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Flashcards in Neural Control of the Heart Deck (17)
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1

Key sympathetic areas of the brain?

CVLM, RVLM, IML

2

Key parasympathetic areas of the brain?

NA, DMNX

3

How was NA pinpointed as an important area?

1) Horsradish peroxidase
2) Antidromic recordings of cardiac branches
3) Micriontophoresis of exciting AAs onto cells of NA

4

NA group axon?s? Resp and baro modulation?

B-fibre axons, discharge pattern shows strong baro and resp modulation

5

DVMN group axons? Resp and baro modulation?

C-fibres axons. No resp or baro modulation.

6

Explain why you would use PI or HR

PI mirrors vagal firing to the heart. Linear relationship between PI and freq of stimulation of R and L cervical vagus nerves.

HR relates directly to CO (double HR, double CO if SV remains =)

7

Time course of sympathetic cf parasympathetic stimulation of the heart and the termination of these effects

Parasympathetic much quicker. Can cut a heart beat short if arrives at correct moment. R > L .

Parasympathetic terminated quicker. Acetylcholinesterase. NA terminated by re-uptake of adrenaline, although some enzymatic breakdown and diffusion away.

8

Effects of ACh on heart

1. Via MuscR via G-proteins to K-ACh to hyperpolarise membrane.

2. Via Musc-R and Gi proteins to reduced AC activity, reduce cAMP and inhibit if current, reducing slope of pacemaker potential.

9

Effect of timing of burst of vagal stimulation arriving at heart?

> slowing if arrives later in cycling. Important to consider when studying other relfexes which involve vagus, eg baroreflex

10

Effect catecholamines on the heart?

1. Increases opening if channels, increasing slope of pacemaker current (+ chronotropic)

2. cAMP also activates PKA which, via phosphorylation, increases the number of functional L-type Ca2+ channels in membrnae, increasing the plateau current and increasing the Ca2+ store and hence the contractile force (+ve inotropic effect). Increased Ca2+ influx in SAN also contributes to +ve chronotropic.

3. Phosphorylates phospholamban, reduces it's inhibitory effect on the SR Ca2+ ATPase pumps (SERCA). It also speeds up re-uptake of Ca2+ by SR, shortening contraction period (lusitropic effect), important for maintaining diastolic filling at higher HRs.

4. Phosphorylated delayed rectifier K+ channels, increases repolarizing outwards iK and shortens AP

11

Define an increase in contractility

An increased energy of contraction from a given initial muscle length (therefore excludes Starling mechanism)

12

What is dP/dt max ? +/-

Maximum rate of increase in left ventricular pressure.

Relatively easy to measure but need a LV pressure measuring system with a good freq response. Detects rapids changes in contractility.

Not a complete pure index of contractility, it is affected to som extent by changes in ventricular contractility.

13

What is Emax?

Slope of line joining end-systolic points on pressure-volume loops.

A good index of contractility. Not affected by changing preload.

Needs measurement of both LV pressure and volume and a means of varying ventricular volume.

14

What two things must be controlled due to their effect on contractility?

HR - Bowditch effect

Afterload - Anrep effect

15

Does the vagus have a direct effect on ventricular and atrial contractility? Any human evidence?

YES for both. Cardiac pacing of a dog heart whilst stimulating vagus led to reduction in contractility as assessed by Emax.

In IHD patients, L thoracic vagal stimulatin seem to reduce Emax. Although subjects were undergoing bypass and were pathological.

16

What is accentuated antagonism? Where is this seen?

Simultaneous symp and parasympathetic stimulation has a greater effect (PS effect) than the PS effect alone.

Effect seen in HR and contractility control.

17

What is HRV? High and low freq? What is it associated with?

Heart Rate Variability.

Low = sympathetic
High = parasympathetic

Higher HRV associated with > survival post-MI