|
|
 |
 |
 |
 |
 |
 |
 |
|
T
sarcoplasmic reticulum, Ca
smooth, cardiac >> skeletal
the action potential
Defective titin might show as reduced passive tension properties of heart muscle cells and might lead to increased filling and over-stretching of the heart during diastole.
myosin
smooth, cardiac or skeletal
Twitch: one action potential, one release and then reuptake of Ca from SR, and one contraction. Summation: repeated action potentials at intermediate levels of stimulation, repeated release and uptake of Ca from SR, but because the reuptake does not have time to occur completely the next contraction occurs with higher [Ca] and is more vigorous than the first. Tetanus: repeated, rapid action potentials, repeated release of Ca; Ca-ATPase cannot keep up with the rates of release, so Ca remains in the cytosol and causes continual contraction, as long as energy supplies are maintained to allow myosin to continue cycling.
The very long depolarization/repolarization cycle for cardiac cells prevents rapid successive contractions or excessive build-up of cytosolic [Ca].
See notes and book for description of A and I bands and Z-lines; ATP in power stroke and release of actin; degrees of overlap of thick/thin filaments.
smooth, smooth
Number of motor units stimulated and degree of stimulation (summation).
Blocks the acetylcholine receptor in muscle membranes, preventing the synapse's chemical signal (acetylcholine) from being reconverted into an electrical one in the muscle membrane. However, the muscle remains functional and can therefore still contract when a muscle action potential is directly initiated with an electrode.
Presence of Ca and ATP: muscle would contract and perhaps get shorter. Absence of Ca and presence of ATP: relax
F. ATP must still be available during fatigue because rigor state has not been reached.
Because a significant amount of Ca enters cardiac cells across the plasma membrane, this treatment would reduce heart contraction.
Contractile force (ATPase activity of myosin), detaching actin from myosin, Ca pumping by PMCA and SERCA during relaxation. In addition, ATP is used for generating the ion gradients used for electrical activity of the heart.
Multiple effects are possible. Caffeine might lead to increased contractile strength initially because more Ca would be released. However, if SR remains "leaky" due to SR channel remaining open too long, possible that relaxation of heart is disrupted. Since caffeine is PDE inhibitor, there may be increased levels of cAMP, which would lead to effects noted above for epinephrine. It is perhaps understandable that one's heart can beat irregularly following too much coffee.
Epinephrine → increased cAMP → phosphorylate Ca entry channel → increased cytosolic Ca for contraction. Increased phosphorylation of phospholamban → more rapid pumping of Ca into SR → increased rate of relaxation and increased Ca pumping during following beat.
Action potential is prolonged due to presence of K channels that inactivate, and Ca channels that open, in response to initial peak of depolarization, resisting repolarization that would otherwise occur when fast Na channels close. Extended duration/plateau phase of the action potential is ended by a second type of K channel, opened very slowly by depolarization, and by slow closing of Ca channels.
b
d
Coronary blood supply exhibits little branching, so blockage of one coronary artery or arteriole can have disastrous consequences for heart, which continually beats and therefore needs a continual supply of nutrients. If this supply is interrupted (e.g., by occlusion of coronary vessel with a blood clot or with athersclerotic plaque), heart muscle cells die, resulting in heart attack. Explanation for measurements of lactic dehydrogenase and troponin in blood is given in text (p. 461).
F. Correct sequence: SA node, atria, AV node, bundle of His, ventricles
Resting membrane potential depends on low [K]out vs high [K]in. Increased [K]out causes cell potential to depolarize towards zero, which opens K channels and inactivates Na channels, leading to a cell that cannot be excited and rapid stoppage of heartbeat.
Single unit smooth muscle has gap junctions, so all cells contract as a unit, as action potentials conduct from one cell to the next.
Smooth muscle can contract without ever exhibiting an action potential. Hormones can elicit contraction through activation of IP3 receptors, without activation of voltage-sensitive Ca channels in plasma membrane.
ACh causes heart to contract more slowly due to effects on SA node (slowing the gradual depolarization phase of the cardiac action potential), while norepinephrine increases contractile strength and rate (effects noted above). ACh causes smooth muscle to relax (dilate), while norepinephrine usually causes smooth muscle to contract. However, there are exceptions to this, depending on the specific adrenergic receptor present (beta 1 vs beta 2).
T. Vagus has tonic activity, which keeps SA node under constant inhibitory pressure. When vagus is cut, the inherent, uninhibited rhythm of SA node can be expressed and heart speeds up.
F. ESV is never 0 ml, but typically ~50 ml.
T. The left ventricle pumps slightly more blood than the right, because of cardiac and pulmonary "shunts" that return some deoxygenated blood directly to the left heart.
a. ii, iii, vii;
b. i, ii, iii;
c. iii, v;
d. ii, iii, iv, vi, viii;
e. i, ii, iii, ix
120, systolic; 80, diastolic
flow decreases by factor of 16 — see Poiseuille's law.
a, b
t = 200 msec, D = 10–5cm2/sec, Dx = radius = 20 um. Since muscle cells are often much larger than this, they have evolved the mechanisms to assure rapid spread of action potential deep into cells (T-tubules) and release of Ca from stores (SR) very close to the site of Ca function in the sarcomere.
See notes
See notes
See notes
120 mm Hg × 1 cm H2O/0.74 mm Hg = 162 cm × 1 in/2.54 cm × 1 ft/12 in = 5.3 ft.
Pulse pressure = systolic - diastolic. Pulse pressure determined by stroke volume, arterial compliance and peripheral resistance. Arteriosclerosis leads to decreased compliance and results in increase in pulse pressure.
Usually use sphygmomanometer to measure blood pressure. Cuff around arm, decreasing blood flow to zero. Gently release pressure, as blood squirts through small opening of artery, turbulent flow gives rise to sound. The pressure at point when first sound is audible is systolic pressure. Pressure at last sound before flow returns to laminar (silent) is diastolic pressure.
Law of Laplace: DP = T (1/r1 + 1/r2). For bubble, DP = 2T/r; for cylinder DP = T/r. This law explains how capillaries can withstand high pressure. Law of Laplace also shows that a dilated or expanded heart will necessarily have to generate more tension to elicit same pressure as a more contracted heart. Thus, Law of Laplace and Starling's law tend to work against each other. In general, Starling's law is important for normal heart function, while debilitating effect of Law of Laplace comes into play at larger than normal heart volumes.
Pressures in the heart, aorta and large arteries are all about the same in a supine person due to fact that little of the energy of the heart has been dissipated in large arteries. When person stands, gravitational forces come into play, and transmural pressures at level of kidney would increase above, and those in head would decrease below, those in the heart.
Slope of this relationship for veins is the compliance, which is larger for veins than for arteries.
If filtration pressure and osmotic pressure are imbalanced, fluid will flow into or out of capillaries. In latter case, edema results. Protein deficiency causes reduction in colloid osmotic pressure, and reduced fluid flow back to capillaries, → edema. Lymphatics drain excess tissue fluid, approx 3 liters per day in systemic circulation. Pulmonary lymphatics are also important for maintaining dry airways for efficient O2 and CO2 exchange.
Pressure in the capillary bed increases.
a, b, g, h (affects area of the capillary available for diffusion to occur); rate of blood flow will be only indirectly important, e.g., if the rate is so slow that the oxygen concentration of the capillary drops to low levels because the oxygen in capillary is not being replenished.
a, b, e
Lymph vessels have valves, like the veins, and muscle pump aids in generating pressures required to move lymph along the lymph vessels.
a. glucose - diffusion
b. oxygen - diffusion
c. carbon dioxide - diffusion
d. proteins - diffusion
e. amino acids - diffusion
f. lactic acid - diffusion
g. water - osmosis, filtration (there is no net diffusion of water across the capillaries since
concentrations of water are identical on the two sides of the capillary membranes)
Osmotic pressure of plasma is due to all dissolved solutes (Na, Cl, HCO3, glucose, amino acids, proteins etc). Colloid osmotic pressure is osmotic pressure due to presence of the plasma proteins only, and is much smaller than total osmotic pressure. Much smaller molecules do not influence water flow across the capillary wall because they are so permeant that they do not elicit any osmotic flow.
Increased flow velocity indicates a vessel is too constricted. This can lead to production of nitric oxide in endothelial cells in the affected area. Nitric oxide in turn leads to relaxation of nearby smooth muscle, and dilation of the affected vessel.
Frank-Starling relationship showed that increased stretch of heart (EDV) caused increased stroke volume and increased systolic pressure. Since each heart has its own P-EDV relationship, moment-to-moment changes in venous return will be compensated automatically by the F-S mechanism. Despite these moment-to-moment changes, the left and right hearts pump nearly the same amounts at any given time, because the left heart's F-S mechanism adjusts to whatever blood flow is delivered from the pulmonary veins (determined almost entirely by the right heart's output). Sympathetic nerves change the relationship between P and EDV, moving to larger P (and therefore larger stroke volume) for any given EDV.
Contractility is the inherent ability of the ventricles to generate tension based on actin-myosin interactions and the amount of Ca reaching the cytosol, both from the SR and through the plasma membrane. Elevation of cytosolic Ca can be increased by sympathetic stimulation.
Flow = CO = arterial pressure/(TPR). Increased stroke volume increases pulse pressure, and arterial compliance increase will decrease pulse pressure.
Arterioles receive sympathetic nerve innervation. Norepinephrine is transmitter. Blood vessels in brain and coronary circulation do not respond very prominently to sympathetic stimulation. Arterioles are often not innervated by parasympathetic fibers, but parasympathetic stimulation can lead to reduction in sympathetic constriction and, therefore, in increased blood flow. Alpha receptors lead to constriction. Skeletal muscle arterioles dilate during sympathetic stimulation.
Local control wins.
Baroreceptors are stretch receptors in the walls of the aortic arch and carotid sinus. They send action potentials (frequency codes pressure) to medulla oblongata (center), which processes information and then sends out sympathetic or parasympathetic impulses depending on whether pressure was too high or too low.
a. increased — many arterioles constrict, leading to increased total peripheral resistance
b. decreased — ↓ BP → ↓ filtration; continued osmotic absorption → ↑ fluid in plasma; with no change in red cells, ↓ hct.
c. increased — leading to increased rate of action potential generation
d, e, and f. all decreased, due to constriction of arterioles and consequent reduction in blood flow
g. reduced — baroreceptors respond to reduced pressure with fewer action potentials
h. increased — response to baroreceptors
i. increased — response to increased sympathetic output