Mucociliary transport in allergic patients with antigen-induced bronchospasm.

Tracheal mucous velocity (TMV) and respiratory mechanics were measured in asymptomatic asthmatic patients with ragweed hypersensitivity before and after inhalation of specific antigen, and with or without cromolyn sodium pretreatment. TMV was measured radiographically, and the airway response to bronchial provocation was monitored by measurements of forced expiratory volume in one sec and specific airway conductance. TMV was significantly less (6.3 +/- 2.3 mm per min, mean +/- SD) in the 6 asymptomatic asthmatic patients than in 7 normal subjects (11.6 +/- 3.6 mm per min, mean +/- SD). In the asthmatic patients, mean TMV diminished to 72 per cent of baseline immediately after bronchial provocation when specific airway conductance was decreased to 65 per cent of baseline or less, with a further decrease in TMV to 47 per cent of baseline after one hour, at which time respiratory mechanics had returned to baseline values. Pretreatment with cromolyn sodium prevented the decrease in TMV after bronchial provocation. We concluded that in asymptomatic patients with allergic asthma, (1) baseline TMV is impaired, (2) inhalation of specific antigen causes a marked decrease in TMV independent of the degree of bronchospasm, and (3) the decrease in TMV may be related to the release of chemical mediators.     

Preservation of ventricular function by treatment of ventricular fibrillation with phenylephrine

Epinephrine promotes resuscitation from ventricular fibrillation because of its peripheral vasoconstrictive effects. However, the beta-adrenergic effects of epinephrine may be detrimental because of the stimulation of myocardial oxygen demand. To test whether functional recovery from fibrillation in hearts treated with a selective alpha-adrenergic agent is greater than in hearts treated with epinephrine, ventricular fibrillation was induced in eight isolated dog hearts while coronary perfusion pressure was maintained at 30 mm Hg. In random order, epinephrine (5 micrograms/min), phenylephrine (50 micrograms/min) or no drug was infused for 5 min. The heart was then defibrillated, the drug infusion stopped and coronary perfusion pressure increased to 100 mm Hg. Coronary blood flow (ml/min per 100 g), arteriovenous oxygen difference (ml O2/dl) and myocardial oxygen consumption (ml O2/min per 100 g) measured after 4 min of ventricular fibrillation were greater with epinephrine (mean +/- SD 30.9 +/- 11.7, 17.5 +/- 1.6 and 5.4 +/- 1.9, respectively) than with phenylephrine (24.4 +/- 6.0, 15.7 +/- 2.6 and 3.8 +/- 1.1, respectively) or no drug (19.8 +/- 5.2, 12.8 +/- 1.8 and 2.6 +/- 0.7, respectively) (p less than 0.05, p less than 0.05 and p less than 0.05, respectively). The slope of the end-systolic pressure-volume relation 10 min after defibrillation and restoration of normal coronary perfusion pressure was depressed (percent of prefibrillation value) most by epinephrine infusion (72 +/- 17%, n = 6), less by no drug infusion (82 +/- 12%, n = 4) and was increased after phenylephrine infusion (143 +/- 17%, n = 6) (p less than 0.002).(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of drinking hot water, cold water, and chicken soup on nasal mucus velocity and nasal airflow resistance.

Nasal mucus velocity and nasal airflow resistance were measured in 15 healthy subjects before and at 5 and 30 minutes after drinking hot water by sip or straw, hot chicken soup by sip or straw, and cold water by sip. A sham drinking procedure with straw was also employed. Hot water by sip increased nasal mucus velocity from 6.2 to 8.4 mm per min, hot chicken soup by sip from 6.9 to 9.2 mm per min, and chicken soup by straw from 6.4 to 7.8 mm per min five minutes after administration. These increases were statistically significant compared to cold water, hot water by straw and sham. All values returned to their baseline at 30 minutes except cold water which significantly decreased the nasal mucus velocity from 7.3 to 4.5 mm per min. There were no significant changes from baseline in nasal airflow resistance 5 and 30 minutes following the above treatments. We conclude that drinking hot fluids transiently increases nasal mucus velocity in part or totally through the nasal inhalation of water vapor. Hot chicken soup, either through the aroma sensed at the posterior nares or through a mechanism related to taste, appears to possess an additional substance for increasing nasal mucus velocity. Finally, hot liquid might be superior to cold liquids in the management of fluids in upper respiratory tract infections.     

Changes in urinary LTE4 and nasal functions following nasal provocation test with ASA in ASA-tolerant and -intolerant asthmatics

Aspirin-induced asthma (AIA) is a syndrome characterized by intolerance to aspirin (ASA), nasal polyps and bronchial asthma, the metabolic shift of arachidonic acid towards the lipoxygenase pathway and hyper-production of cysteinyl-leukotrienes (cys-LTs) being the current pathogenetic hypothesis. The research for both sensitive indicators and safe diagnostic tests is still attracting. Aim of the study was to measure changes in urinary LTE4 excretion and in nasal function (Resistance-Req, and Volume-Vol, assessed by acoustic rhinomanometry (AR)) following a nasal provocation test (NPT) with ASA:LTE4 measurements have been never previously used to our knowledge for assessing nasal responsiveness to ASA. METHODS: After written consent, 118 mild-to-moderate asthmatics (48 males, mean age 41.8 years+/-11.9SD, range 25-70 years; basal FEV1=80.1% pred.+/-5.8SD) underwent NPT by nasal instillation of ASA (total maximal dose 25 mg). Spirometry, acoustic rhinomanometry (AR; TM Hood Lab., USA) and urinary LTE4 (pg/mg creatinine; Cayman Chemical, MI, USA) were measured in baseline and 2h after the ASA challenge. STATISTICS: t-Test between means+/-sd, assuming P<0.05, and linear regression between all variables considered. RESULTS: In 67 ASA-intolerant asthmatics, FEV1 did not change significantly following NPT (81.7% pred.+/-5.1SD in baseline, 80.5% pred.+/-4.1 after NPT, P=ns) even in the presence of a significant decrease of Vol (11.3 cm3+/-4.1SD in baseline, 5.9 cm3+/-4.2SD after NPT, P=0.003), a substantial increase of Req (0.88 cmH2O/l/min+/-0.11SD in baseline, 2.41 cmH2O/l/min+/-0.77 after NPT, P=0.002), and urinary LTE4 excretion (433.0 pg/mg+/-361.7 in bsln, 858.0 pg/mg+/-471.6 90 min after NPT with L-SA, P=0.04). NPT did not affect FEV1 also in 51 ASA-tolerant asthmatics (89.7% pred.+/-6.9 in bsln, 86.6% pred.+/-4.3 after NPT), but in these subjects also Vol (from 14.9 cm3+/-4.2sd to 14.6 cm3+/-3.8SD), Req (0.38 cmH2O/l/min+/-0.14 in bsln, 0.26 cmH2O/l/min+/-0.2 after NPT, P=ns), and urinary LTE4 (333.1 pg/mg+/-202.8 in bsln, 318.0 pg/mg+/-198.7 after NPT, P=ns) remained unchanged. Only pre-NPT LTE4 values proved related to pre-NPT Req and Vol values (r=0.54 and r=-0.71, respectively), but not to patients' age (R=-0.05), and basal FEV1 (r=0.01). CONCLUSIONS: In ASA-intolerant patients, NPT with lysine-aspirin (L-ASA) only induces a substantial nasal obstruction and enhances urinary LTE4 excretion in the absence of any significant bronchial obstruction. Nasal ASA challenge proves a test absolutely safe for asthma patients suspected of ASA intolerance. Measures of urinary LTE4 excretion contributed significantly to magnify the discriminant and the diagnostic value of NPT.     

Comparison of oxygen therapy with nasal continuous positive airway pressure on Cheyne-Stokes respiration during sleep in congestive heart failure

STUDY OBJECTIVES: Both oxygen therapy and nasal continuous positive airway pressure (CPAP) therapy have independently been shown to be effective in the treatment of Cheyne-Stokes respiration (CSR) in patients with congestive heart failure (CHF). The purpose of this study was to compare the short-term effects of oxygen therapy and nasal CPAP therapy on CSR in a group of stable patients with severe CHF. DESIGN: Prospective, randomized, controlled trial. SETTING: University hospital. PATIENTS: Twenty-five stable patients (mean [+/- SD] age, 56 +/- 9) with CHF and a mean left ventricular ejection fraction (LVEF) of 17 +/- 0.8%. INTERVENTIONS AND MEASUREMENTS: All patients had a right heart catheterization prior to the study and an echocardiogram performed to measure LVEF. In addition, all patients had an initial sleep study to identify the presence of CSR. Sleep studies included continuous recordings of breathing pattern, pulse oximetry, and EEG. Those patients identified as having CSR were randomized to a night on oxygen therapy (2 L/min by nasal cannula) and another night on nasal CPAP therapy (9 +/- 0.3 cm H(2)O). RESULTS: Fourteen of the 25 patients (56%) studied had CSR (apnea hypopnea index [AHI], 36 +/- 7 events per hour) during their initial sleep study. Nine of the 14 patients with CSR completed the study. When compared with baseline measurements, both oxygen therapy and nasal CPAP therapy significantly decreased the AHI (from 44 +/- 9 to 18 +/- 5 and 15 +/- 8 events per hour, respectively; p < 0.05), with no significant difference between the two modalities. The mean oxygen saturation increased significantly and to a similar extent with oxygen therapy and nasal CPAP therapy (from 93 +/- 0.7% to 96 +/- 0.8% and 95 +/- 0. 7%, respectively; p < 0.05), as did the lowest oxygen saturation during the night (from 80 +/- 2% to 85 +/- 3% and 88 +/- 2%, respectively; p < 0.05). In addition, the mean percent time the oxygen saturation was < 90% also improved with both interventions (from a baseline of 17 +/- 5 to 6 +/- 3% with oxygen therapy and 5 +/- 2% with nasal CPAP therapy; p < 0.05). When compared with baseline measurements, the apnea-hypopnea length, cycle length, circulation time, and heart rate did not significantly change with either oxygen therapy or nasal CPAP therapy. Total sleep time and sleep efficiency decreased only with nasal CPAP therapy (from 324 +/- 20 to 257 +/- 14 min, and from 82 +/- 3 to 72 +/- 2%, respectively; p < 0.05). The arousal index, when compared with baseline, remained unchanged with both oxygen therapy and nasal CPAP therapy. CONCLUSION: CSR occurs frequently in stable patients with severe CHF. In addition, oxygen therapy and nasal CPAP therapy are equally effective in decreasing the AHI in those CHF patients with CSR.     

Influence of acute alterations in heart rate and systemic arterial pressure on echocardiographic measures of left ventricular perfornmance in normal human subjects.

To study the effects of acute alterations in heart rate and systemic arterial pressure on the mean velocity of left ventricular circumferential fiber shortening (Vcf) and on mean posterior wall velocity (Vpw), we performed ultrasound studies in 25 normal human subjects between the ages of 21 and 29 years. When heart rate was augmented by the administration of intravenous atropine from 64 +/- 2.2 (SEM) to 98 +/- 2.7 beats/min, mean normalized Vcf increased from 1.22 +/- 0.05 to 1.38 +/- 0.06 circumferences (circ)/sec(P less than 0.001). Mean normalized Vpw increased from 0.76 +/- 0.03 to 0.89 +/- 0.04 sec-1 (P less than 0.001). Mean Vcf and mean Vpw uncorrected for end-diastolic diameter increased in a similar fashion (P less than 0.01). After atropine administration, systemic arterial pressure was augmented by means of a phenylephrine infusion in 23 subjects by an average of 39 mm Hg (range 20-50 mm Hg). During the phenylephrine infusion, average heart rate decreased from 96 +/- 2.6 to 91 +/- 3.1 beats/min (NS), while mean normalized Vcf declined from 1.38 +/- 0.06 to 1.09 +/- 0.05 circ/sec (P less than 0.001) and normalized Vpw from 0.89 +/- 0.04 to 0.65 +/- 0.04 sec-1 (P less than 0.001). Nonnormalized velocities exhibited similar alterations (P less than 0.01). We conclude that in the normal human subject mean Vcf and mean Vpw are sensitive to acute alterations in heart rate and systemic arterial pressure. Thus, when ultrasound measures are used for serial assessment of left ventricular performance, the level of heart rate and systemic arterial pressure at which studies are obtained must be considered. Further, the sequential use of atropine and phenylephrine, as described in this study, provides an experimental model for the evaluation of the effects of drug treatment and other interventions on left ventricular performance in man.     

Tracheal mucociliary transport in patients with cystic fibrosis and its stimulation by terbutaline.

Tracheal mucous velocity was measured by observing the motion of teflon discs across the tracheal mucosa through a fiberoptic bronchoscope. The average rate of movement in 14 adult patients with cystic fibrosis was 2.6 mm per min plus or minus 3.3 SD, compared with 20.1 mm per min plus or minus 6.3 in 20 normal subjects of the same age (P less than 0.001). This failure of mucociliary transport may play a role in the pathogenesis of the pulmonary disease in cystic fibrosis. Administration of a beta-adrenergic agent, terbutaline, increased the average mucous velocity in the patients with cystic fibrosis (to 5.5 mm per min plus or minus 3.6 SD, P less than 0.001) but not in control subjects. This observation has potential therapeutic significance.     

The effects of nasal continuous positive airway pressure on platelet activation in obstructive sleep apnea syndrome

OBJECTIVE: A case-controlled study to assess the effects of nasal continuous positive airway pressure (CPAP) on platelet activation in patients with obstructive sleep apnea (OSAS) syndrome. METHODS: We recruited 65 patients with suspected OSAS for this study. Blood samples were taken with the patient in the supine position in the morning immediately after polysomnography, and 1 night and 3 months after the start of nasal CPAP therapy to measure an index of platelet activation (IPA+), which reflected both the quantity and quality of platelet activation. Significant OSAS was defined as an apnea-hypopnea index (AHI) of > or = 10 events per hour. RESULTS: There were 42 patients with significant OSAS and 23 control subjects with AHI < 10 events per hour. The mean (+/- SD) age for the OSAS patients was 48 +/- 9 years, the mean body mass index was 30.7 +/- 4.8, the mean AHI was 47 +/- 25 events per hour, the mean arousal index (AI) was 37 +/- 23 events per hour, and the mean minimum arterial oxygen saturation was 74 +/- 11%. Following multiple linear regression analyses of the clinical and polysomnography parameters, AI was the independent factor that correlated best with the baseline IPA+ (beta-coefficient, 0.386; p = 0.006). Following nasal CPAP treatment with a mean objective CPAP compliance of 3.9 +/- 1.9 h per night, there was a significant decrease in IPA+ from 15.1 +/- 12.2 U (at baseline) to 12.2 +/- 5.2 U (p < 0.001) and 9.8 +/- 4.3 U (p = 0.005), respectively, after 1 night and 3 months, whereas no significant change was noted among the control subjects. Using univariate analysis of variance to compare the changes in IPA+ between the two groups at 3 months with adjustment for the baseline value, nasal CPAP reduced IPA+ by 5.63 (SE, 1.85), whereas IPA+ increased in control subjects by 1.33 (SE, 1.27) [least-squared mean difference between groups, 3.34; 95% confidence interval, 0.42 to 6.26; p = 0.026]. CONCLUSIONS: OSAS, through repeated episodes of arousals, may lead to platelet activation, which can be reduced by nasal CPAP therapy.     

Montelukast protects against nasal lysine-aspirin challenge in patients with aspirin-induced asthma.

Aspirin-induced asthma (AIA) is associated with increased production of cysteinyl leukotrienes (CysLT). Although leukotriene CysLT1-receptor antagonists improve lower airway outcomes in AIA, their effects and dose-response in the upper airway is less well documented. The present study evaluated the dose-response for montelukast (ML) against nasal lysine-aspirin challenge in patients with AIA. A total of 12 patients with a clear-cut history of AIA were randomised in double-blind cross-over fashion to receive single doses of ML 10 mg, ML 40 mg, or placebo (PL), with nasal lysine-aspirin challenge performed 12 h after dosing. Measurements of peak nasal inspiratory flow (PNIF), nasal blockage visual analogue scale (VAS) and forced expiratory volume in one second (FEV1) were made over 120 min after nasal lysine-aspirin challenge. Prechallenge values for mean+/-SEM PNIF (L x min(-1)) were not significantly different comparing all groups: ML 10 mg (132+/-10), ML 40 mg (125+/-12) and PL (132+/-11). There was no significant difference comparing the maximum % PNIF fall from baseline between screening (46+/-6) and PL (45+/-6). The maximum % PNIF fall from baseline was significantly greater with PL (45+/-6) compared to either ML 10 mg (34+/-6) or ML 40 mg (32+/-5). There was also a significantly greater mean % PNIF response over 120 min after lysine-aspirin challenge for PL (26+/-7) compared to either ML 10 mg (14+/-6) or ML 40 mg (17+/-6). There were no significant differences for the maximum or mean % PNIF fall from baseline comparing ML 10 mg and ML 40 mg. A significant increase in nasal blockage VAS score was observed between baseline and 60 min or 120 min with PL but not with ML 10 mg or ML 40 mg. There were no significant differences for either the maximum or mean % FEV1 over 120 min as change from baseline comparing all groups. A single 10 mg dose of montelukast partially protected against the local effects of nasal lysine-aspirin challenge, with no further benefit at 40 mg. Nasal lysine-aspirin challenge appeared to be a reproducible and safe method in assessing patients with aspirin-induced asthma.     

Loss of nocturnal decline of blood pressure in patients with nasal polyposis

The objective of this study was to assess the blood pressure pattern in patients with nasal polyposis. Twenty-seven patients with nasal polyposis (18 males and 9 females), ranging in age from 15 to 72 years (mean 37.1 years) were eligible for inclusion in the study. All patients were hospitalized overnight before surgery. After the basal blood pressure measurements were taken, non-invasive ambulatory blood pressure monitoring was carried out. Oxygen saturation was measured via a finger probe and venous blood sampling was taken for catecholamine level during the full night. All measurements were repeated 4 months after nasal surgery. Mean values for nocturnal decline in blood pressure and heart rate before surgery were less marked than those measured after surgery. Mean decline values (+/- SD) were; 4.6 +/- 2.4 mmHg for systolic blood pressure, 5.8 +/- 3.8 mmHg for diastolic blood pressure, and 7.9 +/- 3.9 beats/min for heart rate before surgery, 9.3 +/- 2.8 mmHg, 8.5 +/- 4.1 mmHg and 10.4 +/- 4.3 beats/min after surgery (p < 0.01), respectively. Whereas mean and minimum SaO2 (%) significantly increased (p < 0.01), catecholamine levels decreased (p < 0.05 for adrenaline, p < 0.01 for noradrenaline) after surgery. A correlation was found between BMI and blood pressure as well as between duration of obstruction and blood pressure. Patients who snored had higher blood pressure values than those who did not. Our data show that in cases of nasal polyposis, hypoxia, hypercapnia, snoring, and sleep disorders may develop and persons with nasal polyposis and snoring have an increased risk of hypertension and loss of nocturnal decline in blood pressure.     

Comparison of two methods of measuring tracheal mucous velocity in anesthetized beagle dogs.

Tracheal mucous velocity measurements were made in 6 beagle dogs using both Sackner's method of radiographing teflon discs and Chopra's method using a gamma camera to detect the movement of instilled labeled material. Dogs were anesthetized by intravenous injection of 30 mg of sodium pentobarbital/kg of body weight in case 1 after pretreatment with atropine and Innovar-Vet; in case 2, without the pretreatment. The mean velocities measured using the 2 techniques were significantly different in both cases: case 1, 3.7 +/- 3.3 mm/min for Sackner's methods and 7.5 +/- 3.7 mm/min for Chopra's method (p less than 0.001); case 2. 3.7 +/- 3.1 mm/min for Sackner's method, and 5.5 +/- 2.1 mm/min for Chopra's method (p less than 0.05). Systematic differences in velocities should be considered when comparing data from investigators using different techniques.     

Effects of nasal mask leak and heated humidification on nasal mucosa in the therapy with nasal continuous positive airway pressure (nCPAP)

The purpose of this study was to determine the objective short-term influence of nasal continuous positive airway pressure (nCPAP) therapy, nasal mask leak (NML) and heated humidifiers (HH) to nasal conditioning of spontaneously breathing subjects. This was a prospective, non-randomized, non-blinded day-time study. Eighteen healthy subjects were enrolled in the study. All subjects received nCPAP therapy for 60 min in three different conditions successively: (1) nCPAP without humidification, (2) nCPAP with a defined leakage of nasal mask (slashed circle 28.3 mm2) and (3) nCPAP with HH. Nasal humidity and temperature were measured in the anterior turbinate area using a miniaturized thermocouple and a relative humidity sensor. The measurements were accomplished at the beginning of therapy, after 60, 120 and 180 min. Absolute humidity (aH) in the anterior turbinate area decreased significantly (p = 0.0075) from 17.41 +/- 3.81 mg/l (baseline) to 15.27 +/- 2.21 mg/l (nCPAP alone). With attachment of a NML, aH decreased from 15.27 mg/l not significantly (p = 0.058) to 13.77 +/- 2.28 mg/l (nCPAP and NML) compared to nCPAP alone. After addition of heated humidification to nCPAP, aH increased again from 13.77 mg/l significantly (p = 0.042) to 15.29 +/- 3.51 mg/l (nCPAP and HH) compared to aH (nCPAP+NML). No difference was found between aH (nCPAP and HH) and aH (nCPAP alone). Airway temperature did not change significantly after application of nCPAP alone, nCPAP and NML, and nCPAP and HH. These data indicate that nCPAP therapy with NML tends to have more remarkable reduction of the nasal humidity than nCPAP therapy without NML. nCPAP with heated humidifier is able to compensate the dehydration effects induced by nCPAP therapy with NML by increasing the aH at the anterior turbinate area to the levels observed during breathing with nCPAP alone.     

Role of mucus and cilia in nasal mucociliary clearance in healthy subjects

Large interindividual variations of nasal mucocilliary clearance across healthy subjects have been previously described. The aim of this study was to evaluate the respective role of the nasal mucus quality and ciliary activity in determining nasal mucociliary clearance and to study changes in these variables across time and with environmental conditions. In 20 healthy nonsmoking volunteers, the in vivo nasal mucociliary clearance was measured with the saccharin test. Then, nasal mucus and ciliated cells were collected. The in vitro ciliary beat frequency of the nasal cells was evaluated by a photometric analysis. The in vitro nasal mucus transport rate was evaluated by use of the frog depleted-palate model. The nasal mucociliary transport time (NMTT) of saccharin was greater than 30 min in seven subjects and was 13.6 +/- 6.1 min (mean +/- SD) in the remaining 13 subjects. NMTT was correlated to the in vitro transport rate of the nasal mucus (r = -0.75, p less than 0.001), but not to the ciliary beating frequency or to ambient temperature, relative humidity, or air pollution indices measured. Moreover, large intraindividual variations of NMTT, measured on two occasions 4 to 8 wk apart, were found to be significantly correlated with changes in mucus transport rate (r = -0.60, p less than 0.05).     

Micronuclei frequencies in exfoliated nasal mucosa cells from pathology and anatomy laboratory workers exposed to formaldehyde

Formaldehyde (FA) is a widely used industrial chemical. Sufficient evidence exists to consider FA as an animal carcinogen. A possible causal role for FA may be considered likely for cancer of the nasopharynx and the nasal cavities in humans. The frequency of micronuclei (MN) in cells of the nasal mucosa was evaluated for 23 individuals in pathology and anatomy laboratories exposed to FA. Twenty-five healthy subjects were selected from the university and hospital staff as a control group. The measured air concentrations of FA in the breathing zone of the laboratory workers were between 2 and 4 ppm. The mean +/- SD values of nasal mucosa MN (per 1000) frequency from exposed and controls were 1.01 +/- 0.62 and 0.61 +/- 0.27, respectively (p < 0.01). Effect of smoking, age, sex and duration of exposure on the genotoxicity parameters analyzed were also evaluated. Our data suggest that low level exposure to FA is associated with cytogenetic changes in epithelial cells of the nasal region and that nasal mucosa cells exposed through respiration is an important target of FA-induced genotoxic effects.     

Ciliary beat frequency and mucociliary clearance. What is the relationship?

Ciliary beat frequency (CBF), measured in vitro, and tracheal mean clearance rate (TMCR), measured in vivo, were studied in 20 nonatopic nonsmokers. CBF, measured by direct examination of nasal cells obtained by a fiberbronchoscopic brush, was 12.1 +/- 1.7 Hz (mean +/- SD). TMCR, assayed by a radioisotope technique, revealed values of 4.3 +/- 1.1 mm/min (mean +/- SD). Both of these values agree with results published by other workers. We attempted to correlate intersubject variation in TMCR with variation in CBF but found no direct relationship, findings similar to those reported in studies done on frog palate epithelium.     

Combined effects of a mechanical nasal dilator and a topical decongestant on nasal airflow resistance.

The goal of this study was to compare the isolated and combined effects of two treatments being used to reduce nasal airflow resistance (NR): an internal nasal mechanical dilator (Nozovent; Prevancure; Sté Pouret, Paris, France) and a topical decongestant, fenoxazoline hydrochloride (Aturgyl; Synthelabo; Le Plessis-Robinson, France). The study was performed in 17 healthy subjects. NR was estimated by active posterior rhinometry at a 0.5 L/s flow under four conditions: in the basal state, with the internal nasal mechanical dilator, after treatment with fenoxazoline hydrochloride, and with both fenoxazoline hydrochloride and the mechanical dilator. The mean NR (+/- SD) decreased from 1.65+/-0.54 cm H2O/L/s in the basal state to 1.02+/-0.27 cm H2O/L/s with the mechanical dilator (p < 0.001), 1.03+/-0.47 cm H2O/L/s with fenoxazoline hydrochloride (p < 0.001), and 0.48+/-0.15 cm H2O/L/s with both the mechanical dilator and fenoxazoline hydrochloride (p < 0.001). The decreases in NR observed after using either the mechanical dilator (deltaNR(N)) or fenoxazoline hydrochloride (deltaNR(A)) were not significantly different. The decrease in NR observed with both (deltaNR(N + A)) was not significantly different from the sum deltaNR(N) + deltaNR(A): 1.16+/-0.53 cm H2O/L/s vs 1.25+/-0.63 cm H2O/L/s, respectively (p > 0.05). deltaNR(N + A) strongly correlated with deltaNR(N) + deltaNR(A): deltaNR(N + A) = 0.80 (deltaNR(N) + deltaNR(A)) + 0.15 (r = 0.96; p < 0.0001). However, the slope of the regression line of deltaNR(N + A) vs deltaNR(N) + deltaNR(A) was significantly lower than unity (p < 0.003). These results demonstrate that, although not totally additive, the effects of using the mechanical dilator and fenoxazoline hydrochloride are cumulative. Further studies that include patients with nasal obstruction would allow us to better evaluate the benefit of a therapy combining both treatments.     

A physiologic comparison of nasal and oral positive airway pressure

STUDY OBJECTIVES: The effectiveness of nasal continuous positive airway pressure (CPAP) in treating obstructive sleep apnea (OSA) is based on raising the intramural pressure above a critical collapsing pressure of the oropharyngeal airway. It is currently unclear whether CPAP delivered orally is also capable of raising pressure in the oropharynx above the critical collapse pressure. DESIGN: We tested a novel oral CPAP device to determine whether the pressure-flow relationships are similar to nasal CPAP and whether the device alters these relationships. Patients were selected based on having moderately severe apnea and were randomized to nasal CPAP, nasal CPAP with oral device, or oral CPAP. SETTING: Johns Hopkins University, The Johns Hopkins Asthma and Allergy Center, Baltimore, MD. PATIENTS: Five men and two women with OSA were studied. INTERVENTIONS: Individual pressure-flow curves were constructed during the application of nasal or oral CPAP. RESULTS: We found the following: (1) a similar effective pressure eliminated inspiratory flow limitation for the nasal or oral CPAP; (2) as pressure in the nose or mouth was lowered below the effective pressure, a linear pressure-flow curve was obtained and a critical closing pressure was described; (3) similar mean (+/- SD) critical pressures of -0.3 +/- 5.3, 1.7 +/- 4.0, and 0.5 +/- 2.8 cm H(2)O, respectively, occurred for nasal CPAP, nasal CPAP with the oral device in place, and oral CPAP conditions (p > 0.1); and (4) the comparable mean values for upstream resistance were 27.8 +/- 19, 19.1 +/- 8.3, and 26.5 +/- 26.7 cm H(2)O/L/s, respectively, for the above three conditions (p > 0.1). CONCLUSIONS: We concluded that comparable upper airway pressure-flow relationships were obtained during oral and nasal breathing. Moreover, effective treatment pressure is obtained when constant pressure is applied through either the nasal or oral route.     

Left ventricular function during stable sustained ventricular tachycardia. Hemodynamic and echo-Doppler analysis

To assess the left ventricular function during sustained stable ventricular tachycardia (VT), ten patients, aged 58 to 74, underwent simultaneous echo-Doppler and hemodynamic studies during sinus rhythm and induced sustained stable monomorphic VT. The VT cycle length was 447 +/- 92 ms (mean +/- SD). During VT, cardiac index fell from 2.32 +/- 0.54 to 1.62 +/- 0.63 L/min/m2 (p less than 0.001), and systemic systolic blood pressure fell from 129 +/- 18 to 107 +/- 18 mm Hg (p less than 0.001), while left ventricular end-diastolic pressure showed a rising trend from 9 +/- 7 to 15 +/- 12 mm Hg, and pulmonary artery wedge pressure rose from 10.2 +/- 1.6 to 24.2 +/- 2.3 mm Hg (p less than 0.005). By echo-Doppler the ejection fraction and the presence and degree of valvular regurgitation were not significantly changed during VT. The mean maximal left ventricular inflow tract velocities, mean time velocity integrals, and the mean time velocity integrals normalized for heart rate (measures of left ventricular diastolic filling) decreased from 0.59 +/- 0.074 to 0.40 +/- 0.053 m/s (p less than 0.05), from 0.12 +/- 0.029 to 0.021 +/- 0.012 m (p less than 0.001), and from 7.43 +/- 1.20 to 3.21 +/- 1.49 m x beats/min (p less than 0.001) during VT, respectively. We conclude that hemodynamic changes during stable sustained VT are neither associated with significant changes in systolic left ventricular function nor related to valvular regurgitation and are likely caused by impaired left ventricular diastolic filling.     

Analysis of the action of angiotensin II on the baroreflex control of heart rate in conscious rabbits

There is considerable evidence that angiotensin II (Ang II) attenuates the baroreflex control of heart rate (HR), but the mechanism and site of this action have not been precisely defined. In the present study the effects of systemically and centrally administered Ang II on the baroreflex control of HR were investigated in conscious, chronically prepared rabbits. Baroreflex curves (HR vs. mean arterial pressure) were generated with iv infusions of phenylephrine or nitroprusside. Background infusion of Ang II at 10 ng/kg.min increased mean arterial pressure from 77.3 +/- 3.0 to 94.3 +/- 4.1 mm Hg (P less than 0.001) without changing HR [212.1 +/- 7.2 to 218.0 +/- 9.8 beats/min (bpm)] and shifted (reset) the baroreflex curve with phenylephrine to a higher pressure level (P less than 0.001) without changing its slope (-1.40 +/- 0.40 to -1.65 +/- 0.46 bpm/mm Hg; P = 0.4). Background infusion of an equipressor dose of phenylephrine did not shift the baroreflex curve or change its slope. Ang II also shifted the baroreflex curve with nitroprusside to a higher pressure level (P less than 0.01), but again the slope was not significantly changed (-2.30 +/- 1.25 to -1.51 +/- 0.52 bpm/mm Hg; P = 0.2). Background intraventricular infusion of Ang II at 1 ng/kg.min had the same effects as iv infusion of Ang II at 10 ng/kg.min; the curve was shifted to a higher pressure level (P less than 0.001), but the slope was not changed (-0.76 +/- 0.47 to -1.143 +/- 0.48 bpm/mm Hg). Intravenous infusion of Ang II at 1 ng/kg.min had no effect on the baroreflex. The resetting of the baroreflex with phenylephrine by iv Ang II (10 ng/kg.min) was not blocked by propranolol: atropine markedly reduced the baroreflex response to phenylephrine in both the absence and presence of Ang II. These results indicate that in conscious rabbits, Ang II resets the baroreflex control of HR, but does not change its sensitivity. This effect apparently results from an action of Ang II on the brain that is mediated by withdrawal of vagal tone to the heart. The resetting of the baroreflex by Ang II can explain the ability of the peptide to increase arterial pressure without decreasing HR.     

Effects of hydration and physical therapy on tracheal transport velocity.

A new tracer method for quantitative measurement of tracheal transport velocity (mm per min) in dogs has been described. Using the same technique, the effects of dehydration, rehydration, postural drainage, and chest percussion on tracheal transport velocity were studied. Mean tracheal transport velocity decreased significantly (14.1 +/- 1.4) after dehydration (P less than 0.05) and reverted to normal (19.0 +/- 1.3) with rehydration in 10 dogs. After postural drainage in 7 dogs, mean tracheal transport velocity increased 39.7 +/- 1.78 (SE) per cent (P less than 0.01). After chest percussion in 6 dogs, mean tracheal transport velocity increased 50.9 +/- 1.22 (SE) per cent. With combined postural drainage and chest percussion, mean tracheal transport velocity increased 50.0 +/- 0.32 (SE) per cent. Although maximal improvement occurred after the combined therapy, the changes were not significantly different from those observed with each therapy alone. These therapeutic measures have been used empirically in the past. The present study gives some objective evidence for their beneficial effects in anesthetized dogs.