MindMap Gallery Blood circulation (2)
This is a mind map about blood circulation (2), including working cells, transmembrane potential and its formation mechanism, transmembrane potential of autonomous cells and its formation mechanism, and physiological characteristics of myocardium.
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Blood circulation (2)
Working cell transmembrane potential and its formation mechanism (atrial myocardium, ventricular myocardium)
ventricle
resting potential
Ik1 (inward rectifying potassium channel)
Non-gated ion channel, affected by membrane potential
depolarization off
Action potential
Issue 0
Fast sodium channels open
Depolarization reaches threshold, sodium current exceeds potassium outward current, and further membrane depolarization is positive feedback
TTX blockade by tetrodotoxin
T-type calcium channel
Issue 1
Clockwise outward current Ito
-30mV is activated
4-aminopyridine blocking
Obvious species differences
Chlorine current
Under the action of catecholamines or when sympathetic nerves are excited, the effect cannot be ignored.
spike potential
Phase 2 (platform phase)
①Asymmetry ②Long duration
L-type calcium channel
-30~-40mV
Activation, deactivation, and resurrection are slow
Current is greater than T type
Permeability is less than that of sodium ions
Delayed rectifier potassium current Ik
Early stage: counteracting L calcium Late stage: main ion flow leading to membrane repolarization
Issue 3
Ik delayed rectification current
Ik1 inward rectifier potassium current
Issue 4
sodium potassium pump
Sodium calcium exchanger 3na 1 calcium
atrium
Resting potential-80
Ito is developed - Stage 2 is not obvious - Stage 2 and Stage 3 are difficult to distinguish
Acetylcholine-sensitive potassium current—K efflux is enhanced and superscheduled—action potential time is significantly shortened
Transmembrane potential of autonomous cells and its formation mechanism
Purkinje cells
4th phase automatic depolarization
Inward ion current If
Inward ion flow that increases over time
If mainly sodium ions
If starts to activate when repolarizing to -60mV, and fully activates when it reaches -100mV
If depolarizes to -50mV in phase 0 and terminates
Cesium Cs blocking
Potassium ion efflux progressively decreases
sinoatrial node cells
Maximum repolarization potential-70mV
The cell membrane lacks Ina channels, and phase 0 production mainly relies on L-type calcium channels, so it is significantly affected by the extracellular calcium ion concentration.
Phase 3 Ik is open and L-type calcium channels are inactivated
Phase 4 Ik off (main) - automatic depolarization
Physiological characteristics of myocardium
Excitability
Prerequisite: Na channel is in standby state
cyclical changes
Valid refractory period
absolute refractory period
local reaction period
Complete tetanic contraction does not occur
Ensure ventricular diastolic alternation
(premature) contraction - compensatory pause
Relative refractory period—sodium ion channels are basically resurrected
supernormal period
Sodium ion channel is completely resurrected - the difference between resting potential and threshold potential
Influencing factors - resting potential, threshold potential level, ion channel properties causing phase 0 depolarization
conductivity
conduction pathway
Sinoatrial node begins - slowest: atrioventricular junction, fastest: Purkinje fibers
Influencing factors
Structural factors: diameter
Physiological factors: phase 0 speed and amplitude, membrane potential level, excitability of membranes adjacent to unexcited parts