The respiratory responses of the fowl to hot climates

1982 ◽  
Vol 97 (1) ◽  
pp. 301-309
Author(s):  
H. Kassim ◽  
A. H. Sykes

Respiratory rate (f) and tidal volume (VT) have been measured at normal and at warm ambient temperatures (Ta) in adult domestic fowl by means of a whole body plethysmograph. Resting values of f = 23 +/− 9 min-1 and of VT = 25.6 +/− 0.9 ml min-1 were found. At Ta 30, 35 or 40 degrees C f increased in direct relation to the severity of the heat stress reaching a maximum values of 273 +/− 12 min-1; VT fell uniformly in all three climates to a minimum of 9.0 +/− 0.5 ml. Total ventilation (V) showed a linear relation with f during first-phase panting. Second-phase panting occurred only at Ta 40 degrees C; V increased at first but subsequently fell as the decline in f became more pronounced.

2014 ◽  
Vol 306 (12) ◽  
pp. R951-R959 ◽  
Author(s):  
Evgeny Bondarenko ◽  
Deborah M. Hodgson ◽  
Eugene Nalivaiko

Both human and animal studies have demonstrated that respiratory parameters change in response to presentation of alerting stimuli, as well as during stress, yet central neuronal pathways that mediate such responses remain unknown. The aim of our study was to investigate the involvement of the amygdala in mediating respiratory responses to stressors of various intensities and duration. Adult male Wistar rats ( n = 8) received microinjections of GABAA agonist muscimol or saline into the amygdala bilaterally and were subjected to a respiratory recording using whole body plethysmography. Presentation of acoustic stimuli (500-ms white noise, 40–90 dB) caused transient responses in respiratory rate that were proportional to the stimulus intensity, ranging from +13 ± 9 cpm to +276 ± 67 cpm for 40- and 90-dB stimuli, respectively. Inhibition of the amygdala significantly suppressed respiratory rate responses to the high-intensity stimuli (70–90 dB). Submitting rats to the restraint stress significantly elevated the mean respiratory rate (+72 ± 8 cpm) and the dominant respiratory rate (+51 ± 12 cpm), as well as the fraction of high-frequency respiratory rate (+10 ± 3%). Inhibition of the amygdala by muscimol significantly suppressed these responses. We conclude that the amygdala is one of the key structures that are essential for expression of respiratory responses to stressful or alerting stimuli in rats.


1981 ◽  
Vol 51 (5) ◽  
pp. 1278-1286 ◽  
Author(s):  
K. A. Yamada ◽  
P. Hamosh ◽  
R. A. Gillis

Respiratory responses to activation of gamma-aminobutyric acid (GABA) receptors in the hindbrain were measured in chloralose-anesthetized cats using a Fleisch pneumotachograph. GABA receptors were activated by intracisternal injections of muscimol and GABA. Muscimol (0.05--6.65 micrograms) administered to seven animals caused a depression of respiratory activity with apnea occurring in each animal. Before apnea occurred, a decrease in tidal volume was observed (from 25.7 +/- 0.9 to 14.7 +/- 1.1 ml). Respiratory rate and inspiratory and expiratory durations were unchanged. GABA (0.05--12.15 mg) administered to five animals produced the same effect as muscimol on respiratory activity. Apnea produced by both agents was reversed by intracisternal administration of the GABA-receptor antagonist drug, bicuculline. Administration of bicuculline to four naive animals increased tidal volume (from 31.3 +/- 1.7 to 36.5 +/- 0.7 ml) but had no effect on either respiratory rate or inspiratory duration. These results indicate that activation of GABA receptors causes respiratory depression and suggest that GABA may be an important neurotransmitter in CNS neural pathways involved in regulating respiratory activity.


1983 ◽  
Vol 54 (3) ◽  
pp. 623-631 ◽  
Author(s):  
S. Iscoe ◽  
R. B. Young ◽  
D. B. Jennings

We measured tidal volume (VT) and inspiratory (TI) and expiratory (TE) durations in five conscious tracheostomized dogs breathing air or 5% CO2 in air either at normal (20 degrees C) or elevated (30 degrees C) ambient temperatures. Respiratory frequency ranged between 16 and 333/min due to changes in both TI and TE. During panting TI exceeded TE. During air inhalation instantaneous ventilation (V) spontaneously ranged from 100 to 1,600 ml . kg-1 . min-1. Hypercapnia, heat stress, or both, increased this range of V by increasing maximum V, primarily due to increases in mean inspiratory flow. Under these conditions, changes in TI accounted for more of the spontaneous changes in breath duration. During inhalation of air and 5% CO2, a positive correlation between VT and TI was obtained for TI between 0.13 and 1.05 s; above 1.05 s VT decreased. Heat stress increased VT at a given TI. We suggest that either the decay rate or position of the inspiratory off-switch threshold curve (Clark and von Euler, J. Physiol. London 222: 267, 1972) varies in conscious dogs. Shifts in either the reset (onset) value or decay rate of the curve yield a positive correlation between VT and TI. This modification to the Clark-von Euler model implies that the primary effect of anesthesia on respiratory control is fixation of the inspiratory off-switch threshold curve.


2015 ◽  
Vol 308 (10) ◽  
pp. R816-R822 ◽  
Author(s):  
Evgeny Bondarenko ◽  
Mirza I. Beig ◽  
Deborah M. Hodgson ◽  
Valdir A. Braga ◽  
Eugene Nalivaiko

The dorsomedial hypothalamus (DMH) and the perifornical area (DMH/PeF) is one of the key regions of central autonomic processing. Previous studies have established that this region contains neurons that may be involved in respiratory processing; however, this has never been tested in conscious animals. The aim of our study was to investigate the involvement of the DMH/PeF area in mediating respiratory responses to stressors of various intensities and duration. Adult male Wistar rats ( n = 8) received microinjections of GABAA agonist muscimol or saline into the DMH/PeF bilaterally and were subjected to a respiratory recording using whole body plethysmography. Presentation of acoustic stimuli (500-ms white noise) evoked transient responses in respiratory rate, proportional to the stimulus intensity, ranging from +44 ± 27 to +329 ± 31 cycles/min (cpm). Blockade of the DMH/PeF almost completely abolished respiratory rate and tidal volume responses to the 40- to 70-dB stimuli and also significantly attenuated responses to the 80- to 90-dB stimuli. Also, it significantly attenuated respiratory rate during the acclimatization period (novel environment stress). The light stimulus (30-s 2,000 lux) as well as 15-min restraint stress significantly elevated respiratory rate from 95 ± 4.0 to 236 ± 29 cpm and from 117 ± 5.2 to 189 ± 13 cpm, respectively; this response was abolished after the DMH/PeF blockade. We conclude that integrity of the DMH/PeF area is essential for generation of respiratory responses to both stressful and alerting stimuli.


2019 ◽  
Vol 19 (2) ◽  
pp. 291-304 ◽  
Author(s):  
Buhari Habibu ◽  
Lukuman Surakat Yaqub ◽  
Tavershima Dzenda ◽  
Mohammed Umaru Kawu

AbstractThis review discusses the thermal conservative and heat dissipating roles of one of the most sensitive thermoregulatory variables (respiratory rate) with the aim of enhancing its application in evaluating both cold and heat adaptation. During cold exposure, livestock enhance the economy of body heat through reduction in respiratory rate with the extent of reduction being greater and commencing at relatively higher ambient temperature in poorly adapted phenotypes. This is accompanied by an increase in tidal volume and alveolar oxygen uptake, but a decrease in partial pressure of oxygen. On the other hand, heat stress induces increase in respiratory rate to enhance evaporative heat loss with the magnitude of such increase being greater and commencing at relatively lower ambient temperature in phenotypes that are poorly-adapted to heat. This is accompanied by a decrease in tidal volume and the development of hypocapnia. The increase in respiratory rate is observed to be greater, moderate and lesser in livestock that are mainly (pigs, rabbits and poultry), moderately (sheep, goats and Bos taurus) and less (Zebu cattle) dependent on respiratory evaporative heat loss, respectively. The changes during chronic heat stress may cause acid-base crisis in all livestock, in addition to reduction in eggshell quality in birds; due to marked decrease in partial pressure of carbon dioxide and a compensatory increase in elimination of bicarbonate. Within and between breed variations in sensitivity of respiratory rhythm to both cold and heat stress has shown high applicability in identifying phenotypes that are more susceptible to thermal stress; with some cellular and metabolic changes occurring to protect the animal from the consequences of hypo- or hyper-thermia. The information in this review may provide basis for identification of genes that support or suppress thermoregulation and may also be of great use in animal breeding, genomics and selective thermal stress mitigation to provide maximum protection and comfort to poorly-adapted phenotypes.


1994 ◽  
Vol 77 (1) ◽  
pp. 434-440 ◽  
Author(s):  
J. R. Jauchem ◽  
M. R. Frei

Ketamine-anesthetized Sprague-Dawley rats were exposed to 2,450-MHz microwaves at an average power density of 60 mW/cm2 (whole body specific absorption rate of approximately 14 W/kg) until lethal temperatures were attained. The effects of propranolol (2 or 10 mg/kg body wt), nadolol (10 mg/kg), and labetalol (10 mg/kg) on physiological responses (including changes in body temperature, heart rate, blood pressure, and respiratory rate) were examined. Lethal temperatures in the labetalol and both propranolol groups were significantly lower than in saline controls. Survival time was significantly less only in the high-dose propranolol group. In all groups, heart rate increased continuously during exposure; blood pressure increased until colonic temperature reached 41–41.5 degrees C and then decreased. These heart rate and blood pressure changes were similar to those that occur during environmental heat stress. Heart rate and blood pressure changes among groups were similar. Respiratory rate, however, was significantly elevated during most of the exposure period in the high-dose propranolol animals. This change in respiration, coupled with the significantly lower survival time in these animals, suggests a vital role of respiration in susceptibility to microwave-induced heating.


1958 ◽  
Vol 51 (3) ◽  
pp. 321-324 ◽  
Author(s):  
W. Bianca

1. In experiments on three calves it was shown that, under severe heat stress, the respiratory rate at first rapidly rose from 88 to a maximum of 218 respirations/min. and then fell to 167 respirations/min., while breathing at first became shallower and then deeper.2. During the phase in which breathing became faster and shallower (panting), the heart rate rose at a mean rate of 13 beats/min. for each degree centigrade increase in rectal temperature. During the phase in which breathing became slower and deeper (‘second-phase breathing’) the mean rate of rise in heart rate was 50 beats/min. for each degree increase in rectal temperature.3. The changes in respiratory rate and in heart rate occurred at mean rectal temperatures of 40·6 and 41·0° C., respectively, and, on average, the change in respiratory rate preceded that in heart rate by 8 min.4. It is concluded that second-phase breathing was the cause of the steep increase in heart rate.5. The steep increase in heart rate is discussed in relation to heat production of the respiratory muscles.


1998 ◽  
Vol 76 (10-11) ◽  
pp. 945-951 ◽  
Author(s):  
Goran Enhorning ◽  
Sandrijn van Schaik ◽  
Claes Lundgren ◽  
Ida Vargas

A whole-body plethysmograph was used for mice. The increase in pressure caused by each inhalation was equivalent to the increase that could be calculated to result from heating and humidification of the inhaled air. However, comprehending that a drop in temperature and humidity would cause an abrupt pressure decline during exhalation was difficult. Pressure changes in the plethysmograph were also studied with an artificial chest, modeling the respiratory mechanics, but without the "inhaled" air being heated or humidified. The "chest" consisted of a metal bellows oscillated by a stepper motor 25 to 175 times per minute. Hereby air (0.05 to 0.20 mL) moved in and out of the bellows. The air passed through a polyethylene tube, the length of which was proportional to "airway resistance" and varied from 5 to 35 cm. It was found that the pressure oscillation was affected not only by "tidal volume" of the mechanical chest but also by "respiratory rate" and by "airway resistance." We concur with previous investigators that the plethysmograph pressure reflects alveolar pressure and that fluctuations cannot be explained by changes in temperature and humidity. Accordingly, tidal volume can only be qualitatively and not quantitatively assessed.Key words: tidal volume, airway resistance, respiratory rate, chest model.


2017 ◽  
Vol 95 (7) ◽  
pp. 3047
Author(s):  
S. M. Mendoza ◽  
R. D. Boyd ◽  
C. E. Zier-Rush ◽  
P. R. Ferket ◽  
K. D. Haydon ◽  
...  

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