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Biomedical subjects

S Furukawa

Publications and source records attributed to S Furukawa.

At least 163 records · Page 9Linked to original sources

Growth hormone/insulin-like growth factor 1 axis alterations contribute to disturbed protein metabolism in cirrhosis patients after hepatectomy.

BACKGROUND/AIM: Liver cirrhosis is accompanied by a fall in whole-body protein turnover and alterations of the growth hormone (GH)/insulin-like growth factor 1 (IGF-1) axis. However, the influence of liver cirrhosis on the GH/IGF-1 axis in the perioperative period, and the contribution of the GH/IGF-1 axis alteration in cirrhosis to postoperative nitrogen metabolism are not known. METHODS: Plasma GH, IGF-1 and IGF binding protein 3 (IGF-BP3) levels were measured sequentially in patients undergoing hepatectomy with or without cirrhosis. Postoperative nitrogen excretion and whole-body protein turnover rate were also determined. RESULTS: Preoperative plasma IGF-1 level showed a negative correlation with indocyanine green retention rate. Cirrhosis patients undergoing hepatectomy had low IGF-1 and IGF-BP3 levels, despite extremely high GH levels in the perioperative period. Perioperative IGF-1 levels were lower in patients with postoperative complications than in those without complications. Postoperative nitrogen excretion was higher and whole-body protein turnover rate was lower in patients with cirrhosis than in those without cirrhosis. The post-operative IGF-1 level showed a positive correlation with whole-body protein turnover rate. CONCLUSIONS: Postoperative hepatic IGF-1 production may be severely disturbed in patients with cirrhosis, and the impaired IGF-1 production contributes to the suppressed postoperative protein metabolism in cirrhosis. It may be appropriate to increase plasma IGF-1 level in patients with cirrhosis to enhance postoperative protein metabolism and improve the postoperative outcome.

Aged↗

cDNA cloning and gene expression of cecropin D, an antibacterial protein in the silkworm, Bombyx mori.

We have isolated a cDNA clone encoding a cecropin D precursor from the fat body of Bombyx mori larvae immunized with bacteria by means of differential display. The cDNA contains 298 bp with a coding region of 183 bp for 61 amino acids plus a termination codon (TAG), a 5'-untranslated region of 36 bp, and a 3'-untranslated region of 79 bp including the poly(A) tail. There is a polyadenylation signal sequence of AATAAA at position 266, 43 nucleotides downstream from the termination codon TAG. The homology of the deduced amino acids is greater to the cecropin D precursor from Hyalophora cecropia (67% identity) than to the precursors of cecropins A and B from B. mori (49% to both). Northern blotting analyses reveal that the gene expression of cecropin D is detectable by 4 h after the bacterial injection and reaches the maximal level at 24 h. That high level is maintained up to 48 h post-immunization. Additionally, the gene is expressed mainly in the fat body and slightly in hemocytes, but it is undetectable in other tissues such as the midgut, the Malpighian tubule and silk gland.

Amino Acid Sequence↗

Prophylactic treatment with growth hormone and insulin-like growth factor I improve systemic bacterial clearance and survival in a murine model of burn-induced gut-derived sepsis.

The purpose of this investigation was to evaluate the effects of GH and IGF-I administration in a murine model of burn-induced gut-derived sepsis. BALB/C mice were treated with 4.8 mg/kg/day of GH, 24 mg/kg/day of IGF-I or saline for 4 days. They were then administered 10(10) E. coli by gavage and subjected to 20% full thickness flame burn. All mice received allogeneic blood transfusion 5 days before burn injury to induce mild immunosuppression. Seventy-three mice were observed for survival and 51 mice were sacrificed at 4 and 20 h postburn. Blood, mesenteric lymph nodes (MLN), spleen and liver were harvested aseptically, and viable bacterial counts in the organs were determined. The small intestine was harvested for the evaluation of villus height and mitoses in the crypts. GH and IGF-I groups showed a significantly better survival than the control group. GH and IGF-I groups had significantly greater villus height and mitoses/crypt than the control group. Translocation of bacteria was not significantly different among groups, however, the relation between the numbers of viable bacteria in MLN and blood suggests that both GH and IGF-I reduced systemic spread of translocated bacteria. It is concluded that GH and IGF-I had positive effects on outcome in this model of burn-induced gut-derived sepsis. It appears that GH and IGF-I may have immune-enhancing effects and that administration of these agents may be useful for burn injury.

Animals↗

Endogenous neurotrophin-3 is retrogradely transported in the rat sciatic nerve.

To address the active transport of neurotrophins, nerve growth factor, brain-derived neurotrophic factor, and neurotrophin-3 in the peripheral nerves, we examined the levels of proteins and messenger RNAs in the sciatic nerve of adult rats following transection, using enzyme immunoassays and reverse transcription polymerase chain reaction method, respectively. Neurotrophin-3 protein increased one day after transection only in the distal segment next to the transection site and returned to the original level two days later. This was considered to reflect accumulation of neurotrophin-3 transported from the periphery toward the neuronal cell bodies, because the neurotrophin-3 messenger RNA level was not changed in any sciatic segments during this experimental period. An increase in brain-derived neurotrophic factor protein was observed simultaneously in both the distal and proximal stumps three days after transection. Brain-derived neurotrophic factor messenger RNA was elevated in the same stumps two days after transection, suggesting that brain-derived neurotrophic factor was produced within the transected stumps. These observations demonstrate that neurotrophin-3, like nerve growth factor, is retrogradely transported in the sciatic nerve but that brain-derived neurotrophic factor is not. This suggests that neurotrophin-3 plays a role in the conveyance of trophic signals from target organs to neurons.

Animals↗

Intravenous immunoglobulin therapy in acute disseminated encephalomyelitis.

Three children ranging in age from 2 to 5 years with acute disseminated encephalomyelitis (ADEM) were successfully treated with high-dose intravenous immunoglobulin (IVIG). Their symptoms were somnolence, fever, headache, vomiting, and resting tremor. In all of these patients, it was difficult to distinguish the condition from viral encephalitis before analyzing the myelin basic protein. ADEM was diagnosed because of increased levels of myelin basic protein in their cerebrospinal fluid and abnormal high-signal intensity on T2-weighted magnetic resonance imaging. All patients were given IVIG at a dose of 400 mg/kg/day for 5 consecutive days. The patients rapidly regained consciousness in 14 hours, 2 days, and 4 days and demonstrated a complete clinical improvement within 18 days, 10 days, and 7 days of the initiation of the treatment, respectively. IVIG may prove useful as an alternative treatment to corticosteroids for ADEM.

Child, Preschool↗

Enteral administration of glutamine in purulent peritonitis.

The intestinal hypomotility associated with purulent peritonitis is generally regarded as a contraindication to enteral nutrition. However, enteral nutrition may be feasible in suppurative peritonitis if administered with great caution, i.e., assuring the appropriate amount, delivery speed, and osmolality of the enteral formulation. Glutamine (Gln) increases muscle protein synthesis and decreases muscle protein degradation in sepsis, regardless of the route of administration. Therefore, administering small amounts of supplemental Gln via the enteral route to peritonitis patients may be beneficial. Two purulent peritonitis patients received L-Gln through a jejunostomy tube. The average amount of supplemental Gln was 16 g/d. Systemic inflammatory responses, i.e., high temperature and a high serum C-reactive protein level, persisted throughout the treatment period. Femoral arterial and venous blood samples were drawn simultaneously for determination of amino acid levels before and after 7 d of Gln supplementation. Enterally administered Gln was well-tolerated by both patients. There was an increase in plasma Gln levels after Gln supplementation. Moreover, the release of Gln, alanine, and phenylalanine from the lower extremities was lower after as compared to before Gln supplementation. Enteral administration of Gln may be feasible even in purulent peritonitis.

Amino Acids↗

Nerve growth factor release with mast-cell-derived mediators in a patient with systemic mastocytosis after middle-wave ultraviolet irradiation.

BACKGROUND: The symptoms of a 56-year-old man with systemic mastocytosis became worse with exposure to sunlight. We evaluated mast-cell-derived mediators and cytokines before and after exposure to ultraviolet light in the patient. METHODS: The patient was irradiated with middle-wave ultraviolet light, so-called ultraviolet light B, and the levels of mediators and cytokines were measured serially. The point mutation Asp816Val in c-kit was investigated by analyzing polymerase chain reaction products from the complementary DNA of peripheral blood mononuclear cells. RESULTS: Before irradiation, the levels of mast-cell-derived mediators and metabolites were elevated. Among various cytokines measured, including soluble c-kit and stem cell factor, only the level of nerve growth factor was elevated. After irradiation, the nerve growth factor level was further increased along with the levels of mast-cell-derived mediators and metabolites. The point mutation Asp816Val in c-kit was not detected in peripheral blood mononuclear cells. CONCLUSIONS: Middle-wave ultraviolet light may activate mast cells to release nerve growth factor and mediators in systemic mastocytosis.

Cytokines↗

Decreased interferon-gamma (IFN-gamma)-producing T cells in patients with acute Kawasaki disease.

Kawasaki disease (KD) is an acute febrile illness of early childhood, in which the activation of monocytes/macrophages plays a central role in the development of vasculitis during the acute stage of disease. In this study we investigated peripheral blood T cells of 10 patients with KD, focusing on the Th1 and Th2 imbalance, using intracellular cytokine staining and analysis of the cytokine-producing T cells by flow cytometry. We observed a decrease in the numbers of IFN-gamma-producing, but not IL-4-producing, CD3+ T cells, during the acute stage. Our results suggest that there is an imbalance of Th1 and Th2 subsets during the acute stage of KD.

CD3 Complex↗

Induction of gene expression of antibacterial proteins by chitin oligomers in the silkworm, Bombyx mori.

Activation of antibacterial protein genes by various chitin oligomers (from dimer to hexamer) was investigated by Northern blot analysis using cDNAs encoding cecropin B, attacin and lebocin from Bombyx mori as probes. All chitin oligomers tested were found to strongly trigger expression of cecropin B, attacin and lebocin genes. Furthermore, gene expression triggered by chitin oligomers was confirmed to occur specifically in the fat body and haemocytes. These results suggest that chitin oligomers have the same characteristics as those of lipopolysaccharide (LPS) and peptidoglycan in triggering gene expression of insect antibacterial proteins.

Animals↗

[A new exanthematous disease in newborn infants caused by exotoxins producing Staphylococcus aureus; exotoxins production of the isolates and serum levels of antitoxin antibody in the patients and umbilical cord blood].

Recently, in Japan newly neonatal exanthematous disease was elucidated to be caused by staphyloccocal supcrantigcnic exotoxins, mainly TSST-1. We studied exotoxins producibility of 43 strains of S. aureus isolated from neonates with exanthematous disease and examined antibody titers to staphylococcal enterotoxin A, B, C (SEA, SEB, SEC) and toxic shock syndrome toxin 1 (TSST-1) of the patients and control (umbilical cord blood from term infants). The results were as follows 1.34 of 43 strains (79%) isolated from the patients were SEC and TSST-1 producing MRSA, 5 strains (12%) were SEB, SEC, and TSST-1 producing MRSA, 1 strain (2%) was SEB and TSST-1 producing MRSA, 2 strains (12%) were SEB producing MSSA and did not produce TSST-1. The 1 strain (2%) was MSSA which produced SEC and TSST-1. 2. 16 neonates with exanthematous disease, who showed typical clinical signs and laboratry findings of thrombocytopenia, with SEC and TSST-1 producing MRSA isolates had significantly low anti-TSST-1 antibody titers at onset (p < 0.05), compared with the control (umbilical cord blood from term infants): TSST-1 appeared to the causative agent for the disease. In two neonates with exanthematous disease, with SEB- and non- TSST-1-producing MSSA isolates, anti-SEB antibody titers were low at onset, so SEB appeared to the causative agent for the disease. 3. In Japan, low anti-TSST-1 antibody titers were found in the umbilical blood samples from about 70% of term infants; and low anti-SEB or anti-SEC antibody titers were found in samples from only about 10% of them, that is, a number of term infants had anti-SEB and anti-SEC antibodies. The majority of S. aureus isolated from neonates with exanthematous disease were enterotoxin- and TSST-1-producing MRSAs. The results of our study by measuring antitoxin antibody titers suggested that SEB and SEC might not be pathogenically responsible, but TSST-1 was considered to be responsible for the majority of exanthematous disease. Prevalence of TSST-1-producing MRSA in the neonatal and premature baby ward is the main cause for the high incidence of this disease in Japan, whereas the low antibody titer to TSST-1 in the mother, in comparison with the anti-enterotoxin antibody titers, may also be a predisposing factor.

Antibodies, Bacterial↗

Lymphotoxin inhibits Chlamydia pneumoniae growth in HEp-2 cells.

Cytokines such as gamma interferon and tumor necrosis factor alpha (TNF-alpha) inhibit the intracellular replication of Chlamydia pneumoniae or Chlamydia trachomatis. In this study, we found that another cytokine, lymphotoxin (TNF-beta), restricts the growth of C. pneumoniae in HEp-2 cells. When lymphotoxin (10 U/ml) was added during incubation from 8 to 16 h postinoculation, inclusion body formation was severely reduced. In addition, we observed activation of nitric oxide production and the nuclear transition of NF-kappaB in HEp-2 cells in response to lymphotoxin. These results suggest that inhibition of chlamydial growth by lymphotoxin is mediated, at least in part, by nuclear transition of NF-kappaB, resulting in induction of nitric oxide synthase to produce nitric oxide, a potent bacteristatic agent. This is the first report on antichlamydial activity of lymphotoxin through induction of nitric oxide.

Animals↗

Sodium/calcium exchange contributes to contraction and relaxation in failed human ventricular myocytes.

Defects in myocyte contraction and relaxation are key features of human heart failure. Sodium/calcium exchanger-mediated contribution to contraction and relaxation were separated from other mechanisms [L-type calcium current, sarco(endo)plasmic reticulum (SR) Ca(2+)-ATPase] based on voltage, temperature, and selective blockers. Rod-shaped left ventricular myocytes were isolated from failed human explants (n = 29) via perfusion with collagenase-containing Krebs solution. Action potentials using perforated patch and contractions using an edge detector were recorded at 0.5-1.5 Hz in Tyrode solution at 25 degrees C and 37 degrees C. Contraction duration was dependent on action potential (AP) duration at 37 degrees C but not at 25 degrees C, suggesting the role of the exchanger in relaxation and linking myocyte relaxation to the repolarization phase of the AP. Voltage-clamp experiments from -50 to +10 mV for 1,500 ms in Tyrode or Na(+)- and K(+)-free solutions after conditioning pulses triggered biphasic contractions that included a rapid SR-mediated component and a slower voltage-dependent exchanger-mediated component. We used thapsigargin to block the SR, which eliminated the rapid component, and we used an exchanger blocker, Kanebo 7943, which eliminated the slow component. The exchanger was shown to contribute to contraction through reverse-mode exchange, as well as to play a key role in relaxation of human ventricular myocytes.

Action Potentials↗

Effect of lung volume reduction surgery on diaphragm length in severe chronic obstructive pulmonary disease.

Lung volume reduction surgery (LVRS) has been suggested as improving respiratory mechanics in patients with severe chronic obstructive pulmonary disease (COPD). We hypothesized that LVRS might lengthen the diaphragm, increase its area of apposition with the chest wall, and thereby improve its mechanical function. To determine the effect of bilateral LVRS on diaphragm length, we measured diaphragm length at TLC, using plain chest roentgenograms (CXRs), in 25 patients (11 males and 14 females) before LVRS and 3 to 6 mo after LVRS. A subgroup of seven patients (reference data) also had diaphragm length measurements made with CXRs, using films made within a year before their presurgical evaluation. Right hemidiaphragm silhouette length (PADL) and the length of the most vertically oriented portion of the right hemidiaphragm muscle (VDML) were measured. Diaphragm dome height was determined from the: (1) distance between the dome and transverse diameter at the manubrium; and (2) highest point of the dome referenced horizontally to the vertebral column. Patients also underwent spirometry, measurements of lung volumes and diffusion capacity, an incremental symptom-limited maximum exercise test, and measurements of 6 min walk distance (6MWD) and transdiaphragmatic pressures during maximum static inspiratory efforts (Pdimax sniff) and bilateral supramaximal electrophrenic twitch stimulation (Pditwitch) both before and 3 mo after LVRS. Patients were 58 +/- 8 yr of age, with severe COPD and hyperinflation (FEV1 = 0.68 +/- 0.23 L, FVC = 2.56 +/- 7.3 L, and TLC = 143 +/- 22% predicted). Following LVRS, PADL increased by 4% (from 13.9 +/- 1.9 cm to 14.5 +/- 1.7 cm; p = 0.02), VDML increased by 44% (from 2.08 +/- 1.5 cm to 3.00 +/- 1.6 cm, p = 0.01), and diaphragm dome height increased by more than 10%. In contrast, diaphragm lengths were similar in subjects with CXRs made before LVRS and within 1 yr before evaluation. The increase in diaphragm length correlated directly with postoperative reductions in TLC and RV, and also with increases in transdiaphragmatic pressure with maximal sniff (Pdimax sniff), maximal oxygen consumption (V O2max), maximal minute ventilation (V Emax), and maximum voluntary ventilation following LVRS. We conclude that LVRS leads to a significant increase in diaphragm length, especially in the area of apposition of the diaphragm with the rib cage. Diaphragm lengthening after LVRS is most likely the result of a reduction in lung volume. Increases in diaphragm length after LVRS correlate with postoperative improvements in diaphragm strength, exercise capacity, and maximum voluntary ventilation.

Diaphragm↗

Relationship between resting hypercapnia and physiologic parameters before and after lung volume reduction surgery in severe chronic obstructive pulmonary disease.

Patients with severe chronic obstructive pulmonary disease (COPD) have varying degrees of hypercapnia. Recent studies have demonstrated inconsistent effects of lung volume reduction surgery (LVRS) on PaCO2; however, most series have excluded patients with moderate to severe hypercapnia. In addition, no study has examined the mechanisms responsible for the reduction in PaCO2 post-LVRS. We obtained spirometry, body plethysmography, diffusion capacity, respiratory muscle strength, 6-min walk test, and incremental symptom-limited maximal exercise data in 33 consecutive patients pre- and 3 to 6 mo post-LVRS, and explored the relationship between changes in PaCO2 and changes in the measured physiologic variables. All patients underwent bilateral LVRS via median sternotomy and stapling resection by the same cardiothoracic surgeon. Patients were 57 +/- 8 yr of age with severe COPD, hyperinflation, and air trapping (FEV1, 0.73 +/- 0.2 L; TLC, 7.3 +/- 1.6 L; residual volume [RV], 4.8 +/- 1.4 L), and moderate resting hypercapnia (PaCO2, 44 +/- 7 mm Hg; range, 32 to 56 mm Hg). Post-LVRS, PaCO2 decreased by 4% (PaCO2 pre 44 +/- 7 mm Hg, PaCO2 post 42 +/- 5 mm Hg; p = 0.003). Patients with higher baseline values of PaCO2 had the greatest reduction in PaCO2 post-LVRS (r = -0.61, p < 0.001). Significant correlations existed between reduction in PaCO2 and changes in FEV1 (r = -0.56; p = 0.0007), maximal inspiratory pressure (PImax) (r = -0.46; p = 0.009), diffusing capacity of the lungs for carbon monoxide (DLCO) (r = -0.47; p = 0.008), and RV/TLC (r = 0.41; p = 0. 02). Correlation existed also between reduction in PaCO2 and breathing pattern at maximal exercise: maximal minute ventilation (V Emax) (r = -0.47; p = 0.009), and tidal volume (VT) (r = -0.40; p = 0.02). The changes in PaCO2 post-LVRS showed marked intersubject variability. We conclude that LVRS, by reducing hyperinflation, air trapping, and improving respiratory muscle function, enables the lung and chest wall to act more effectively as a pump, thereby increasing alveolar ventilation and reducing baseline resting PaCO2. In addition, patients with higher baseline levels of PaCO2 demonstrate the greatest reduction in PaCO2 post-LVRS, and should not be excluded from receiving LVRS.

Aged↗

Prospective randomized trial comparing bilateral lung volume reduction surgery to pulmonary rehabilitation in severe chronic obstructive pulmonary disease.

Several uncontrolled studies report improvement in lung function, gas exchange, and exercise capacity after bilateral lung volume reduction surgery (LVRS). We recruited 200 patients with severe chronic obstructive pulmonary disease (COPD) for a prospective randomized trial of pulmonary rehabilitation versus bilateral LVRS with stapling resection of 20 to 40% of each lung. Pulmonary function tests, gas exchange, 6-min walk distance, and symptom-limited maximal exercise testing were done in all patients at baseline and after 8 wk of rehabilitation. Patients were then randomized to either 3 additional months of rehabilitation or LVRS. Thirty-seven patients met study criteria and were enrolled into the trial. Eighteen patients were in the medical arm; 15 of 18 patients completed 3 mo of additional pulmonary rehabilitation. Thirty-two patients underwent LVRS (19 in the surgical arm, 13 crossover from the medical arm). After 8 wk of pulmonary rehabilitation, pulmonary function tests remained unchanged compared with baseline data. However, there was a trend toward a higher 6-min walk distance (285 +/- 96 versus 269 +/- 91 m, p = 0.14) and total exercise time on maximal exercise test was significantly longer compared with baseline values (7.4 +/- 2.1 versus 5.8 +/- 1.7 min, p < 0.001). In 15 patients who completed 3 mo of additional rehabilitation, there was a trend to a higher maximal oxygen consumption (V O(2)max) (13.3 +/- 3.0 versus 12.6 +/- 3.3, p < 0.08). In contrast, at 3 mo post-LVRS, FVC (2.79 +/- 0.59 versus 2.36 +/- 0.55 L, p < 0.001) and FEV(1) (0.85 +/- 0.3 versus 0.65 +/- 0.16 L, p < 0.005) increased whereas TLC (6.53 +/- 1.3 versus 7.65 +/- 2.1 L, p < 0.001) and residual volume (RV) (3.7 +/- 1.2 versus 4.9 +/- 1.1 L, p < 0.001) decreased when compared with 8 wk postrehabilitation data. In addition, Pa(CO(2)) decreased significantly 3 mo post-LVRS compared with 8 wk postrehabilitation. Six-minute walk distance (6MWD), total exercise time, and V O(2)max were higher after LVRS but did not reach statistical significance. However, when 13 patients who crossed over from the medical to the surgical arm were included in the analysis, the increases in 6MWD (337 +/- 99 versus 282 +/- 100 m, p < 0.001) and V O(2)max (13.8 +/- 4 versus 12.0 +/- 3 ml/kg/min, p < 0.01) 3 mo post-LVRS were highly significant when compared with postrehabilitation data. The Sickness Impact Profile (SIP), a generalized measure of quality of life (QOL), was significantly improved after 8 wk of rehabilitation and was maintained after 3 mo of additional rehabilitation. A further improvement in QOL was observed 3 mo after LVRS compared with the initial improvement gained after 8 wk of rehabilitation. There were 3 (9.4%) postoperative deaths, and one patient died before surgery (2.7%). We conclude that bilateral LVRS, in addition to pulmonary rehabilitation, improves static lung function, gas exchange, and QOL compared with pulmonary rehabilitation alone. Further studies need to evaluate the risks, benefits, and durability of LVRS over time.

Combined Modality Therapy↗

Spontaneous pinealoma in a male Crj:CD (SD) IGS rat.

A pinealoma (benign) was found in a 61-week-old male Crj:CD (SD) IGS rat. The neoplasm was located between the cerebral hemispheres and the cerebellum. Histologically, the tumor cells consisted of two cell types: large, pale-staining cells and small dark-staining cells. A fibrovascular stroma divided the tumor cells into incomplete lobules or nest structures. Relatively numerous mitoses were noted in the tumor cells. Ultrastructurally, the tumor cells contained dense-cored vesicles, approximately 120 nm in diameter.

Animals↗

Improvements in lung function, exercise, and quality of life in hypercapnic COPD patients after lung volume reduction surgery.

STUDY OBJECTIVE: To determine the impact of preoperative resting hypercapnia on patient outcome after bilateral lung volume reduction surgery (LVRS). METHODS: We prospectively examined morbidity, mortality, quality of life (QOL), and physiologic outcome, including spirometry, gas exchange, and exercise performance in 15 patients with severe emphysema and a resting PaCO2 of > 45 mm Hg (group 1), and compared the results with those from 31 patients with a PaCO2 of < 45 mm Hg (group 2). RESULTS: All preoperative physiologic and QOL indices were more impaired in the hypercapnic patients than in the eucapnic patients. The hypercapnic patients exhibited a lower preoperative FEV1, a lower diffusing capacity of the lung for carbon monoxide, a lower ratio of PaO2 to the fraction of inspired oxygen, a lower 6-min walk distance, and higher oxygen requirements. However, after surgery both groups exhibited improvements in FVC (group 1, p < 0.01; group 2, p < 0.001), FEV1 (group 1, p=0.04; group 2, p < 0.001), total lung capacity (TLC; group 1, p=0.02; group 2, p < 0.001), residual volume (RV; group 1, p=0.002; group 2, p < 0.001), RV/TLC ratio (group 1, p=0.03; group 2, p < 0.001), PaCO2 (group 1, p=0.002; group 2, p=0.02), 6-min walk distance (group 1, p=0.005; group 2, p < 0.001), oxygen consumption at peak exercise (group 1, p=0.02; group 2, p=0.02), total exercise time (group 1, p=0.02; group 2, p=0.02), and the perceived overall QOL scores (group 1, p=0.001; group 2, p < 0.001). However, because the magnitude of improvement was similar in both groups, and the hypercapnic group was more impaired, the spirometry, lung volumes, and 6-min walk distance remained significantly lower post-LVRS in the hypercapnic patients. There was no difference in mortality between the groups (p=0.9). CONCLUSIONS: Patients with moderate to severe resting hypercapnia exhibit significant improvements in spirometry, gas exchange, perceived QOL, and exercise performance after bilateral LVRS. The maximal achievable improvements in postoperative lung function are related to preoperative level of function; however, the magnitude of improvement can be expected to be similar to patients with lower resting PaCO2 levels. Patients should not be excluded from LVRS based solely on the presence of resting hypercapnia. The long-term benefit of LVRS in hypercapnic patient remains to be determined.

Aged↗