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while air from the caudal air sac travels up the mediodorsales and parabronchi and ending
in the cranial air sacs, completing one respiratory cycle.
Three types of chemoreceptors in birds undertake regulation of the respiratory
cycle. They are the intrapulmonary chemoreceptors (IPC), arterial chemoreceptors, and
the central chemoreceptors. IPCs, which are located in the lungs function similar to
pulmonary stretch receptors in mammals in that they regulate breath size and arterial
PCO2 levels. IPCs regulate ventilation by decreasing breath size as their activity
becomes more frequent (Sturkies). IPC activity is inversely proportional to PCO2 levels,
as PCO2 levels increase, the firing rate of IPCs decrease (Sturkies). Arterial
chemoreceptors are located in the carotid/ thoracic bodies and are innervated by the
vagus nerve. They are sensitive to changes in pH, CO2, and O2 levels and are stimulated
in birds during hypoxia, showing increased action potential frequency as the level of O2
decreases causing an increase in ventilation (Sturkies). The final type of chemoreceptor,
central chemoreceptors lie in respiratory control centers in the brain stem. Central
chemoreceptors, which respond to hypercapnic hypoxia, increase action potential
frequency, causing the depth and rate of respiration to increase (cite).
Consequently, we can postulate that the effect of increasing CO2 inspiration in the
avian lung causes a concerted effort from all three chemoreceptors to increase ventilatory
efforts in a counter balance fashion in order to bring CO2 levels back to the physiological
standard. IPC activity decreases as CO2 levels increase which allows a deeper breath size,
while arterial and chemoreceptor activity increases, causing respiration in the bird to
become deeper and more frequent. Also in the addition of DNP, which causes protons in
the mitochondria to leak, thus uncoupling electron transport and phosphorylation
reactions makes ATP synthesis less efficient (cite). As a result hyper metabolism occurs
to compensate for the inefficiency, which causes local accumulation of CO2 in the tissue,
strengthening the effect of this chemoreceptor regulation causing a further increase in
respired volume.
Methods
In this study white leghorn chickens (Gallus Domesticus) were anesthetized using
a combination of sodium pentobarbital, diazepam, and ketamine. Initial anesthesia was
administered through the medial petal vein in order to prepare the chicken for surgery
(lab manual). Once an appropriate plane of anesthesia was determined, the chicken was
cannulated in the specific order of the ulnar vein, trachea, carotid artery, and the caudal
thoracic airsac (lab manual). For a more in depth look at the procedure look at the NPB
111L lab manual pages 9-21 for an in depth description on the procedures. The ulnar vein
was cannulated in order to introduce anesthesia during the experiment using a dual
stopcock with a large syringe filled with heparinized saline and a smaller syringe filled
with anesthetic which was injected via PE90 tubing (lab). Tracheal cannulation was done
in order to introduce artificial ventilation from the MKS. Carotid arteries were cannulated
in order to observe blood pressure from a blood pressure transducer. The air sac was
cannulated in order to measure oscillatory pressure.
Three direct measurements were made: core body temperature, pressure between
air in the caudal thoracic air sac and the air outside of the trachea, and gas flow during
respiration. The plethysmographic transducer was used to measure the pressure of the
caudal thoracic air sac and the trachea. The pneumotachometer and the statham pressure
transducer were used to measure the flow of gas as the bird respired.
Results
Temperatur
e
Tidal
Volume
Expiratory
Tidal
Volume
Inspiratory
Respiratory
Rate
Minute
Ventilation
Heart Rate
Mean
Arterial
Pressure
Systolic
Diastolic
Pulse
Pressure
Temperatur
e
Tidal
Volume
Expiratory
Tidal
Volume
Inspiratory
Respiratory
Rate
Minute
Ventilation
Heart Rate
4% CO2
34.2
Control
End
34
mL
19.5
16.2
18.5
28.4
18.1
mL
18.7
16.7
21.1
25.7
16.8
BPM
(Breaths
)
mL/min
11.6
16.1
8.5
15.5
14.34
310
311
417
449
259
BPM
(Beats)
mmHg
155
136
174
165
172
62
59
54
62
64
mmHg
mmHg
mmHg
103
42
61
106
35
71
106
28
78
107
40
67
101
45
56
4% CO2
34.57
Control
End
34.6
18.9
22
25.6
28
21.6
mL
17
20
21
27.3
18.4
BPM
(Breaths
)
mL/min
22.3
26
28
28.9
27
425
626
758
970
755
BPM
(Beats)
224
250
254
263
208
Mean
mmHg
68
64
69
119
77
Arterial
Pressure
Systolic
mmHg
109
113
116
136
118
Diastolic
mmHg
47
40
46
110
57
Pulse
mmHg
62
73
70
26
61
Pressure
Data was gathered and analyzed using Biopac BSL analysis 4.0. For all of the
tabulated values the I-beam tool was used to highlight sections of the graph of the raw
data. Temperature was calculated using the mean function in Biopac and sampling
approximately 10 seconds of data. Inspiratory tidal volume was calculated from the
tracheal airflow raw data source channel using the negative integration function and
highlighting the tracheal flow from peak to trough. Expiratory tidal volume was
calculated from the same data channel as the inspiratory tidal volume but used the
positive integration function. Respiratory rate was calculated from the airflow raw data
source channel and used the RR function where the window was set from 5-60. Minute
Ventilation was calculated by multiplying expiratory tidal volume and respiratory rate.
Post DNP
33.8
33.6
0 0.5 1 1.5 2 2.5 3 3.5 4 4.5
% CO2
For the
cardiovascular data all measurements used the blood pressure raw data source channel,
heart rate was measured using the BPM function. Systolic pressure was gathered by using
the max function on the peak portion of the blood pressure cycle and averaged over 10
cycles. Diastolic pressure was measured in the same way but used the min function on the
trough portion of the blood pressure. Mean arterial pressure (MAP) was calculated using
the formula [(2 x diastolic)+systolic]/3. Pulse pressure was calculated by subtracting the
systolic and diastolic pressures.
Post DNP
5
0
0 0.5 1 1.5 2 2.5 3 3.5 4 4.5
% CO2
Figure
A shows the relationship between core temperature as % CO2 inspired by the chicken
increased. As % CO2 increased so did the core body temperature, which is modeled by
both trend lines showing a positive slope. Between the pre DNP and the Post DNP
injection trials, the average temperature for the post DNP trials had a higher core body
temperature than the pre DNP trials, which is also evident in the trend line for the post
DNP trial being shifted farther up than the pre DNP trials.
Post DNP
5
0
0 0.5 1 1.5 2 2.5 3 3.5 4 4.5
% CO2
DNP plays a
hand in increasing inspiratory tidal volumes.
Post DNP
10
5
0
0 0.5 1 1.5 2 2.5 3 3.5 4 4.5
% CO2
In figure D
respiratory frequencies are plotted against increasing CO2 levels. Like the previous
figures the pre DNP and post DNP trend lines showed a positive slope, which meant that
respiratory rate also increased as CO2 levels increased. The same upward shift of the
trend line was also observed between the pre and post DNP injection trials in figure D. As
a result post DNP respiratory rate also higher than the pre DNP respiratory rate.
200
0
0 0.5 1 1.5 2 2.5 3 3.5 4 4.5
% CO2
is guided by the interaction of all 3 sets of chemoreceptors in the bird. This idea is
supported in a similar study done by (M.R Fedde et al). In this study ventilatory
sensitivity in response to the inspiration of low CO2 partial pressures were used to test the
idea that IPCs are not the sole chemoreceptors used in response to counteract a rise in
arterial CO2 levels. As inspiration of CO2 partial pressure increased in the study tidal
volume, minute ventilation and arterial CO2 also increased while respiratory frequency
stayed the same. These results indicate that at low partial pressures of CO2 (where IPC
inhibition of tidal volume is the greatest) an observed increase in Vm and tidal volume
indicates that arterial and central chemoreceptors are responsible for the increase in
ventilatory efforts (M.R Fedde).
Effects of DNP
In figures A-E post injection trials of DNP show higher overall body temperature,
tidal volume, respiratory rate, and minute ventilation as inspired CO2 increases. This is
due to the physiological mechanism of DNP as an uncoupler allowing H+ to leak and
makes energy production inefficient. As a result the cell enters hyper metabolism in order
to bring energy production back to normal. A consequence of hyper metabolism is the
accumulation of CO2 and H+ in the blood and tissues causing an elevation of blood CO2
levels that affects ventilatory effort by increasing the signal frequencies of central and
arterial chemoreceptors leading to a stronger response. A study done by (Gleeson)
demonstrated this effect. In this study, respiratory adjustments of DNP were measured,
specifically tidal volume (TV), oxygen consumption (VO2), Vm and blood CO2 (PaCO2)
levels. An Injection of DNP was associated with an increase in VO2, and Vm from the
control however PaCO2 and TV initially increased then returned to control values after 10
seconds (Gleeson). This study suggests that only the central and arterial chemoreceptors