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EFFECTS OF INDUCED RESPIRATORY CHANGES ON CARDIAC, VENTILATORY, AND THERMOREGULATORY PARAMETERS IN HEALTHY SPRAGUE-DAWLEY RATS
Citation:
Wichers, L. B., W. H. Rowan, D L. Costa, W P. Watkinson, AND M. J. Campen. EFFECTS OF INDUCED RESPIRATORY CHANGES ON CARDIAC, VENTILATORY, AND THERMOREGULATORY PARAMETERS IN HEALTHY SPRAGUE-DAWLEY RATS. Presented at American Thoracic Society, Orlando, FL, May 21-26, 2004.
Description:
EFFECTS OF INDUCED RESPIRATORY CHANGES ON CARDIAC, VENTILATORY, AND THERMOREGULATORY PARAMETERS IN HEALTHY SPRAGUE-DAWLEY RATS. LB Wichers1, WH Rowan2, DL Costa2, MJ Campen3 and WP Watkinson2 1UNC SPH, Chapel Hill, NC, USA; 2USEPA, ORD/NHEERL/ETD/PTB, RTP, NC, USA; 3LRRI, Albuquerque, NM, USA.
Numerous toxicological studies have recently employed automated whole-body plethysmography (WBP) to obtain ventilation parameters in rodents. This is a relatively new application for these systems and the data obtained are largely derived from airflow curves. The present study integrated radiotelemetry and WBP systems to gain better insight into the meaning of these derived parameters. The WBP system was validated using positive (CO2) and negative (buprenorphine) ventilatory controls. Sprague-Dawley rats (n=4) were implanted with radiotelemeters to monitor ECG, pleural pressure, and core temperature (Tco); naive animals (n=4) were subjected to the same exposure regimen as the telemetered rats. Animals were placed in WBP chambers and exposed for 5 min via whole-body inhalation to CO2 (FiCO2 = 0.05). After a 30?min recovery period, animals were injected with buprenorphine (i.p., 30 mg/kg) and returned to their respective chambers. This was followed by an additional CO2 exposure (5 min) and recovery period. Two days after CO2 and buprenorphine exposures, animals were subjected to nebulized methacholine (MCh) with doses ranging from 12?500 mg/ml. Methacholine induced progressive increases in enhanced pause (Penh) up to approximately 6 times the baseline, while 5% CO2 alone doubled Penh values. However, pleural pressure changes were greater during CO2 exposures (12.7?0.7 mmHg) than during 500 mg/ml MCh (8.6?1.9 mmHg). Lung compliance decreased 18% during 500 mg/ml MCh, but remained essentially unchanged in response to CO2. Additionally, we observed decreases in HR (20-100 bpm) and Tco ( 0.2 C) in telemetered rats with initial CO2 exposure. This experimental design provides a novel approach to substantiate data obtained from WBP and is a useful methodology for simultaneous collection of cardiovascular and respiratory parameters. (Abstract does not represent USEPA policy. This research was supported in part by EPA CT826513.)