9.2 Arterial And Cardiopulmonary Reflexes Flashcards
State the key terminology used from the key paper of Raven et al (2005)??
Threshold : increases in carotid sinus pressure decrease MAP/HR
Saturation : further increase in CSP have no effect on MAP/HR
Slope : gain / sensitivity of the system
Max gain : the sensitivity at the centre point.
Disucss Smyth et al (1969) and their use of the oxford method??
IV infusion of angiotensin increased vasoconstriction and blood pressure.
Gave graded doses of 0.25ug to produce rises in SBP of 25-35mmhg. Also showed an increase in the R-R interval - but requires medical supervision and is exercise restricted.
Correlation between SBP and R-R interval (r=0.93)
Discuss Fadel et al (2013) - variable pressure neck chamber??
This is a fully automated non-invasive method.
Stimulate the carotid sinus receptors and oscillatory neck pressure loads the carotid baroreceptor, oscillatory neck suction unloads the carotid baroreceptor.
This method can be used to investigate dynamic relationship between the carotid baroreflex and physiological variables (e.g. HR/ABP/MSNA/BF).
Discuss the key paper from Sheriff (1990)??
Looked at denervation of sino-aortic baroreceptors in mild treadmill running dogs
Results showed an increase in ABP became unrestrained ~doubled the pressor responses - indicated that ABR control of ABP was functional during exercise therefore ABR was necessary for the normal CV response to exercise.
Discuss the resetting of the carotid baroreflex (Fadel and Raven, 2011)???
The CP : equal depressor and pressor responses to BP change
The OP : pre stimulus BP
Response curves HR and BP progressively rest during ex in an intensity dependent manner with no sig changes in sensitivity.
For HR : OP moves away from the CP and closer to the
threshold , which results in a reduction in the response range of HR - which is a more optimal position to counter hypertensive stimuli
For MAP : OP remains close to CP
Discuss Carrington (2002)???
Looked at central command and the baroreflex.
P’s performed voluntary (CC and EPR) and involuntary (EPR) exercise with circulatory occlusion during and post exercise.
For both groups, the SBP is greater in voluntary than invoked contraction.
For baroreflex sensitivity, reduced in the older group relative to young in both forms of exercise.
The rightward shift in the regression indicating the ‘resetting’ of the baroreflex, which shows the large influence that CC has on resetting the baroreflex.
- this is limited by ex intensity
Ogoh (2003) looked at exercise intensity :- investigated the contribution of CO and TVC to CBR mediated changes in MAP, how and what did he find??
Performed mild to heavy ex x3 20 min cycling at 90/120/150 b/min.
5 second pulses of neck pressure and neck suctions from +40 to -80 torr.
Showed no changes in SV either at rest or during exercise. The CBR-mediated changes in CO were due to reflex changes in HR.
Showed that carotid-cardiac and carotid-MAP response curves were reset upward and rightward during exercise with no change in sensitivity.
The operating and response ranges were unchanged from rest to heavy exercise.
Discuss Raven et al (2005)??
As exercise intensity increased :
- %Q progressively decreased @time of the peak HR response?
- small %contribution of Q at rest was eliminated with even mild exercise @ peak MAP response.
- %TVC at the time of both the peak HR response and the peak MAP response ⬆️ with exercise intensity
Discuss Gallagher (2001)??
Had subjects perform a 3.5 min knee ext (20%mvc) and then 7 minutes of cycling (20% Vo2 max)
He measured carotid baroreflex function via neck collar pressure.
For MAP - for static at time points Ex2-Ex3, MAS (antishock trousers to simulate afferent feedback). For dynamic at all time points other than rest, MAS significantly higher.
Also, EPR activation resets at the carotid-cardiac baroreflex curve rightward only to higher operating pressures (Op remains close to the CP). EPR acts as modulator in resetting the carotid baroreflex due to feedback nature of the EPR.
Discuss orthostatic hypotension (Stewart and Clarke, 2011)??
The orthostatic component of ‘lightheadedness’ or ‘dizziness’ on rapid standing - you could faint.
These transient dissipate after 30-60 seconds
HR increases as BP fall.
Discuss the key literature of (Walker, 1980)?? Who investigated the interactions of CPR and EPR, discuss the methodology
CPR manipulation via :⬇️CBV via 5 mmhg LBNP to reduce loading on cardiopulmonary receptors - results in ⬆️CPR, ⬆️SNS , ⬆️vascular resistance
EPR manipulation via : 2 min static handgrip, 10% MVC (metabolic washout), 20% MVC (no metabolic washout)
Discuss the key literature of (Walker, 1980)?? Who investigated the interactions of CPR and EPR, discuss the results found ?
The results indicated an interaction between the CPR and EPR.
LBNP + Hg(20%) was significantly higher for MAP delta change, sig lower (as was LBNP +Hg(10%)) for forearm blood flow delta change. Both these were sig higher for forearm vascular resistance delta change. No signifance to HR.
WhAt is LBNP (Tyako et al, 2016)????
Stimulates orthostasis by lower body suction , draws blood from upper to lower half of the body (mild - 20mmhg, moderate - 50mmhg)
MAP remains stable, CVP drops.
Discuss Ogah (2007) who investigated the role of CBV on BR function during dynamic exercise??
Upright vs supine cycling (60-80rpm) (enhance muscle pump) - same o2 uptake, same CC and EPR response.
⬆️CBV relocated the carotid - MAP BR function curve downward and leftward.
⬆️CBV during exercise resulted in significant BP reductions at same exercise intensity
⬆️CBV and loading the CBR reduced ex induced increased in MAP and CBR resetting.
- demonstrates CBV influences CBR resetting during dynamic exercise
