Biomedical subjects
Publications and source records attributed to R A Sauder.
Horses intended for slaughter in Western Canada are frequently transported in double-deck trailers, where headroom may be restricted. Poll and withers height was estimated from type photographs of various horse breeds. The headroom required by Canadian legislation and codes of practice may not be sufficiently restrictive to protect the welfare of sport type horses when transported.
BACKGROUND: Corticosteroids used in combination with bronchodilators are significantly more effective than placebo combined with bronchodilators in the acute treatment of bronchospasm. Because the time course for this effect is not known, and is of importance in the preoperative preparation of patients with reactive airway disease, the authors investigated the time course by which methylprednisolone increased sensitivity to the beta-adrenergic agonist, albuterol, in a dog model with airway hyperresponsiveness. METHODS: Airway responsiveness to methacholine alone and in the presence of albuterol was determined before treatment with methylprednisolone in nine Basenji greyhounds. Each dog was then treated with methylprednisolone for 1 week. Airway responsiveness to methacholine in combination with albuterol was determined after 24 h, 48 h, and 1 week of methylprednisolone treatment. RESULTS: Albuterol alone did not alter airway responsiveness to methacholine in Basenji greyhounds before methylprednisolone treatment and after 24 h of methylprednisolone treatment. Methylprednisolone, however, significantly decreased pulmonary responses to methacholine in albuterol-pretreated dogs at 48 h. CONCLUSIONS: The authors concluded that methylprednisolone increased sensitivity to the beta-adrenergic agonist, albuterol, within 48 h.
This study investigated the effect of chronic methylprednisolone treatment on the ability of albuterol and aminophylline to inhibit methacholine-induced airway constriction in Basenji-Greyhound (BG) dogs in vivo. Pulmonary responsiveness to methacholine was measured in five untreated BG dogs and in the same dogs pretreated with albuterol or aminophylline (which has been shown in this model to release endogenous catecholamines). Each dog was studied before, during, and after daily subcutaneous methylprednisolone for 6 wk. Changes in pulmonary resistance and dynamic compliance with methacholine aerosol challenge were measured. Neither baseline pulmonary function nor pulmonary responsiveness to aerosolized methacholine was significantly altered by albuterol, aminophylline, or chronic methylprednisolone administration alone. However, pretreatment with albuterol or aminophylline significantly attenuated airway responses to methacholine in BG dogs chronically receiving methylprednisolone. Because the reduced sensitivity to albuterol and aminophylline was restored by chronic methylprednisolone treatment, we conclude that at least part of the beneficial effects of corticosteroids on airways in BG dogs is through modulation of beta-adrenergic function.
To determine if corticosteroids would prevent beta-adrenergic-antagonist-induced increases in airway reactivity, we evaluated the ability of chronic methylprednisolone administration to prevent propranolol-induced airway hypereactivity to methacholine aerosol in the basenji-greyhound (BG) dog model of asthma. Initial studies included the measurement of lung resistance (RL) and dynamic compliance (Cdyn) with and without propranolol pretreatment in 5 BG and 5 mongrel dogs. A single dose of propranolol (2 mg/kg) did not significantly alter airway reactivity in the mongrels. The dose of methacholine needed to increase RL by 200% (ED200RL) was 0.20 +/- 0.05 mg/ml (mean +/- standard error of the mean [SEM]) in untreated and 0.18 +/- 0.04 mg/ml in propranolol-treated mongrels. In contrast, propranol significantly increased methacholine-reactivity in the BGs. The ED200RL for methacholine was 0.17 +/- 0.03 mg/ml in untreated and 0.05 +/- 0.02 mg/ml (P less than 0.05) in propranolol-treated BG dogs. Following the initial studies, the 5 BG dogs were given methylprednisolone (2 mg.kg-1.day-1) for 4 weeks, after which time propranolol no longer increased methylacholine reactivity in the BGs. The ED200RL was 0.16 +/- 0.03 mg/ml after 4 weeks of methylprednisolone and 0.22 +/- 0.06 mg/ml after propranolol administration in the BGs given 4 weeks of methylprednisolone treatment. The attenuation of propranolol-induced bronchoconstriction by corticosteroids may be a clinically useful intervention in asthmatic patients receiving beta-adrenergic antagonists in the perioperative period. However, further studies are needed to define the effective dose and duration of corticosteroid therapy that is needed.
We investigated the correlation between collateral airway reactivity and other indexes of lung reactivity in response to aerosol and intravenous (iv) challenges. In four anesthetized mongrel dogs, we measured the peripheral airway resistance (Rp) to gas flow out of a wedged lung segment in different lobes on multiple occasions. We obtained dose-response curves of peripheral airways challenged with iv histamine or aerosols through the bronchoscope. During the same iv bolus challenge, whole lung airway pressure (Paw) responses to histamine were also measured. On separate occasions, changes in lung resistance (RL) were measured after the whole lung was challenged with a histamine aerosol. Reactivity was assessed from the dose-response curves for Rp and RL as the PD50 (dose required to produce a 50% increase); for changes in Paw we calculated the PD15 (dose required to produce a 15% increase over baseline). Results for Rp showed considerably more variability among different lobes in a given animal with the aerosol challenge through the bronchoscope than with the iv challenge. With aerosol challenge there were no significant differences in the mean PD50 for Rp among any of the animals. However, with the iv challenge two of the dogs showed significant differences from the others in reactivity assessed with Rp (P less than 0.01). Moreover, the differences found in the peripheral airways with iv challenge reflected differences found in whole lung reactivity assessed with either iv challenge (Paw vs. Rp, r2 = 0.96) or whole lung aerosol challenge (RL vs. Rp, r2 = 0.84). We conclude that the measurement of the collateral resistance response to iv challenge may provide a sensitive method for assessing airway reactivity.
The application of 70% helium-30% oxygen mixtures by tight-fitting face mask in the emergency management of large airway obstruction is well known. We present the case of an infant with severe large airway obstruction and respiratory failure that was unresponsive to the more traditional approaches of airway management, including the delivery of He-O2 by face mask, endotracheal intubation, and conventional mechanical ventilation with oxygen alone. This case was successfully managed with He-O2, when concentrations of O2 were lower than those previously reported in association with conventional mechanical ventilation, until the obstruction could be surgically corrected. We suggest using a new combination of the low-density helium-oxygen gas mixtures and conventional mechanical ventilation, both of which are readily available in most intensive care units.
Pulmonary reactivity to methacholine after equipotent beta-blocking doses of propranolol and esmolol was compared in seven basenji-greyhound dogs during thiopental-fentanyl anesthesia. Equipotent doses of esmolol and propranolol were determined by both heart rate effects and by isoproterenol response curves. Propranolol (2 mg/kg) was administered intravenously as a bolus dose and esmolol (0.4-0.5 mg.kg-1.min-1) was administered by continuous infusion. Both esmolol and propranolol significantly decreased heart rate and mean arterial pressure (P less than 0.001). Baseline pulmonary resistance and dynamic compliance did not change after the administration of either propranolol or esmolol. However, propranolol significantly shifted the methacholine dose-response curve to the left so that methacholine (0.3 mg/ml) increased pulmonary resistance by 7.9 +/- 0.97 cmH2O.l-1.s-1 (mean +/- SEM of seven dogs) after pretreatment with propranolol but only 4.4 +/- 0.89 cmH2O.l-1.s-1 (P less than 0.05) without propranolol pretreatment (control). Esmolol, however, did not significantly shift the methacholine dose-response curve. Methacholine (0.3 mg/ml) increased resistance 4.0 +/- 0.89 cmH2O.l-1.s-1 during esmolol administration. This study shows that at equipotent beta 1-blocking doses, propranolol, but not esmolol, produces significant increases in pulmonary reactivity to methacholine.
Rapid intravenous (iv) infusion of protamine sulfate is associated with hypotension in humans. A possible mechanism for this hypotension is the release of inflammatory mediators, including histamine, from tissue mast cells lining the blood vessels. To determine whether protamine caused nonimmunologic release of histamine, histamine released from dispersed human skin mast cells exposed to protamine sulfate was measured. Skin from seven adult patients was washed, chopped into small tissue fragments, and incubated with collagenase, hyaluronidase, and DNAase. Dispersed mast cells were harvested after 12 h of short-term tissue culture, washed, and challenged with protamine sulfate. Histamine release was measured using an automated histamine analyzer and expressed as a per cent of total released histamine measured minus the spontaneous histamine release. Spontaneous histamine release averaged 6 +/- 1%. Protamine produced dose-related histamine release. At a concentration of 3 X 10(-3) M, protamine sulfate released 14 +/- 2% (P less than 0.05), which significantly differed from spontaneous release. This study demonstrates that protamine sulfate causes nonimmunologic histamine release in dispersed human skin mast cells. However, histamine release occurred only at concentrations much greater than those used in clinical practice. Thus, these data do not support the hypothesis that nonimmunologic histamine release is a likely mechanism for protamine-induced hypotension in vivo.
To investigate the inhibitory effects of beta-adrenergic agonists and aminophylline on pulmonary responsiveness, we evaluated the ability of albuterol and aminophylline to attenuate pulmonary responses to aerosol challenge with methacholine and histamine in intact Basenji-Greyhound (BG) and selected mongrel dogs. Pulmonary responses were measured in untreated dogs and in dogs pretreated with albuterol (1 and 2.5 micrograms/kg) or aminophylline. Before aerosol challenge, baseline pulmonary resistance (RL) and dynamic compliance (Cdyn) were not significantly different between the BGs and the mongrels. In the untreated dogs, pulmonary responses to methacholine and histamine aerosols were not different between the BGs and the mongrels. Pretreatment with albuterol (1 microgram/kg) or aminophylline significantly attenuated the pulmonary response to methacholine in the mongrels but was without effect in the BGs. Albuterol (2.5 micrograms/kg) significantly attenuated the pulmonary response to methacholine in the BGs and the mongrels; however, this attenuation was significantly greater (P less than 0.05) in the mongrels than in the BGs. In response to histamine challenge, no differences were seen between the BGs and the mongrels in the control state (no pretreatment) or after pretreatment with albuterol or aminophylline. This study demonstrates that in BGs pulmonary responsiveness to methacholine but not histamine is resistant to inhibition by beta-adrenergic agonists. This may result from a qualitative or quantitative defect in either the cholinergic or beta-adrenergic receptor or to an abnormality distal to the receptors in the signal transduction mechanism at a site where the two signals interact.
We report three unusual, catastrophic cases in which a significant decrease in leak pressure around a tracheal tube was noted before the discovery of the ultimate airway problem. A brief review of potential causes of a decrease in leak pressure is included and management of these difficult cases is discussed.
We studied transepithelial potential difference (PD) in normal persons, patients with chronic disease, and patients with cystic fibrosis (CF), using the technique described by Knowles and co-workers. A maximal PD value (PDmax) and an average PD value (PDmean) were determined for each study of the nasal respiratory epithelium. The voltage response to superfusion of 10(-4) mol/L amiloride onto nasal mucosa was noted. The PD of the palm, wrist, and between two fingertips was also measured. Nasal PDmax and PDmean of the CF group were more negative than the control (P less than 0.01) and chronic disease groups (P less than 0.01). After application of amiloride, the voltage change in nasal PD was greater in the CF group than in the non-CF control groups (P less than 0.01). There were no clinically significant differences in the PD of the palm, wrist, or fingertips of the three groups. These data confirm the observation that patients with CF have hyperpolarized nasal epithelia that demonstrate greater change in response to amiloride than that in non-CF controls. These results indicate a possible role for the use of in vivo nasal PD measurements as a diagnostic test for cystic fibrosis.
We studied airway reactivity (AR) to aerosolized histamine, carbachol, and citric acid in lambs 1 mo of age to adulthood. Awake lambs were intubated and studied in a plethysmograph that measured dynamic compliance (Cdyn), resistance of the lung (RL), and functional residual capacity (FRC). Pleural pressure was measured using a Silastic balloon in the pleural space, and airway opening pressure (Pao) was measured using a catheter placed 1-2 cm distal to the nasotracheal tube. At the ages of 1, 3, 5, and 7 mo and adulthood, measurements of Cdyn, RL, and FRC were obtained in 46 sheep (22 males, 24 females). AR to carbachol, histamine, and citric acid was measured in each sheep in randomized order on three separate days by giving increasing concentrations of the drug in a noncumulative fashion. The dose that would have caused a 35% reduction in Cdyn (ED65Cdyn), a doubling of RL (ED200RL), or a 50% increase in FRC (ED150FRC) was calculated. In both males and females, base-line Cdyn increased (r = 0.81, P less than 0.01) with age, as did FRC (r = 0.87, P less than 0.01). There was no significant change in RL in either sex with age or in the group as a whole. There was a significant increase in AR to both histamine and carbachol with increasing age as measured by a decrease in ED65Cdyn (P less than 0.01 and P less than 0.05, respectively) with age. There was no significant change in AR with age as measured by RL or FRC for any of the three bronchoconstrictors tested.(ABSTRACT TRUNCATED AT 250 WORDS)
Pulmonary alveolar proteinosis is a rare disease that usually affects the adult patient, but is now being recognized as a possible cause of neonatal respiratory distress. In the adult patient, whole lung lavage, as described by Ramirez-R in 1965, is considered the most effective therapy for management of this condition. The lavage can be accomplished safely and with relative ease by using a Carlens or Robertshaw tube to isolate and lavage one lung while ventilating the other. The unavailability of a small double-lumen tube makes this procedure impossible in the pediatric age group. Therefore, whole lung lavage has been possible in only a few children in the past with the help of cardiopulmonary bypass to allow simultaneous oxygenation during the pulmonary lavage. Due to the hazards and technical difficulties of cardiopulmonary bypass, total pulmonary lavage can not be considered a practical option in the very small infant. A 15-week-old infant is reported, weighing 2 kg with a diagnosis of pulmonary alveolar proteinosis, who underwent total pulmonary lavage safely on three different occasions without employing cardiopulmonary bypass. A double-lumen Swan-Ganz catheter, introduced transbronchoscopically through the side-arm of a rigid, 3.5-mm Storz bronchoscope was used to isolate and lavage one lung while ventilation to the other lung was maintained through the bronchoscope. A Nellcor oximeter, utilized for transcutaneous monitoring, revealed satisfactory oxygen saturation during the entire pulmonary lavage. The transbronchoscopic lavage was monitored under direct vision with a video monitor, ensuring correct position of the bronchoscope and the catheter at all times.(ABSTRACT TRUNCATED AT 250 WORDS)
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