was alleviated by SNP or SNAP pretreatment, in both SHR and WKY rats. In both SHR and WKY rats, AE elevated levels of NO(x) (2.6 and 28.7%, respectively), TNF-alpha (52.7 and 158.6%, respectively) and IL-1beta (108.4 and 224.1%, respectively) in the lung perfusate and cGMP levels in lung tissues (35.8 and 111.2%, respectively). Pretreatment with l-LAME or l-Nil exacerbated, whereas SNP or SNAP abrogated, the increases in these factors, except in the case of NO(x) (levels were decreased by l-LAME or l-Nil pretreatment and increased by SNP or SNAP pretreatment). 6. Air embolism caused increases in the lung weight (LW)/bodyweight ratio, LW gain, protein concentration in bronchoalveolar lavage and Evans blue dye leakage. These AE-induced changes were less in lungs isolated from SHR compared with normotensive WKY rats. 7. The results suggest that ALI and associated changes following air embolism in lungs isolated from SHR are less than those in WKY rats. Nitric oxide production through inducible NOS isoforms reduces air embolism-induced lung injury and associated changes. Spontaneously hypertensive rats appear to be more resistant than WKY rats to air embolism challenge.

N-acetylcysteine attenuates the acute lung injury caused by phorbol myristate acetate in isolated rat lungs.

Acute lung injury (ALI) caused by phorbol myristate acetate (PMA) is characterized by pulmonary edema and inflammatory cells infiltration. PMA-activated neutrophils in vivo and in vitro to release free radicals, pro-inflammatory cytokines, nitric oxide (NO) and other mediators. These mediators may be the causes of pulmonary hypertension and increased microvascular permeability. In the present study, we used isolated perfused rat lungs from Sprague-Dawley (SD) rats. The purpose was to evaluate the effects of pretreatment of N-acetylcysteine (NAC) on the PMA-induced ALI and associated changes. PMA (2 microg kg(-1)) was introduced into the lung perfusate. NAC (150 mg kg(-1)) was administered 10 min before PMA. Thirty isolated lungs were randomly assigned to receive vehicle (dimethyl sulfoxide, DMSO, the solvent for PMA, 100 microg g(-1)), PMA alone and PMA with NAC pretreatment. There were 10 lungs in each group. We measured the lung weight (LW) to body weight (BW) ratio (LW/BW), LW gain (LWG), exhaled nitric oxide (NO) and protein concentration in bronchoalveolar lavage (PCBAL). The pulmonary arterial pressure (PAP) and microvascular permeability (K(fc)) were assessed. The concentration of nitrate/nitrite, methyl guanidine (MG), tumor necrosis factor(alpha) (TNF(alpha)) and interleukin-1(beta) (IL-1(beta)) in lung perfusate were determined. In addition, we also evaluate the lung injury by histopathological examination and by grading system for the lung injury score (LIS). PMA caused severe ALI as evidenced by the marked increases in LW changes, exhaled NO, PCBAL, histopathological changes, and LIS. It also increased the nitrate/nitrite, MG, TNF(alpha), and IL-1(beta) in lung perfusate. Pretreatment with NAC significantly attenuated these changes and abrogated the extent of ALI. Our results suggest that NAC exerts strong protective effects on the PMA-induced ALI and associated alterations. The mechanisms are possibly attributable to its antioxidant actions, inhibition of pro-inflammatory cytokines, and restoration of glutathione enzymes.