Week 3 Flashcards
What is the difference between arteries and veins?
Arteries take blood from the heart, veins take blood to the heart
What are the consequences of the increase in the surface of capillaries?
- Larger surface (more options for transfer)
- Slower speed (more time for transfer)
- Lower pressure (capillaries are fragile)
What is the Bohr effect?
Heme-iron binds oxygen in the lung where the pH is high and releases in tissues where the pH is low.
What is the optimal BP?
Lower than 120/80
In which blood vessels is BP measured?
Large arteries in systemic circuit
What is pulse pressure?
systolic - diastolic
What is MAP?
Mean arterial pressure: diastolic + 1/3 pulse pressure
What is the immediate response to a change in BP?
baroreceptors in carotid arteries sense pressure -> ANS -> change in cardiac output or vascular resistance
What is the longer term response to a change in BP?
- less vasopressin
- RAAS: low BP -> renin (from kidney) -> angiotensinogen (from liver) into angiotensin I -> ACE converts I into II -> secretion of aldosterone -> aldosterone and angiotensin II: kidney, retain water and salt in the body. Angiotensin II also is a powerful vasoconstrictor.
- Natriuretic peptides (ANPs): vessel dilation, decrease sodium reabsorption, supress RAAS, suppress ANS
What happens when there is a high water intake?
o Higher ECF volume -> kidneys excrete salt and water (slow) -> normal osmolarity
o Higher BP -> ANS lowers BP (rapid) -> normal osmolarity
What is excitation-contraction coupling?
Action potential spreads through transverse tubules to the sarcoplasmic reticulum -> release of calcium from the SR -> calcium binds to troponin to expose active sites on the actin filament -> cross-bridge cycling and muscle contraction.
Action potential Calcium Troponin Expose actin Contraction
What are the treatments of AF?
Electrical cardioversion Surgical ablation Pharmacological cardioversion Anticoagulation to avoid stroke Symptom control Lifestyle changes
What are the three types of AF remodelling?
- electrical; reduced calcium transient (1 day)
- metabolic; mitochondrial dysfunction/ oxidative stress (continuous)
- structural; degradation of contractile proteins (long term)
What are possible compounds that could decrease cardiac diseases?
Vit B3 and vitamin C
Vit D3 and n-3 not much evidence
What is done for cardiac reperfusion?
PCI; go in arteries with a catheter
What are the mechanisms of IRI?
- free radical damage
- inflammation
- influx of calcium
Explain what ROS damage does in the mechanism of IRI
Free radical damage; damaged mitochondria produce ROS due to incomplete reduction of oxygen and by infiltrating leukocytes. Reperfusion -> more ROS -> lipid peroxidation and protein modifications (membrane damage, protein breakdown and DNA mutations).
Explain what inflammation does in the mechanism of IRI
Inflammation; influx of leukocytes, plasma protein and cytokines
Explain what calcium influx does in the mechanism of IRI
Influx of calcium; during ischemia, SR is damaged, so it doesn’t recycle calcium -> toxic amount of calcium in muscle cell -> hypercontraction.
Explain the function of HIF1
Gene transcription (EPO, Slc2a1 and VEGF).
What does VEGR do?
Angiogenesis
What does EPO do?
Erythropoiesis
What does Slc2a1 do?
Increase glucose supply
What causes HIF1-alpha knock out mice to die?
Cardiac and vascular defects and decreased RBC production
