Heated humidified high-flow nasal oxygen prevents intraoperative body temperature decrease in non-intubated thoracoscopy.

PURPOSE: In patients receiving non-intubated video-assisted thoracic surgery (NIVATS), transnasal humidified rapid-insufflation ventilatory exchange (THRIVE) has been applied instead of oxygen mask for better oxygenation. However, the THRIVE effects on intraoperative temperature decrease have not been investigated. METHODS: Pre- and postoperative temperatures, measured by an infrared tympanic ear thermometer, taken before sending patients to the operation room and immediately upon their arrival in the postoperative anesthesia unit, were collected from medical records of patients who received NIVATS either with oxygen mask or THRIVE. Intraoperative temperature decrease, calculated by preoperative temperature minus postoperative temperature, was compared between different groups. Multiple linear regression analysis was performed to determine factors associated with intraoperative temperature decrease. RESULTS: Records of 256 adult patients with forced-air warming were retrospectively analyzed. 172 patients of them received THRIVE and 84 patients received oxygen mask. Preoperative temperatures were comparable between groups (THRIVE: 36.25 ± 0.46 °C; mask: 36.30 ± 0.39 °C, p = 0.43). Postoperative temperatures were significantly higher in patients using THRIVE than those using oxygen masks (36.05 ± 0.59 vs 35.87 ± 0.62 °C, p = 0.025). Significantly less intraoperative temperature decrease was shown in THRIVE group (THRIVE: 0.20 ± 0.69 °C; mask: 0.43 ± 0.69 °C, p = 0.04). According to the multiple linear regression analysis, significant temperature decrease was associated with the advanced age (ßage = 0.01) but not the anesthetic duration. Using THRIVE was correlated with significantly less body temperature decrease (ßTRIVE = - 0.24). CONCLUSIONS: THRIVE effectively prevents intraoperative temperature decrease during NIVATS, especially in old patients.

Ovalbumin sensitizes vagal pulmonary C-fiber afferents in Brown Norway rats.

Sensitization of vagal lung C fibers has been postulated to contribute to the development of asthma, but support for this notion is still lacking. We investigated the characteristics and function of pulmonary C fibers (PCFs) in ovalbumin (OVA)-sensitized Brown Norway rats, an established animal model of asthma. Rats were sensitized with intraperitoneal injection of OVA or were treated with saline (control). In study 1, with the use of open-chest and artificially ventilated rats, inhalation of 5% OVA aerosol evoked an augmented increase in total lung resistance in the OVA-sensitized rats, compared with the control rats. Bilateral vagotomy or subcutaneous pretreatment with a high-dose of capsaicin for blocking of C-fiber function equally attenuated this augmented total lung resistance response, suggesting the involvement of PCFs. In study 2, with the use of anesthetized, spontaneously breathing rats, right atrial injection of capsaicin (1 microg/kg; a PCF stimulant) evoked an augmented apneic response in the OVA-sensitized rats, compared with the control rats. In study 3, with the use of open-chest, paralyzed, and artificially ventilated rats, the afferent PCF responses to right atrial injection of capsaicin (0.5 and 1.0 microg/kg), phenylbiguanide (8 microg/kg; a PCF stimulant), or adenosine (0.2 mg/kg; a PCF stimulant) were enhanced in the OVA-sensitized rats, compared with the control rats. However, the baseline activities of PCFs and their afferent responses to mechanical stimulation by lung hyperinflation in the OVA-sensitized and control rats were comparable. Our results suggested that OVA-sensitized Brown Norway rats possess sensitized vagal PCFs, which may participate in the development of the airway hyperreactivity observed in these animals.

A frizzled homolog functions in a vertebrate Wnt signaling pathway.

BACKGROUND: Wnts are secreted proteins implicated in cell-cell interactions during embryogenesis and tumorigenesis, but receptors involved in transducing Wnt signals have not yet been definitively identified. Members of a large family of putative transmembrane receptors homologous to the frizzled protein in Drosophila have been identified recently in both vertebrates and invertebrates, raising the question of whether they are involved in transducing signals for any known signaling factors. RESULTS: To test the potential involvement of frizzled homologs in Wnt signaling, we examined the effects of overexpressing rat frizzled-1 (Rfz-1) on the subcellular distribution of Wnts and of dishevelled, a cytoplasmic component of the Wnt signalling pathway. We demonstrate that ectopic expression of Rfz-1 recruits the dishevelled proten-as well as Xenopus Wnt-8 (Xwnt-8), but not the functionally distinct Xwnt-5A-to the plasma membrane. Moreover, Rfz-1 is sufficient to induce the expression of two Xwnt-8-responsive genes, siamois and Xnr-3, in Xenopus explants in a manner which is antagonized by glycogen synthase kinase-3, which also antagonizes Wnt signaling. When Rfz-1 and Xwnt-8 are expressed together in this assay, we observe greater induction of these genes, indicating that Rfz-1 can synergize with a Wnt. CONCLUSIONS: The results demonstrate that a vertebrate frizzled homolog is involved in Wnt signaling in a manner which discriminates between functionally distinct Wnts, which involves translocation of the dishevelled protein to the plasma membrane, and which works in a synergistic manner with Wnts to induce gene expression. These data support the likely function of frizzled homologs as Wnt receptors, or as components of a receptor complex.

Glycosylation and surface expression of the influenza virus neuraminidase requires the N-terminal hydrophobic region.

A full-length double-stranded DNA copy of an influenza A virus N2 neuraminidase (NA) gene was cloned into the late region of pSV2330, a hybrid expression vector that includes pBR322 plasmid DNA sequences and the simian virus 40 early region and simian virus 40 late region promoters, splice sequences, and transcription termination sites. The protein encoded by the cloned wild-type NA gene was shown to be present in the cytoplasm of fixed cells and at the surface of "live" or unfixed cells by indirect immunofluorescence with N2 monoclonal antibodies. Immunoprecipitation and sodium dodecyl sulfate-polyacrylamide gel electrophoretic analysis of [35S]methionine-labeled proteins from wild-type vector-infected cells with heterospecific N2 antibody showed that the product of the cloned NA DNA comigrated with glycosylated NA from influenza virus-infected cells, remained associated with internal membranes of cells fractionated into membrane and cytoplasmic fractions, and could form an immunoprecipitable dimer. NA enzymatic activity was detectable after simian virus 40 lysis of vector-infected cells. These properties of the product of the cloned wild-type gene were compared with those of the polypeptides produced by three deletion mutant NA DNAs that were also cloned into the late region of the pSV2330 vector. These mutants lacked 7 (dlk), 21 (dlI), or all 23 amino acids (dlZ) of the amino (N)-terminal variable hydrophobic region that anchors the mature wild-type NA tetrameric structure in the infected cell or influenza viral membrane. Comparison of the phenotypes of these mutants showed that this region in the NA molecule also includes sequences that control translocation of the nascent polypeptide into membrane organelles for glycosylation.

Enhanced sympathetic outflow and decreased baroreflex sensitivity are associated with intermittent hypoxia-induced systemic hypertension in conscious rats.

Long-term exposure to intermittent hypoxia (IH), such as that occurring in association with sleep apnea, may result in systemic hypertension; however, the time course changes in arterial pressure, autonomic functions, and baroreflex sensitivity are still unclear. We investigated the changes in cardiovascular neural regulations during the development of chronic IH-induced hypertension in rats. Sprague-Dawley rats were exposed to repetitive 1.25-min cycles (30 s of N2+45 s of 21% O2) of IH or room air (RA) for 6 h/day during light phase (10 AM-4 PM) for 30 days. Arterial pressure was measured daily using the telemetry system during RA breathing. The mean arterial pressure (MAP) and interpulse interval (PPI) signals were then used to assess the autonomic functions and spontaneous baroreflex sensitivity by auto- and cross-spectral analysis, respectively. Stable MAP, low-frequency power of MAP (BLF), and low-frequency power (LF)-to-high frequency power (HF) ratio of PPI (LF/HF) were significantly higher in IH-exposed rats, compared with those of RA-exposed rats. Elevation of the MAP, BLF, LF/HF, and minute ventilation started 5 days after IH exposure and lasted until the end of the 30-day observation period. Additionally, IH-exposed rats had significant lower slope of MAP-PPI linear regression (under a successively descending and ascending) and magnitude of MAP-PPI transfer function (at frequency ranges of 0.06-0.6 Hz or 0.6-2.4 Hz) after IH exposure for 17 days. However, RA-exposed rats did not exhibit these changes. The results of this study indicate that chronic IH-induced hypertension is associated with a facilitation of cardiovascular sympathetic outflow and inhibition of baroreflex sensitivity in conscious rats.

Cone beam CT for determining breast cancer margin: an initial experience and its comparison with mammography and specimen radiograph.

PURPOSE: To assess the ability of cone beam CT (CBCT) in determining the breast cancer margin using, to compare the results with mammography and specimen radiography, and to explore the clinical potential of CBCT for breast imaging. METHODS: Specimens of 46 breast cancer patients were imaged by using a prototype CBCT system. Each patient underwent mammography, CBCT and X-ray of breast surgical specimen within 6 months. Images of mammography, breast surgical specimen radiography and CBCT were evaluated by an experienced radiologist. Indicators, such as: morphology, glitch, density, invasion, structural distortion and calcification, were observed. RESULT: There was no significant difference of the calcification, glitch and morphology among three methods. However, there was significant difference in indicators of breast tumor invasion among three methods. There was statistical significance in detecting invasions of breast cancer cells in peripheral tissues among three methods. CONCLUSION: CBCT shows no superiority over mammography and specimen radiography in determining tumor's outline and detecting calcification. On the other hand, CBCT demonstrates its advantage in determining the 3 dimensional position of a lesion which could be a potential clinical application in future practices of breast imaging.

Processing of dengue type 4 and other flavivirus nonstructural proteins.

Dengue type 4 (DEN4) and other flaviviruses employ host and viral proteases for polyprotein processing. Most proteolytic cleavages in the DEN4 nonstructural protein (NS) region are mediated by the viral NS2B-NS3 protease. The N-terminal third of NS3, containing sequences homologous to serine protease active sites, is the protease domain. To determine required sequences in NS2B, deletions were introduced into DEN4 NS2B-30% NS3 cDNA and the expressed polyproteins assayed for self-cleavage. A 40 amino acid segment within NS2B was essential. Sequence analysis of NS2B predicts that this segment constitutes a hydrophilic domain surrounded by hydrophobic regions. Hydrophobicity profiles of other flavivirus NS2Bs show similar patterns. Cleavage of DEN4 NS1-NS2A requires an octapeptide sequence at the NS1 C terminus and downstream NS2A. Comparison of the analogous octapeptide sequences among flaviviruses indicates a consensus cleavage sequence of (P8)/Met/Leu-Val-Xaa-Ser-Xaa-Val-Ala(P1), where Xaa are non-conserved amino acids. The effects on cleavage of amino acid substitutions in this consensus sequence were analyzed. Most substitutions of the conserved residues interfered with cleavage, whereas substitutions of non-conserved residues had little or no effect. These findings indicate that the responsible enzyme recognizes well-defined sequences at the cleavage site.

Reflex changes in breathing pattern evoked by inhalation of wood smoke in rats.

The acute ventilatory response to inhalation of wood smoke was studied in 58 anesthetized Sprague-Dawley rats. Wood smoke (approximately 6 ml) was inhaled spontaneously via a tracheal cannula. Within the first two breaths of smoke inhalation, either a slowing of respiration (SR) (n = 39) or an augmented inspiration (AI) (n = 19) was elicited consistently in each rat. The SR was primarily due to a prolongation of expiratory duration, whereas the AI was characterized by a two-step inspiratory flow leading to an exceedingly large tidal volume. Both initial responses, usually accompanied by bradycardia and hypotension, were reduced by inhaling smoke at a decreased concentration. After these initial responses, a delayed tachypnea developed and reached its peak 6-10 breaths after inhalation of smoke. Both the SR and AI were completely abolished by bilateral cervical vagotomy. In contrast, the delayed tachypneic response was not prevented by vagotomy but was significantly attenuated by denervation of peripheral chemoreceptors. We conclude that the initial responses to inhalation of several tidal breaths of wood smoke are mediated through vagal bronchopulmonary afferents, whereas the delayed tachypnea may involve nonvagal mechanisms that include a stimulation of peripheral chemoreceptors.

Stimulation of vagal pulmonary C fibers by inhaled wood smoke in rats.

This study investigated the stimulation of vagal pulmonary C fibers (PCs) by wood smoke. We recorded impulses from PCs in 58 anesthetized, open-chest, and artificially ventilated rats and delivered 6 ml of wood smoke into the lungs. Within 1 or 2 s after the smoke delivery, an intense and nonphasic burst of discharge [delta = +7.4 +/- 0.7 (SE) impulses/s, n = 68] was evoked in 60 of the 68 PCs studied and lasted for 4-8 s. This immediate stimulation was usually followed by a delayed and more sustained increase in C-fiber activity (delta = +2.0 +/- 0.4 impulses/s). The overall stimulation was not influenced by removal of smoke particulates (n = 15) or by pretreatment with vehicle (n = 8) for dimethylthiourea (DMTU; a hydroxyl radical scavenger) or indomethacin (Indo; a cyclooxygenase inhibitor). The immediate-phase stimulation was not affected by pretreatment with Indo (n = 8) but was largely attenuated by pretreatment with DMTU (n = 12) or by a combined treatment with DMTU and Indo (DMTU + Indo; n = 8). Conversely, the delayed-phase stimulation was partially suppressed either by DMTU or by Indo but was totally abolished by DMTU + Indo. These results suggest that 1) the stimulation of PCs is linked to the gas phase of wood smoke and 2) hydroxyl radical, but not cyclooxygenase products, is involved in the immediate-phase stimulation, whereas both metabolites are responsible for evoking the delayed-phase stimulation.

Inhibitory effect of inhaled wood smoke on the discharge of pulmonary stretch receptors in rats.

We investigated the inhibition of slowly adapting pulmonary stretch receptors (PSRs) by inhaled wood smoke. Impulses were recorded from PSRs in 68 anesthetized, open-chest, and artificially ventilated rats. Eighty-one of one hundred five PSRs were inhibited within one or two breaths when 6 ml of wood smoke were delivered into the lungs. As a group (n = 105), PSR activity significantly decreased from a baseline of 19.0 +/- 1.3 (SE) to a lowest level of 12.9 +/- 1.2 impulses/breath at the fourth or fifth breath after smoke delivery. This afferent inhibition usually persisted for 5-18 breaths. In contrast, smoke delivery did not affect transpulmonary pressure. Delivery of gas-phase smoke or a hypercapnic gas mixture containing CO2 at a concentration (15%) matching that in the smoke produced a nearly identical inhibition in the same PSRs (n = 10). This afferent inhibition was largely prevented by pretreatment with acetazolamide (an inhibitor of carbonic anhydrase; n = 10) but was not affected by pretreatment with the vehicle for acetazolamide (n = 8) or isoproterenol (a bronchodilator; n = 10). These results suggest that 1) an increase in H+ concentration resulting from hydration of CO2 in the smoke may be responsible for the inhibitory effect of wood smoke on the discharge of PSRs and 2) changes in lung mechanics are not the cause of this afferent inhibition.

Role of vagal afferents in the acute ventilatory responses to inhaled wood smoke in rats.

Spontaneous inhalation of wood smoke (approximately 6 ml) via tracheostomy immediately evoked either a slowing of respiration (SR) or an augmented inspiration (AI) in each of the 76 anesthetized Sprague-Dawley rats studied. The SR was abolished after perineural capsaicin treatment of both cervical vagi (PCT; n = 20) but persisted during cooling of both vagi to 6.7 degrees C (VGC, n = 12); PCT selectively blocked the conduction of unmyelinated C fibers, whereas VGC differentially blocked the conduction of myelinated fibers. In contrast, the AI was eliminated during VGC (n = 10) but was unaffected by PCT (n = 5). Furthermore, after the SR was abolished in rats with PCT, an AI became the dominant immediate response to inhaled wood smoke. Conversely, after the AI was eliminated in rats receiving VGC, a SR was instantly evoked by inhaled wood smoke. Removal of smoke particulates did not affect the SR (n = 17) but did prevent the AI in 5 of the 12 rats studied. These results suggest the following: 1) the SR is a reflex resulting from stimulation of bronchopulmonary C-fiber nerve endings by the gas-phase smoke; 2) the AI results from excitation of lung irritant receptors by the gas-phase and/or smoke particulates; and 3) in intact animals, both types of vagal bronchopulmonary afferents are probably activated by inhaled wood smoke.

Increased immunogenicity and protective efficacy in outbred and inbred mice by strategic carboxyl-terminal truncation of Japanese encephalitis virus envelope glycoprotein.

We constructed recombinant vaccinia viruses expressing the full-length envelope (E) glycoprotein of Japanese encephalitis virus (JEV) or a strategically truncated E glycoprotein, approximately 80% of the N-terminal sequence, and compared their antigenic structure and protective immunity in mice. The truncation site in the JEV E glycoprotein sequence corresponds to the position that had been shown to increase the immunogenicity of dengue type 4 or type 2 virus E glycoprotein. Analysis of the JEV E glycoprotein in recombinant virus-infected cells showed that C-terminally truncated E retains an antigenic structure similar to that of the full-length E glycoprotein. The full-length JEV E glycoprotein was detected predominantly intracellularly, while a small fraction (< 2%) was present on the cell surface. On the other hand, the truncated 80% E glycoprotein exhibited an alteration in the intracellular transport pathway resulting in increased accumulation (10-25%) on the cell surface and secretion (6-10%) into the medium. The C-terminally truncated E glycoprotein induced a greater antibody response and a higher level of protective immunity than did the full-length E glycoprotein in outbred CD-1 mice as well as in two strains of inbred mice that differ in their resistance to intraperitoneal (ip) JEV infection. In the case of outbred CD-1 and inbred C57/Bl mice, which possess a dominant autosomal genetic locus that controls resistance to a high dose of ip infection of JEV or the capacity to acquire resistance to intracerebral JEV infection, truncated E glycoprotein induced a higher titer of JEV neutralizing antibodies.

Immunization of monkeys with baculovirus-dengue type-4 recombinants containing envelope and nonstructural proteins: evidence of priming and partial protection.

Groups of rhesus monkeys were immunized with baculovirus-dengue type-4 (DEN-4) recombinant-infected cell extracts. One recombinant contained all of the DEN-4 structural proteins and two nonstructural (NS) proteins (C-M-E-NS1-NS2a), while the other was a fusion protein containing a portion of the respiratory syncytial virus G glycoprotein and DEN-4 envelope glycoprotein (RSVG-E). Both preparations were immunogenic; all monkeys receiving either immunogen responded with the production of antivirion antibodies in enzyme immunoassays. All except one monkey receiving the recombinant b(C-M-E-NS1-NS2a) made antibodies to NS1. One monkey that received b(RSVG-E) showed the production of low levels of neutralizing antibodies. Following challenge with unmodified DEN-4 virus, seven of nine monkeys in the immunized group became infected and were viremic for a mean of 4.1 days. The control, sham-inoculated monkeys were also viremic; the mean number of days of viremia in this group was 4.7 days. The remaining monkeys in the immunized group (n = 7), although not protected, had evidence of priming. Hemagglutination inhibition antibody responses following challenge indicated an anamnestic response in this group of animals. Based on these results, it was concluded that future immunization schedules should be altered to optimize immune responses and that immunization with more potent and purified immunogens would probably result in higher seroconversion rates and antibody levels in monkeys.

Attenuation and immunogenicity in humans of a live dengue virus type-4 vaccine candidate with a 30 nucleotide deletion in its 3'-untranslated region.

The recombinant dengue virus type-4 vaccine candidate 2AA30 was attenuated in rhesus monkeys due to an engineered 30-nucleotide deletion in the 3'-untranslated region of the viral genome. A clinical trial to evaluate the safety and immunogenicity of a single dose of 2Adelta30 was conducted with 20 adult human volunteers. The vaccine candidate was well tolerated and did not cause systemic illness in any of the 20 volunteers. Viremia was detectable in 14 volunteers at a mean level of 1.6 log10 plaque-forming units/ml of serum, although all 20 volunteers seroconverted with a seven-fold or greater increase in serum neutralizing antibody titer on day 28 post-vaccination (mean titer = 1:580). A mild, asymptomatic, macular rash developed in 10 volunteers, and a transient elevation in the serum level of alanine aminotransferase was noted in five volunteers. The low level of reactogenicity and high degree of immunogenicity of this vaccine candidate warrant its further evaluation and its use to create chimeric vaccine viruses expressing the structural genes of dengue virus types 1, 2, and 3.

Effects of natriuretic peptides and dopamine on single-unit activity of dorsomedial arcuate neurons in rat brain slices.

The effects of atrial natriuretic peptide (ANP) and C-type natriuretic peptide (CNP) on single-unit activity of dorsomedial arcuate (DM-ARC) neurons were reported. The modulatory effect of CNP on dopamine's (DA) action was also studied. ANP alone in 0.05-0.5 nmol doses induced 26% inhibition and 14% excitation of 37 DM-ARC neurons; the majority (60%) were not responsive. CNP, however, inhibited 46% and excited 4% of 74 DM-ARC neurons. Dose-dependent inhibitory effects of CNP were also observed. In 71 neurons tested with both CNP and DA, more neurons were inhibited by DA (66%) than those by CNP (46%). About one-third (34%) of them were inhibited by both. Furthermore, in 41 neurons inhibited by DA, more than half (54%) of their responses were potentiated by co-administration of CNP. In conclusion, CNP by itself exhibited a predominantly inhibitory action on DM-ARC neurons; and it also potentiated the inhibitory effect of DA on these neurons.

Inhibitory effect of dopamine on dorsomedial arcuate neurons in rat brain slices: potentiation by coadministration of cocaine.

Whether dopamine (DA) can have a direct effect on the tuberoinfundibular dopaminergic neurons has been a controversial issue. The present report used single-unit recording of neurons in dorsomedial region of the arcuate nucleus, where most tuberoinfundibular dopaminergic neurons are located, to study this question. By focusing our recording in this region, we found that DA in 25-250 nmol ranges inhibited a significant number of arcuate neurons tested (74.2% of 182 units). The inhibitory effect of DA was not only prominent in most cases, it also persisted in low Ca2+, high Mg2+ solution in several trials. Cocaine, a drug of abuse whose main effect is due to its inhibition of DA transporters and increasing the DA concentration in synaptic clefts, also inhibited a significant number of arcuate neurons by itself (51.5% of 97 units), although its effects were lesser than those of DA. Nevertheless, when coadministered with DA, cocaine significantly potentiated the inhibitory effect of DA in 82% of DA-responsive units (n = 39). These results clearly demonstrate that DA exhibits a predominantly inhibitory effect on presumed DA neurons in dorsomedial arcuate nucleus. The effects of cocaine further support this notion.

Endothelial dysfunction in type 2 diabetes mellitus subjects with peripheral artery disease.

We strived to characterize the endothelial function status in type 2 diabetic patients with peripheral artery disease which was detected by ankle-brachial index by utilizing high frequency ultrasounds. Predictors of endothelial dysfunction were investigated. We chose 23 type 2 diabetic patients had ankle-brachial index <0.97 (0.15-0.95; mean=0.74+/-0.20), 31 diabetic patients had ankle-brachial index >/=1.0 and 28 non-diabetic subjects for study. Older age, a longer duration of diabetes, higher systolic blood pressure, higher prevalence of history of hypertension were observed in patients with peripheral vascular disease. Type 2 diabetic patients showed impaired flow-mediated dilatation than non-diabetic and it showed more impaired in patients with peripheral vascular disease. Nitroglyerin-induced dilatation showed a trend of impairment in patients with peripheral vascular disease but did not reach statistical significance. Age (r=-0.259, P=0.019), baseline brachial artery diameter (r=-0.321, P=0.003), ankle-brachial index (r=0.259, P=0.002) and hypertension history (P=0.01) were significantly associated with flow-mediated dilatation. However, after adjusting for age, only baseline diameter and ankle-brachial index were independent predictors of flow-mediated dilatation. In conclusion, we demonstrated flow-mediated dilatation was impaired in type 2 diabetic patients and it was further impaired in patients with peripheral vascular disease. Nitroglycerin-induced dilatation showed a trend of impairment but did not reach statistical significance.

Successful resuscitation of patient with massive coronary air embolism occluding two vessels during coronary angiography--a case report.

Massive coronary air embolism is usually disastrous although successful resuscitation has been reported previously. To what extent a patient with coronary air embolism can be resuscitated is not known. The authors report a rare case of massive air embolism to the left coronary arteries and successful resuscitation by vigilantly maintaining an effective driving force to dissipate the air lock.

Inhibitory influence of lung vagal C-fiber afferents on the delayed ventilatory response to inhaled wood smoke in rats.

We studied the influences of lung vagal afferents on the delayed ventilatory response to inhaled wood smoke in 35 Sprague-Dawley rats. Wood smoke (approximately 6 ml) was inhaled via tracheostomy when animals breathed spontaneously. Immediately after inhalation, wood smoke evoked a slowing of respiration or an augmented inspiration, followed by a delayed tachypnea. Owing to the increase in respiratory frequency, the delayed ventilatory response usually resulted in an increase in minute ventilation (VI). The smoke-induced increase in VI was elevated after perineural capsaicin treatment of both cervical vagi (PCT, n = 12), but was unaltered during cooling of both vagi to 6.7 degrees C (VGC, n = 9); PCT selectively blocked the conduction of unmyelinated C-fibers, whereas VGC differentially blocked the conduction of myelinated fibers. Furthermore, the smoke-induced increase in VI after PCT was unaffected by an additional application of VGC (n = 12), whereas it was magnified by an additional application of PCT during VGC (n = 9). This magnification was not changed after a subsequent bilateral vagotomy (n = 21). Removal of smoke particulates did not affect the increase in VI evoked by smoke inhalation (n = 14). These results suggest that 1) the smoke-induced delayed ventilatory response is restrained by the inhibitory input from lung vagal C-fibers, whereas it was not influenced by the input from irritant receptors and 2) the gas phase of wood smoke is responsible for eliciting this delayed ventilatory response.

Effects of practice on identification of multidimensional stimuli.

This study investigated the effects of practice on the identification of multidimensional stimuli. Subjects were instructed to perform a two dimensional identification task. The stimuli could be identified either physically or connotatively. There were two orders of reporting the two dimensions of a stimulus. Analysis showed that method of identification and order of report significantly affected speed of identification. Physical identification was faster than identification of meaning. An appropriate order of report shortened response times, and increased practice reduced response times. Practice in multidimensional identification seemed to follow the same laws and trends of unidimensional performance. The effects of practice on multimensional identification could be represented by straight lines if response times were plotted against the logarithm of the number of trials as noted in unidimensional performance. Further, practice attenuated initial differences in response times between physical identification and identification of meaning.