Acute Effects of Ozone on Heart Rate and Body Temperature in the Unanesthetized, Unrestrained Rat Maintained at Different Ambient Temperatures

Watkinson, William P.; Aileru, Azeez A.; Dowd, Sean; Doerfler, Donald L.; Tepper, Jeffrey S.; Costa, Daniel L.

doi:10.3109/08958379309034498

Cited by 26 publications

(18 citation statements)

References 11 publications

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“…The acute hypothermic response to O 3 has been reported in a variety of rodent studies (Slade et al, 1997;Watkinson et al, 1993Watkinson et al, , 1996. The mechanism of action of this effect is not well understood.…”

Section: Discussionmentioning

confidence: 99%

“…Rats were weighed weekly, after the second day of O 3 exposure. An O 3 concentration of 1.0 ppm was selected for the current study because past studies have demonstrated marked hypothermic and bradycardic effects in telemetered rats exposed to this concentration (Watkinson et al, 1993(Watkinson et al, , 1996. We were unclear how the adult versus senescent animals would respond to O 3 and selected a dose that we expected to be effective over the 13-week exposure period.…”

Section: Exposuresmentioning

confidence: 99%

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Episodic ozone exposure in adult and senescent Brown Norway rats: acute and delayed effect on heart rate, core temperature and motor activity

Gordon

Johnstone

Aydin

et al. 2014

Inhalation Toxicology

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Setting exposure standards for environmental pollutants may consider the aged as a susceptible population but the few published studies assessing susceptibility of the aged to air pollutants are inconsistent. Episodic ozone (O₃) is more reflective of potential exposures occurring in human populations and could be more harmful to the aged. This study used radiotelemetry to monitor heart rate (HR), core temperature (T(c)) and motor activity (MA) in adult (9-12 months) and senescent (20-24 months) male, Brown Norway rats exposed to episodic O₃ (6 h/day of 1 ppm O₃ for 2 consecutive days/week for 13 weeks). Acute O₃ initially led to marked drops in HR and T(c). As exposures progressed each week, there was diminution in the hypothermic and bradycardic effects of O₃. Senescent rats were less affected than adults. Acute responses were exacerbated on the second day of O₃ exposure with adults exhibiting greater sensitivity. During recovery following 2 d of O₃, adult and senescent rats exhibited an elevated T(c) and HR during the day but not at night, an effect that persisted for at least 48 h after O₃ exposure. MA was elevated in adults but not senescent rats during recovery from O₃. Overall, acute effects of O₃, including reductions in HR and T(c), were attenuated in senescent rats. Autonomic responses during recovery, included an elevation in T(c) with a pattern akin to that of a fever and rise in HR that were independent of age. An attenuated inflammatory response to O₃ in senescent rats may explain the relatively heightened physiological response to O₃ in younger rats.

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Section: Discussionmentioning

confidence: 99%

Section: Exposuresmentioning

confidence: 99%

Episodic ozone exposure in adult and senescent Brown Norway rats: acute and delayed effect on heart rate, core temperature and motor activity

Gordon

Johnstone

Aydin

et al. 2014

Inhalation Toxicology

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“…With respect to nonpulmonary end points, these studies used radiotelemetry procedures to examine HR, T co , and electrocardiographic changes in rats and mice over a variety of experimental conditions. These studies were among the first to report consistent, robust concentration-related decreases in the abovementioned parameters in rodents following exposure to routine experimental levels of O 3 .…”

mentioning

confidence: 81%

Cardiovascular and Systemic Responses to Inhaled Pollutants in Rodents: Effects of Ozone and Particulate Matter

Watkinson¹,

Campen²,

Nolan³

et al. 2001

Environmental Health Perspectives

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539Over the past decade our laboratory has been investigating the nature and extent of specific extrapulmonary responses observed in rodents following exposure to ambient pollutants and other xenobiotic agents. These responses are characterized by primary decreases in important indices of cardiac and thermoregulatory functions, along with secondary decreases in associated parameters. The summation of these effects, termed the hypothermic response (1), has both physiological and behavioral components, appears to be most pronounced in (and possibly unique to) the rodent, and may significantly impact the interpretation of experimental data and its subsequent extrapolation to the human situation. Typically, healthy adult rats may exhibit decreases in heart rate (HR) of 50-100 beats per minute (bpm) and decreases in core temperature (T co ) of 1.5-2.5°C following routine exposures to moderate levels of ambient pollutants, such as ozone (O 3 ) or particulate matter (PM). In addition, there appear to be similar, albeit related, decreases in other functional parameters, including metabolism, minute ventilation, blood pressure, and cardiac output. Furthermore, it has been demonstrated that the magnitudes of these observed decreases may be significantly modulated by changes in experimental conditions. For example, experimental stresses related to exercise, restraint, and handling, as well as the imposition of changes in ambient temperature (T a ), have all been shown to have profound effects on these responses. Finally, it has been proposed that a moderate hypothermic response may afford protection and improve survivability following toxic exposures, whereas a more severe response may actually potentiate the toxicity. Although the underlying mechanisms of the hypothermic response are still largely unexplored and unknown, preliminary experimental evidence suggests that these effects may be mediated, at least partly, via components of the parasympathetic nervous system. O 3 is a ubiquitous ambient pollutant and a known pulmonary irritant (2). In a series of earlier studies from our laboratory (3-6), we investigated both the pulmonary and systemic consequences of O 3 exposures (0.25-2.0 ppm) in rodents. With respect to nonpulmonary end points, these studies used radiotelemetry procedures to examine HR, T co , and electrocardiographic changes in rats and mice over a variety of experimental conditions. These studies were among the first to report consistent, robust concentration-related decreases in the abovementioned parameters in rodents following exposure to routine experimental levels of O 3 .More recently, the putative toxicity of PM has attracted considerable attention, and numerous epidemiological studies published over the last few years have reported a slight but consistent association between the concentration of ambient PM and the incidence of adverse health effects in man (7-12). Despite limited supporting experimental evidence, there is a growing consensus that higher levels of PM in the air are associated with in...

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“…Similar studies have shown that when O 3 exposure is repeated daily, some of the pulmonary effects attenuate as the exposures continue (6,13,17,25). An inhalation experiment in rats from our laboratory has also demonstrated that the magnitudes of selected extrapulmonary responses consequent to O 3 exposure, e.g., decreases in heart rate (HR) and core body temperature (T co ), are concentration related and can be modified by changing ambient temperature (T a ) during the exposure (29). Presently, little is known about the influence of T a on O 3 toxicity and adaptation in the lung.…”

mentioning

confidence: 57%

Ozone toxicity in the rat. III. Effect of changes in ambient temperature on pulmonary parameters

Wiester

Watkinson

Costa

et al. 1996

Journal of Applied Physiology

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Pulmonary toxicity of ozone (O3) was examined in adult male Fischer 344 rats exposed to 0.5 parts/million O3 for either 6 or 23 h/day over 5 days while maintained at an ambient temperature (Ta) of either 10, 22, or 34 degrees C. Toxicity was evaluated by using changes in lung volumes and the concentrations of constituents of bronchoalveolar lavage fluid that signal lung injury and/or inflammation. Results indicated that toxicity increased as Ta decreased. Exposures conducted at 10 degrees C were associated with the greatest decreases in body weight and total lung capacity and the greatest increases in lavageable protein, lysozyme, alkaline phosphatase activity, and percent neutrophils. O3 effects not modified by Ta included increases in residual volume and lavageable potassium, glucose, urea, and ascorbic acid with exposure at 34 degrees C. Most effects were attenuated during the 5 exposure days and/or returned to normal levels after 7 air recovery days, regardless of prior O3 exposure or Ta. It is possible that Ta-induced changes in metabolic rate may have altered ventilation and, therefore, the O3 doses among rats exposed at the three different Ta levels.

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Acute Effects of Ozone on Heart Rate and Body Temperature in the Unanesthetized, Unrestrained Rat Maintained at Different Ambient Temperatures

Cited by 26 publications

References 11 publications

Episodic ozone exposure in adult and senescent Brown Norway rats: acute and delayed effect on heart rate, core temperature and motor activity

Episodic ozone exposure in adult and senescent Brown Norway rats: acute and delayed effect on heart rate, core temperature and motor activity

Cardiovascular and Systemic Responses to Inhaled Pollutants in Rodents: Effects of Ozone and Particulate Matter

Ozone toxicity in the rat. III. Effect of changes in ambient temperature on pulmonary parameters

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