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Flashcards in Integration of Reflexes Deck (20)
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Why is the HR and TPR response to the chemoreflex variable?

Chemoreflex = bradyycardia, vasoconstriction and an increase in ventilation.

But the increase in VE can activate SAR which cause a vasodilation and a tachycardia.


How can two reflexes interact?

Change operating point, curve shifts to right. This may alter sensitivity at the extremes due to maximal stimulation and extreme inhibition at either ends respectively. Should always look at responses in mid-range.

Change sensitivity.

Shift curve up = no change in one variable despite an increase in the other.


What is respiratory sinus arrhythmia?

Lung afferents inhibit CVMN -> decrease HR

Large stretch of lung -> activate HB reflex -> inhibiton of respiratory drive -> lack of inhibition of CVMN -> increase in HR


What are the probable sites for respiratory modulation of central respiratory drive?

1. Pre-synaptic inhibition of baro-R afferents
2. NTS neurones
3. inhibition of excitatory interneurones to CVMs
4. the CVMs


What is the evidence against pre-synpatic inhibition of Baro-R afferents

Their membrane potentials dont show resp modulation


Evidence against inhibition of NTS neurones?

Little convergence of neurones which show both cardiac and respiratory rhythm


Evidence against inhibition of excitatory neurons to CVM/inhibition of CVM itself

Apply excitatory AA DLH to CVM. Causes response to CSN stimulation even during inspiration. Therefore Baro-R is still reaching CVM, so gating cannot be earlier in that path.


Where is the main site of respiratory modulation of CVM?

At the CVM itself due to input from inspiratory drive. Input is ACh, as atropine abolishes resp modulation of CVM discharge.

Some gating by pulmonary SARs


Who first demonstrated the dive reflex?

Bert, 1870

Bradycardia of breath holding more profound with head immersion in water than in air


What nerve supplies the R on the face which are activated by the dive reflex?

V1, V2


Dive reflex?

Reduced CO
Widespread vasoconstrcition
? small rise in BP in man


What maintains the bradycardia?

Activation of CB due to hypoxia/hypercapnia. Hyperoxic blood prevented the bradycardia.


What happens to BP and blood flow?

BP stays the same in the seal.

Blood flow pretty much stops in aorta and renal circulation. Brain only area preserved.


What does the apnoea do?

Maintains bradycardia. The chemo-R would otherwise cause an increase in ventilation, stimulate lung receptors and cause a tachycardia.


Any effect on the spleen during diving?

Yes. Contracts. Supply RBCs? HCT and Hb concentration seen to fall following dive


What is the effect of breath holding in expiration?

Greater bradycardia. Lack of central insp drive or pulm receptor stimulation inhibitng CVMs


Is the dive reflex oxygen conserving in man?

Facial immersion decreased the falli n oxygen saturation in trained breath-hold divers (Andersson 2002)


Stimulus and response of the defence/alerting response?

Stimulus = anything unexpected, novel, noxious. Species and individual specific. Hypoxia

Behavioural response - ear pricking to hissing and full blown rage
CV response - tachycardia, increase contractility, vasoconstriction skin, kidney, gut, vasodilation of skeletal muscle.
Other- pupil dilation, piloerection, increased respiration


What areas of the brain are involved?

Amygdala, hypothalamus, periaqueductal grey of midbrain and medulla


Mechanism of vasodilation?

Reduced symp, adrenergic vasoconstriction
circulating adrenaline