Far-infrared rays enhance mitochondrial biogenesis and GLUT3 expression under low glucose conditions in rat skeletal muscle cells

Far-infrared rays (FIR) are known to have various effects on atoms and molecular structures within cells owing to their radiation and vibration frequencies. The present study examined the effects of FIR on gene expression related to glucose transport through microarray analysis in rat skeletal muscle cells, as well as on mitochondrial biogenesis, at high and low glucose conditions. FIR were emitted from a bio-active material coated fabric (BMCF). L6 cells were treated with 30% BMCF for 24 h in medium containing 25 or 5.5 mM glucose, and changes in the expression of glucose transporter genes were determined. The expression of GLUT3 (Slc2a3) increased 2.0-fold (p < 0.05) under 5.5 mM glucose and 30% BMCF. In addition, mitochondrial oxygen consumption and membrane potential (ΔΨm) increased 1.5- and 3.4-fold (p < 0.05 and p < 0.001), respectively, but no significant change in expression of Pgc-1a, a regulator of mitochondrial biogenesis, was observed in 24 h. To analyze the relationship between GLUT3 expression and mitochondrial biogenesis under FIR, GLUT3 was down-modulated by siRNA for 72 h. As a result, the ΔΨm of the GLUT3 siRNA-treated cells increased 3.0-fold (p < 0.001), whereas that of the control group increased 4.6-fold (p < 0.001). Moreover, Pgc-1a expression increased upon 30% BMCF treatment for 72 h; an effect that was more pronounced in the presence of GLUT3. These results suggest that FIR may hold therapeutic potential for improving glucose metabolism and mitochondrial function in metabolic diseases associated with insufficient glucose supply, such as type 2 diabetes.

Far-infrared rays enhance mitochondrial biogenesis and GLUT3 expression under low glucose conditions in rat skeletal muscle cells

Far-infrared rays (FIR) are known to have various effects on atoms and molecular structures within cells owing to their radiation and vibration frequencies. The present study examined the effects of FIR on gene expression related to glucose transport through microarray analysis in rat skeletal muscle cells, as well as on mitochondrial biogenesis, at high and low glucose conditions. FIR were emitted from a bio-active material coated fabric (BMCF). L6 cells were treated with 30% BMCF for 24 h in medium containing 25 or 5.5 mM glucose, and changes in the expression of glucose transporter genes were determined. The expression of GLUT3 (Slc2a3) increased 2.0-fold (p < 0.05) under 5.5 mM glucose and 30% BMCF. In addition, mitochondrial oxygen consumption and membrane potential (ΔΨm) increased 1.5- and 3.4-fold (p < 0.05 and p < 0.001), respectively, but no significant change in expression of Pgc-1a, a regulator of mitochondrial biogenesis, was observed in 24 h. To analyze the relationship between GLUT3 expression and mitochondrial biogenesis under FIR, GLUT3 was down-modulated by siRNA for 72 h. As a result, the ΔΨm of the GLUT3 siRNA-treated cells increased 3.0-fold (p < 0.001), whereas that of the control group increased 4.6-fold (p < 0.001). Moreover, Pgc-1a expression increased upon 30% BMCF treatment for 72 h; an effect that was more pronounced in the presence of GLUT3. These results suggest that FIR may hold therapeutic potential for improving glucose metabolism and mitochondrial function in metabolic diseases associated with insufficient glucose supply, such as type 2 diabetes.

Profiling of remote skeletal muscle gene changes resulting from stimulation of atopic dermatitis disease in NC/Nga mouse model

Although atopic dermatitis (AD) is known to be a representative skin disorder, it also affects the systemic immune response. In a recent study, myoblasts were shown to be involved in the immune regulation, but the roles of muscle cells in AD are poorly understood. We aimed to identify the relationship between mitochondria and atopy by genome-wide analysis of skeletal muscles in mice. We induced AD-like symptoms using house dust mite (HDM) extract in NC/Nga mice. The transcriptional profiles of the untreated group and HDM-induced AD-like group were analyzed and compared using microarray, differentially expressed gene and functional pathway analyses, and protein interaction network construction. Our microarray analysis demonstrated that immune response-, calcium handling-, and mitochondrial metabolism-related genes were differentially expressed. In the Kyoto Encyclopedia of Genes and Genomes (KEGG) and Gene Ontology pathway analyses, immune response pathways involved in cytokine interaction, nuclear factor-kappa B, and T-cell receptor signaling, calcium handling pathways, and mitochondria metabolism pathways involved in the citrate cycle were significantly upregulated. In protein interaction network analysis, chemokine family-, muscle contraction process-, and immune response-related genes were identified as hub genes with many interactions. In addition, mitochondrial pathways involved in calcium signaling, cardiac muscle contraction, tricarboxylic acid cycle, oxidation-reduction process, and calcium-mediated signaling were significantly stimulated in KEGG and Gene Ontology analyses. Our results provide a comprehensive understanding of the genome-wide transcriptional changes of HDM-induced AD-like symptoms and the indicated genes that could be used as AD clinical biomarkers.

Expression of potassium channel genes predicts clinical outcome in lung cancer

Lung cancer is the most common cause of cancer deaths worldwide and several molecular signatures have been developed to predict survival in lung cancer. Increasing evidence suggests that proliferation and migration to promote tumor growth are associated with dysregulated ion channel expression. In this study, by analyzing high-throughput gene expression data, we identify the differentially expressed K⁺ channel genes in lung cancer. In total, we prioritize ten dysregulated K⁺ channel genes (5 up-regulated and 5 down-regulated genes, which were designated as K-10) in lung tumor tissue compared with normal tissue. A risk scoring system combined with the K-10 signature accurately predicts clinical outcome in lung cancer, which is independent of standard clinical and pathological prognostic factors including patient age, lymph node involvement, tumor size, and tumor grade. We further indicate that the K-10 potentially predicts clinical outcome in breast and colon cancers. Molecular signature discovered through K⁺ gene expression profiling may serve as a novel biomarker to assess the risk in lung cancer.

Prediction of itching diagnostic marker through RNA sequencing of contact hypersensitivity and skin scratching stimulation mice models

Pruritus (itching) is classically defined as an unpleasant cutaneous sensation that leads to scratching behavior. Although the scientific criteria of classification for pruritic diseases are not clear, it can be divided as acute or chronic by duration of symptoms. In this study, we investigated whether skin injury caused by chemical (contact hypersensitivity, CHS) or physical (skin-scratching stimulation, SSS) stimuli causes initial pruritus and analyzed gene expression profiles systemically to determine how changes in skin gene expression in the affected area are related to itching. In both CHS and SSS, we ranked the Gene Ontology Biological Process terms that are generally associated with changes. The factors associated with upregulation were keratinization, inflammatory response and neutrophil chemotaxis. The Kyoto Encyclopedia of Genes and Genomes pathway shows the difference of immune system, cell growth and death, signaling molecules and interactions, and signal transduction pathways. Il1a , Il1b and Il22 were upregulated in the CHS, and Tnf, Tnfrsf1b, Il1b, Il1r1 and Il6 were upregulated in the SSS. Trpc1 channel genes were observed in representative itching-related candidate genes. By comparing and analyzing RNA-sequencing data obtained from the skin tissue of each animal model in these characteristic stages, it is possible to find useful diagnostic markers for the treatment of itching, to diagnose itching causes and to apply customized treatment.

Far-infrared radiation stimulates platelet-derived growth factor mediated skeletal muscle cell migration through extracellular matrix-integrin signaling

Despite increased evidence of bio-activity following far-infrared (FIR) radiation, susceptibility of cell signaling to FIR radiation-induced homeostasis is poorly understood. To observe the effects of FIR radiation, FIR-radiated materials-coated fabric was put on experimental rats or applied to L6 cells, and microarray analysis, quantitative real-time polymerase chain reaction, and wound healing assays were performed. Microarray analysis revealed that messenger RNA expressions of rat muscle were stimulated by FIR radiation in a dose-dependent manner in amount of 10% and 30% materials-coated. In 30% group, 1,473 differentially expressed genes were identified (fold change [FC] > 1.5), and 218 genes were significantly regulated (FC > 1.5 and p < 0.05). Microarray analysis showed that extracellular matrix (ECM)-receptor interaction, focal adhesion, and cell migration-related pathways were significantly stimulated in rat muscle. ECM and platelet-derived growth factor (PDGF)-mediated cell migration-related genes were increased. And, results showed that the relative gene expression of actin beta was increased. FIR radiation also stimulated actin subunit and actin-related genes. We observed that wound healing was certainly promoted by FIR radiation over 48 h in L6 cells. Therefore, we suggest that FIR radiation can penetrate the body and stimulate PDGF-mediated cell migration through ECM-integrin signaling in rats.

Expression profile of mitochondrial voltage-dependent anion channel-1 (VDAC1) influenced genes is associated with pulmonary hypertension

Several human diseases have been associated with mitochondrial voltage-dependent anion channel-1 (VDAC1) due to its role in calcium ion transportation and apoptosis. Recent studies suggest that VDAC1 may interact with endothelium-dependent nitric oxide synthase (eNOS). Decreased VDAC1 expression may limit the physical interaction between VDAC1 and eNOS and thus impair nitric oxide production, leading to cardiovascular diseases, including pulmonary arterial hypertension (PAH). In this report, we conducted meta-analysis of genome-wide expression data to identify VDAC1 influenced genes implicated in PAH pathobiology. First, we identified the genes differentially expressed between wild-type and Vdac1 knockout mouse embryonic fibroblasts in hypoxic conditions. These genes were deemed to be influenced by VDAC1 deficiency. Gene ontology analysis indicates that the VDAC1 influenced genes are significantly associated with PAH pathobiology. Second, a molecular signature derived from the VDAC1 influenced genes was developed. We suggest that, VDAC1 has a protective role in PAH and the gene expression signature of VDAC1 influenced genes can be used to i) predict severity of pulmonary hypertension secondary to pulmonary diseases, ii) differentiate idiopathic pulmonary artery hypertension (IPAH) patients from controls, and iii) differentiate IPAH from connective tissue disease associated PAH.

Effects of hydrogen peroxide on voltage-dependent K+ currents in human cardiac fibroblasts through protein kinase pathways

Human cardiac fibroblasts (HCFs) have various voltage-dependent K+ channels (VDKCs) that can induce apoptosis. Hydrogen peroxide (H2O2) modulates VDKCs and induces oxidative stress, which is the main contributor to cardiac injury and cardiac remodeling. We investigated whether H2O2 could modulate VDKCs in HCFs and induce cell injury through this process. In whole-cell mode patch-clamp recordings, application of H2O2 stimulated Ca2+-activated K+ (K(Ca)) currents but not delayed rectifier K+ or transient outward K+ currents, all of which are VDKCs. H2O2-stimulated K(Ca) currents were blocked by iberiotoxin (IbTX, a large conductance K(Ca) blocker). The H2O2-stimulating effect on large-conductance K(Ca) (BK(Ca)) currents was also blocked by KT5823 (a protein kinase G inhibitor) and 1 H-[1, 2, 4] oxadiazolo-[4, 3-a] quinoxalin-1-one (ODQ, a soluble guanylate cyclase inhibitor). In addition, 8-bromo-cyclic guanosine 3', 5'-monophosphate (8-Br-cGMP) stimulated BK(Ca) currents. In contrast, KT5720 and H-89 (protein kinase A inhibitors) did not block the H2O2-stimulating effect on BK(Ca) currents. Using RT-PCR and western blot analysis, three subtypes of K(Ca) channels were detected in HCFs: BK(Ca) channels, small-conductance K(Ca) (SK(Ca)) channels, and intermediate-conductance K(Ca) (IK(Ca)) channels. In the annexin V/propidium iodide assay, apoptotic changes in HCFs increased in response to H2O2, but IbTX decreased H2O2-induced apoptosis. These data suggest that among the VDKCs of HCFs, H2O2 only enhances BK(Ca) currents through the protein kinase G pathway but not the protein kinase A pathway, and is involved in cell injury through BK(Ca) channels.

Improvement Characteristics of Bio-active Materials Coated Fabric on Rat Muscular Mitochondria

This study surveys the improvement characteristics in old-aged muscular mitochondria by bio-active materials coated fabric (BMCF). To observe the effects, the fabric (10 and 30%) was worn to old-aged rat then the oxygen consumption efficiency and copy numbers of mitochondria, and mRNA expression of apoptosis- and mitophagy-related genes were verified. By wearing the BMCF, the oxidative respiration significantly increased when using the 30% materials coated fabric. The mitochondrial DNA copy number significantly decreased and subsequently recovered in a dose-dependent manner. The respiratory control ratio to mitochondrial DNA copy number showed a dose-dependent increment. As times passed, Bax, caspase 9, PGC-1alpha and beta-actin increased, and Bcl-2 decreased in a dose-dependent manner. However, the BMCF can be seen to have had no effect on Fas receptor. PINK1 expression did not change considerably and was inclined to decrease in control group, but the expression was down-regulated then subsequently increased with the use of the BMCF in a dose-dependent manner. Caspase 3 increased and subsequently decreased in a dose-dependent manner. These results suggest that the BMCF invigorates mitophagy and improves mitochondrial oxidative respiration in skeletal muscle, and in early stage of apoptosis induced by the BMCF is not related to extrinsic death-receptor mediated but mitochondria-mediated signaling pathway.

Taxifolin Glycoside Blocks Human ether-a-go-go Related Gene K+ Channels

Taxifolin glycoside is a new drug candidate for the treatment of atopic dermatitis (AD). Many drugs cause side effects such as long QT syndrome by blocking the human ether-a-go-go related gene (hERG) K+ channels. To determine whether taxifolin glycoside would block hERG K+ channels, we recorded hERG K+ currents using a whole-cell patch clamp technique. We found that taxifolin glycoside directly blocked hERG K+ current in a concentration-dependent manner (EC50=9.6+/-0.7 microM). The activation curve of hERG K+ channels was negatively shifted by taxifolin glycoside. In addition, taxifolin glycoside accelerated the activation time constant and reduced the onset of the inactivation time constant. These results suggest that taxifolin glycoside blocks hERG K+ channels that function by facilitating activation and inactivation process.

A Preliminary Study for the Effect of Multidivisional Program for Social Skill Improvement on Senile Dementia / 가정의학회지

BACKGROUND: Aging population correspond with an increase in the numbers of dementia patients. Dementia decreases the quality of life of patients and care-givers. However, current pharmacological treatment is limited by modest efficacy and adverse effect. Nonpharmacological treatment for dementia has been considered to be a substitute treatment. Recently we developed a special planned program for dementia with depression. The aim of this study was to evaluate therapeutic effect of this program. METHODS: We included patients aged 65 and older who diagnosed dementia with depression in a geriatric institution from April to June, 2006. We surveyed their sex, age, education period, and histories of hypertension, smoking, and alcohol intake. Patients in experimental group carried out our program, including cooking, painting, recreation, and activity, 9 times for 60 minutes a session. All included patients were checked Korean Mini-Mental State Examination (K-MMSE) and Korean Form of Geriatric Depression Scale (KGDS) before starting program and after 3 months when programs finished. RESULTS: There was no difference in demographic factors between two groups. K-MMSE was significantly improved in experimental group compared with control group (P = 0.01). And, the KGDS was significantly improved in experimental group compared with control group (P = 0.00). CONCLUSION: Multidivisional program for social skill improvement was effective on treatment for patients of dementia with depression. Nonpharmacological treatment for dementia with depression would be developed and studied to enhance the qualities of life of patients and care of dementia.

Regional Differences in Mitochondrial Anti-oxidant State during Ischemic Preconditioning in Rat Heart

Ischemic preconditioning (IPC) is known to protect the heart against ischemia/reperfusion (IR)-induced injuries, and regional differences in the mitochondrial antioxidant state during IR or IPC may promote the death or survival of viable and infarcted cardiac tissues under oxidative stress. To date, however, the interplay between the mitochondrial antioxidant enzyme system and the level of reactive oxygen species (ROS) in the body has not yet been resolved. In the present study, we examined the effects of IR- and IPC-induced oxidative stresses on mitochondrial function in viable and infarcted cardiac tissues. Our results showed that the mitochondria from viable areas in the IR-induced group were swollen and fused, whereas those in the infarcted area were heavily damaged. IPC protected the mitochondria, thus reducing cardiac injury. We also found that the activity of the mitochondrial antioxidant enzyme system, which includes manganese superoxide dismutase (Mn-SOD), was enhanced in the viable areas compared to the infarcted areas in proportion with decreasing levels of ROS and mitochondrial DNA (mtDNA) damage. These changes were also present between the IPC and IR groups. Regional differences in Mn-SOD expression were shown to be related to a reduction in mtDNA damage as well as to the release of mitochondrial cytochrome c (Cyt c). To the best of our knowledge, this might be the first study to explore the regional mitochondrial changes during IPC. The present findings are expected to help elucidate the molecular mechanism involved in IPC and helpful in the development of new clinical strategies against ischemic heart disease.

Erratum: Korean J Physiol Pharmacol 2006 Feb;10(1):19-24. Differential Functional Expression of Clotrimazole-sensitive Ca2+ -activated K+ Current in Bal-17 and WEHI-231 Murine B Lymphocytes

No abstract available.

Differential Functional Expression of Clotrimazole-sensitive Ca2+-activated K+ Current in Bal-17 and WEHI-231 Murine B Lymphocytes

The intermediate conductance Ca2+-activated K+ channels (SK4, IKCa1) are present in lymphocytes, and their membrane expression is upregulated by various immunological stimuli. In this study, the activity of SK4 was compared between Bal-17 and WEHI-231 cell lines which represent mature and immature stages of murine B lymphocytes, respectively. The whole-cell patch clamp with high-Ca2+ (0.8microM) KCl pipette solution revealed a voltage-independent K+ current that was blocked by clotrimazole (1 mM), an SK4 blocker. The expression of mRNAs for SK4 was confirmed in both Bal-17 and WEHI-231 cells. The density of clotrimazole-sensitive SK4 current was significantly larger in Bal-17 than WEHI-231 cells (-11.4+/-3.1 Vs. -5.7+/-1.15 pA/pF). Also, the chronic stimulation of B cell receptors (BCR) by BCR-ligation (anti-IgM Ab, 3microgram/ml, 8~12 h) significantly upregulated the amplitude of clotrimazole-sensitive current from -11.4+/-3.1 to -53.1+/-8.6 pA/pF in Bal-17 cells. In WEHI-231 cells, the effect of BCR-ligation was significantly small (-5.7+/-1.15 to -9.0+/-1.00 pA/pF). The differential expression and regulation by BCR-ligation might reflect functional changes in the maturation of B lymphocytes.

Higher Expression of TRPM7 Channels in Murine Mature B Lymphocytes than Immature Cells

TRPM7, a cation channel protein permeable to various metal ions such as Mg2+, is ubiquitously expressed in variety of cells including lymphocytes. The activity of TRPM7 is tightly regulated by intracellular Mg2+, thus named Mg2+-inhibited cation (MIC) current, and its expression is known to be critical for the viability and proliferation of B lymphocytes. In this study, the level of MIC current was compared between immature (WEHI-231) and mature (Bal-17) B lymphocytes. In both cell types, an intracellular dialysis with Mg2+-free solution (140 mM CsCl) induced an outwardly-rectifying MIC current. The peak amplitude of MIC current and the permeability to divalent cation (Mn2+) were several fold higher in Bal-17 than WEHI-231. Also, the level of mRNAs for TRPM7, a molecular correspondence of the MIC channel, was significantly higher in Bal-17 cells. The amplitude of MIC was further increased, and the relation between current and voltage became linear under divalent cation-free conditions, demonstrating typical properties of the TRPM7. The stimulation of B cell receptors (BCR) by ligation with antibodies did not change the amplitude of MIC current. Also, increase of extracellular [Mg2+]c to enhance the Mg2+ influx did not affect the BCR ligation-induced death of WEHI-231 cells. Although the level of TRPM7 was not directly related with the cell death of immature B cells, the remarkable difference of TRPM7 might indicate a fundamental change in the permeability to divalent cations during the development of B cells.

Anesthetic Management of Emergent Cesarean Section of a Patient with a Latex-Induced Allergic Reaction: A case report / 대한마취과학회지

Since the first report appeared in 1979, the incidence of potentially life threatening allergic reactions to latex has increased. We performed Cesarean section on a 28 yr old women who showed a severe latex allergic reaction that induced fetal distress. In the 39 th week of pregnancy, delivery was induced with oxytocin and a vaginal examination was performed using latex gloves. Chest tightness, dyspnea, urticaria, maternal hypotension (78/50 mmHg) and fetal bradycardia (40-90 beats/min) appeared suddenly 10 min after the vaginal examination. In addition to the subcutaneous injection of 0.3 mg epinephrine, diphenhydramine 45.5 mg and dexamethasone 4 mg was administered intravenously. Anesthesia was induced with thiopental and succinycholine, and maintained with isoflurane and epidural lidocaine. After operation, no additional problems were evident, except an itching sense. Potentially life threatening allergic reactions to latex should be considered in those with a high risk of latex allergy, and efforts should be made to provide this group with a latex-free environment.

Gluteal Compartment Syndrome: A Case Report / 대한정형외과학회잡지

A 33-year-old female visited to our hospital complaining of severe painful swelling in her right buttock. Ten hours previously, she had fallen down stairs. Motor power of her ankle and foot were zero to trace and the intracompartment pressure of the gluteal region was 50 mmHg. MRI showed diffuse intramuscular edema of right gluteal muscle. Emergency fasciotomy of the gluteal compartment was per-formed and her neurologic signs gradually improved at a postoperative 24 hours. She recovered completely at postoperative 14 days without further sequelae.

Effects of Aprotinin on Acute Lung Injury by Endotoxin in Rabbits / 대한마취과학회지

BACKGROUND: Aprotinin, a serine protease inhibitor, has an anti-inflammatory and hemostatic effect and has been used to reduce perioperative blood loss and lung injury after cardiopulmonary bypass in cardiac surgery. Acute respiratory distress syndrome (ARDS), which results in clinical manifestations due to non-cardiogenic permeability edema is a fatal condition associated with a mortality rate of 50 to 80%. The purpose of this study was to evaluate the effects of aprotinin on acute lung injury induced by bacterial endotoxin in rabbits. METHODS: Nineteen rabbits were anesthetized with intravenous xylazine, Ketamine and vecuronium and ventilated with a Harvard apparatus maintaining normocapnea. In 7 rabbits, 2 mg/Kg of lipopolysaccharide from E. coli was infused intravenously for 30 min (Toxin group) and in another 7 rabbits aprotonin loading with 200,000 KIU/Kg followed by a continuous infusion of 50,000 KIU/Kg/hr was performed 30 min before the endotoxin infusion throughout the experiment (Aprotinin group). At 1, 2, 3, and 4 hours after endotoxin infusion, arterial blood gas, blood cell count, prothrombin time, activated partial thromboplastin time, fibrinogen, and hemodynamic profiles were checKed. At four hours, the animals were dissected at which time the lungs were divided into three regions for wet/dry weight ratio (WW/DW), myeloperoxidase activity and microscopic examination. RESULTS: In the Aprotinin group, pulmonary vascular resistance, arterial oxygen partial pressure and coagulation function were well preserved compared with the Toxin group. Furthermore, lung WW/DW, myeloperoxidase activity, and inflammatory responses also increased less in the Aprotinin group. CONCLUSIONS: The results of the current data showed that aprotinin has prophylactic effects against acute lung injury and coagulation impairment induced by bacterial endotoxin in rabbits.

The Method to Increase the Ratio of Location of a Catheter in the Superior Vena Cava by Subclavian Cannulation / 대한마취과학회지

BACKGROUND: Subclavian cannulation is useful for the patients who need long-term maintenance of central venous catheters, but the inadequate location of catheters produces some complications. In pediatric populations, the abnormal placement of subclavian catheters in the internal jugular vein (IJV) is frequent because the angle formed by the subclavian vein and IJV is much larger than in adults. We would therefore propose a technique which will increase the location ratio of subclavian catheters in the superior vena cava (SVC). METHODS: One hundred twenty three patients who received elective or emergent operations were divided into 4 groups which consisted of the 'neck rotation away from the cannulation site' group (RA), 'neck rotation toward the cannulation site' group (RT), 'neck tilt away from the cannulation site' group (TA), 'neck tilt toward the cannulation site' group (TT). We cannulated each group and verified the location of the catheter tip in chest PA for each group. RESULTS: The calculation for the ratio of SVC location to the total cannulation of each group (%SVC) was done and the X2 test was done. Total %SVC was 73.2% and %SVC of each group were 64.9% for the RA group, 77.3% for the RT group, 61.8% for the TA group, and 93.3% for the TT group. A considerable difference was found for total %SVC in the X2 test. The location ratio of the TT group was higher than the others and there was no difference found between the RA, RT, TA groups. CONCLUSIONS: We can conclude that tilting the neck toward the cannulation site would produce a higher ratio of SVC location of the subclavian catheter than other neck positions.

The Ventilatory Effect of Hybrid Ventilation in Rabbits

PURPOSE: Intratracheal pulmonary ventilation (ITPV) is developed to decrease dead space ventilation. A reverse thrust catheter (RTC) is introduced into an endotracheal tube through an adapter. Bias gas through the RTC exits from the catheter tip. The flow of gas is redirected outward away from the lung. Gas is intermittently introduced into the lung as tidal volume (VT) by an expiratory valve. ITPV can be combined with pressure control mode, resulting in hybrid ventilation (HV). We hypothesized that HV might decrease VT, compared with volume controlled ventilation (VCV) or pressure controlled ventilation (PCV) alone. METHODS: HV was compared with VCV and PCV in 7 tracheostomized rabbits. We aimed at maintaining PaCO2 levels normal as the respiratory rates (RR) were set at 20, 40, 80, and 120/min. Blood pressure and airway pressures were monitored and dead space ratio was calculated. RESULTS: The dead spaces (VD) of VCV are 30+/-4 mL, 18+/-4 mL, 14+/-4 mL, and 12+/-5 mL and the VD of PCV are 24+/-6 mL, 16+/-3 mL, 15+/-4 mL and 12+/-4 mL at the respiratory rates of 20/min, 40/min, 80/min, and 120/min, respectively. The VD of HV are 13+/-6 mL, 9+/-3 mL, 7+/-2 mL, and 5+/-1 mL, respectively. The VT and PIP of HV are significantly lower than those of VCV and PCV at the same RR. CONCLUSION: It can be concluded that HV can be applied to minimize the airway pressures and dead space ventilation of VCV and PCV.