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Flashcards in Experimental Evidence Deck (17)
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1

Alam and Smirk

1938

PECO sustained the BP response to exercise until cessation of occlusion

2

Roswell

1986

HR response was not maintained by PECO

3

McCloskey and Mitchell

1972

Group III / Group IV afferents. Used rats treated during neonatal period with capsaicin to destroy group IV and then gadolinium to block group III.

Metabosensitive = group IV
Mechanosensitive = group III

4

Coote

1971

Electrical stimulation of hind limb vental roots led to a graded response which was slower than during voluntary exercise.

Response was absolished by cutting dorsal roots

5

Coote and Gladwell

2002

Passive stretch of hind limb -> HR response, suggesting mechanoreceptors mediate the HR response to exercise

6

Krogh and Linard

1913

Immediate increase in HR and Ve which they suggested was too fast for a reflex or blood borne mechanism.

HR increase is slower in electrically stimulated exercise than during voluntary exercise

7

McCloskey

1981

NMJ blockade. BP response mirrored % MVC not absolute force, therefore mirroring RPE

8

Goodwin

1972

Vibration agonist or antagonist muscle, activating stretch reflex which reduces or increase perceived effort needed to maintain same absolute force. Stretch reflex inhibits/assists CC, not actual force generation.

HR and BP responses were either reduced or increased respectively - in proportion to effort and presumably CC

9

Lind, Taylor

1964

As time goes on EMG activity, RPE and BP and HR responses progressively increase. Similar reasoning to NMJ blockade evidence. Absolute force is the same

10

Williamson

2002

Hypnosis of easily hypnotisable subjects elicited HR, BP and RPE responses. Not seen in non-hypnotisable subjects.

11

McCubbin

1956

CSN multifibre recordings at different CSP. Control vs perinephritic hypertensive dogs

Hypertensive firing less than control
Silent at 60mmHg, normal still firing.
Baro-R reset to higher pressure, maintain rather than inhibit chronic hypertension

12

Cowley

1973

SAD dogs. = stripped adventitia around CS and AA. Treated with 5% phenol and isopropyl alcohol. Cut L cervicovagus trunk and R medial bundle of vagus.

Quiet root. Monitored BP. Showed more diurnal variation.

BP rose, then fell, 1/52 after operation stabilished at 10mmHg above control. Concluded no change when peripheral baro-R lost, therefore no role in long term control BP.

But, ? evidence presented. Used a "typical" dog, but there were some displaying great variation. 10mmHg is also a decent elevation BP, ? significance. ? housing conditions, quiet room with no stimulus.

13

Persson

1989

Denervation cardiopulmonary-R + SAD -> sustained hypertension. They concluded that SAD did not cause any long term chance in mean BP, although there was more variation, and suggested the cardipulmonary-R were able to compensate. Denervation cardiopulmonary-R + SAD --> increase in mean BP.

14

Animal model evidence long term control BP?

Baboons display a 10mmHg rise in mean BP
Rats show no change mean BP unless they are on a salt challenged diet

15

Thrasher

2004

Chronic baroreceptor unloading. AA and 1 CS denervated, the other unloaded via carotid ligation. MAP remained above control levels suggesting baroreflex can influence long term control.

16

Lohmeir

2010

Chronic electrical activation baroreflex. Even after 3weeks inhibition of sympathetic system and BP was still occuring, suggesting little or no peripheral or central adaptation.

Findings oppose initial SAD data, by proposing that the baroreceptors are able to have long term sympathetic and BP inhibitory effects during chronic activation such as that seen in hypertension.

16

Lohmeir

2010

Chronic electrical activation baroreflex. Even after 3weeks inhibition of sympathetic system and BP was still occuring, suggesting little or no peripheral or central adaptation.

Findings oppose initial SAD data, by proposing that the baroreceptors are able to have long term sympathetic and BP inhibitory effects during chronic activation such as that seen in hypertension.