Alveolar macrophages and they are involved in Phagocytosis

1. transport of O2 and substrates to cells
2. transport of CO2 and metabolites from cells
3. distribution of hormones
4. defense
5. hemostasis
6. thermoregulation

Primary – SA node
Secondary – AV node

Determinant of PRELOAD.
Increasing venous return will increase the volume of blood entering the heart during diastole (increased end diastolic volume)

-Volume Receptors: Atrial Receptors:
-Low pressure stretch receptors in the walls of the atria acting as volume receptors.
-LOCATED WHERE THERE IS LOW PRESSURE (opposite of baroreceptors)

Lysozyme: enzyme that can break down microbial membrane. It is found in the mucous lining the respiratory tract.

Atherosclerosis is when the coronary artery can get blocked. Blockage can cause impairment of oxygen supply.

Intercalated discs – they allow the cardiac muscle cells to contract in a wave-like pattern so that the heart can work as a pump.

1. Atrial contraction
2. Isovolumetric contraction
3. Rapid ejection
4. Reduced ejection
5. Isovolumetric ejection
6. Rapid filling
7. Reduced filling

-Excessive Perfusion pressure: leads to capillary damage, endothelial injury, and fluid exudation
-If perfusion is too high, this can result in fluid exudation, causing edematous changes in the tissues. This also causes damage to the capillaries due to damage to the epithelial cells that make up the capillary wall
-Seen in some cases of heart failure.

Peyer’s patches: loosely defined lymph nodes where white blood cells reside and they’re producing features. Specifically, there are beta cells that are producing antibodies known as IgA.
IgA is a specific mucosal protective antibody.
IgA is produced by the beta cells in Peyer’s Patches and when produced, IgA lines the GI tract, inhibiting microbes to bind and colonize.

What is- Which species have a Dual Circulatory System??
Fish:
• Single circulator circuit
• Heart – single atrium and single ventricle
Amphibians:
• Double circulatory circuit
• Heart – 2 atria and single ventricle
Mammals, birds, crocodilians:
• Fully developed septum that separates the atria and the ventricles
• DUAL CIRCULATORY SYSTEM!!!!!

o SA node (generates pacemaker) Atrial muscle (spreads over both atria through pathways composed of specialized myocytes) AV Node (impulse hits AV node where there’s a small pause before traveling to Bundle of His) Bundle of His Purkinje Fibers Ventricular Muscle

Allows animal or person to maintain a stroke volume and cardiac output under sympathetic conditions.
Strengthens the contractions by regulating the contractility in the myocardium.
Sympathetic nervous system influences this effect.

• Hemorrhage: see chart in binder for more
o Barorecpetors (high pressure) and atrial volume receptor (low pressure) both contribute to the restoration of blood volume (MAP)

Inflammatory response is a body’s second line of defense against invasion by pathogens. It’s an innate response that is caused by a series of events.
1. Damaged tissues release histamines, increasing blood flow to the area
2. Histamines cause capillaries to leak, releasing phagocytes and clotting factors into the wound.
3. Phagocytes engulf bacteria, dead cells, and cellular debris.
4. Platelets move out of the capillary to seal the wounded area.

1. Blood comes back to the heart (in right atrium) through the very large vein (vena cava)
2. Blood goes from RA into RV
3. RV pumps blood into lungs through pulmonary artery
4. Blood goes up into lungs, collects O2 (needed for tissues to survive), then returns from the lungs via pulmonary veins.
5. Blood travels from LA into LV
6. From LV, blood gets pumped up into aorta
7. Aorta is the major distribution channel that takes oxygenated blood back to body.

• Cardiac muscle is a functional syncytium, meaning that all cells/ mycocytes are electrically and mechanically coupled.
o Electrical coupling is important because that’s how the electrical signals spread from cell to cell via gap junctions.
o When the muscle contracts, the ability for the muscle to act as a functional syncytium depends upon these gap junctions and desmosomes (proteins) which provide stability and link all cells together.
-Gap junction (nexus) – electrochemical link
-Desmosome – anchors the cells together
-Actin filament – mechanical link

The parasympathetic nerve is able to interfere with the release of noradrenaline. The parasympathetic nerve will release ACh, which binds to the presynaptic muscarinic receptors that sit on the sympathetic nerve terminal. This reduces NAd release and we’ll no longer have a sympathetic stimulation on the atrial myocyte.
• This is how the parasympathetic system is able to affect contractility of the atrial muscle via inhibiting the function of the sympathetic system and decreasing contractility of the atrial muscle.

- Sensors: monitor pressure and whether it’s too high or low
- Integrating system: assess correctness of pressure by sending info to brain
- Effectors: mechanisms to return pressure to required levels by switching a factor on or off

• Impairment of the mucociliary escalator can lead to virus infections, trauma (dust), or toxins (ammonia). All three of these invasions can destroy the mucociliary elevator
• The mucociliary elevator: the continued movement of cilia that is involved in preventing microbes from adhering, binding, and colonizing. It serves as an important defense barrier because it facilitates continuous movement of microbes.
• When the mucociliary elevator is damaged (ex: due to inhalation of toxic compounds), the host becomes immunocompromised. Now, there is a potential that there will be damage caused to the mucociliary elevator and lead to the colonization of microbes.

All the fluid exits to the lymphatic vessels. The fluid itself is called lymph. In parallel to the blood circulation, this circulation is called the lymphatic circulation.
• The lymphatic system’s function is to return excess fluid exiting the capillary beds back into the blood circulation/ cardiovascular system. This happens right next to the right atrium through a large lymphatic vessel called the lymphatic duct.
o Abnormal accumulation of interstitial fluid is known as edema. Edema can occur when there is:
-Excess filtration
-Defective resorption
-Defective lymphatic drainage
-Increased capillary permeability
-Increased capillary pressure
-Decreased plasma protein (OP)
-Decreased lymphatic drainage

1. There is no “funny current” in a ventricular muscle cell. The resting membrane in phase 4 is more negative than that of the sinoatrial node, making it harder to move a ventricular muscle towards positivity.
2. Phase 0: When the muscle cell sees a depolarization signal arriving, a special set of voltage sensitive channels in the membrane, called “Fast Sodium Channels”, opens allowing rapid movement of sodium into the cell
3. Phase 1: The fast sodium channels are closing but around the same time, voltage sensitive L – Type Calcium Channels are opening in order to allow calcium into the cell to allow for the contraction to occur. Cardiac muscle contraction lasts longer then that of SA Node contraction.
4. Phase 2: This action potential has a characteristic plateau phase, where Ca2+ enters during this time. The K+ permeability of the membrane is very los, so K+ isn’t moving out to counter that depolarization.
5. Phase 3: Ca2+ channels close and K+ leaves through now open K+ channels, creating repolarization of ventricular cell.
-Refractory Period – Phases 0, 1, 2, 3: allows for muscle to fully relax before receiving another response to contract again.

- Parasympathetic (vagal) innervation
o ACh release slows heart rate.
-Muscarinic receptor antagonists increase HR. Can be admin. Via drugs
o Parasympathetic nerve terminals release ACh as the parasympathetic transmitter. This transmitter binds to the muscarinic receptors on the cells in the SA Node, which causes the DECREASE in HR.
♣ Stimulation of the vagus nerve releases ACh which binds to its receptors, opening fewer sodium channels and slowing down the rate of that depolariszation phase.
-It takes longer to reach threshold
-Decrease in action potentials per unit time = decrease in heart rate.
-Parasympathetic nerves: release acetylcholine and open fewer channels for If (predominates).
• Sympathetic innervation
o Noradrenaline (NAd) release accelerates HR
-B-adrenoreceptor antagonists slow HR. Can be admin via B-blocking drugs. Blocking the receptor will decrease HR.
o The release of noradrenaline increases HR by binding to B-adrenergic receptors that sit on the cells inside the SA node.
-Anagonizing those receptors is necessary so that noradrenaline can bind to them and accelerate HR.
o Stimulation of the sympathetic nerve will cause more leaky sodium channels to open to generate If current.
♣ This increases the speed at which this depolarization takes place, causing the cells to reach the threshold more quickly
• Increase action potentials = increase heart rate.

1. BP decreases (detected by baroreceptors) so we want to switch on all processes in the heart and vessels that’ll increase MAP
2. Sensors detect decreased dilation of arteries because of dropped BP.
3. All info is transmitted from baroreceptors to Medulla Oblongata to have info sorted
4. Medulla Oblongata sorts coordinated response to heart and vessels.
5. We switch off parasympathetic system (which is normally inhibiting) because we want to increase HR, SV, and TPR
6. Switch on sympathetic system to increase HR, which will increase CO
-CO is one of the determinants of MAP
7. Sympathetic system is also important in enhancing contractility. We switch sympathetic system on so that heart muscle will contract more forcefully.
-Increase SV = increase CO = increase MAP
8. Stimulate sympathetic vasoconstrictor fibers in the walls of the vessels, release noradrenaline so arterioles and other vessels can constrict.
-Arterioles hold most of the peripheral resistance within them so we get a strong effect on TPR, which will increase BP.