Biological Physiology Lab Exam 2
Biological Physiology Lab Exam 2 BIOL 5600
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This 9 page Study Guide was uploaded by Brianna Sanguily on Saturday April 23, 2016. The Study Guide belongs to BIOL 5600 at Auburn University taught by Dr. Mendonća in Winter 2016. Since its upload, it has received 75 views. For similar materials see Biomedical physiology in Biology at Auburn University.
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Date Created: 04/23/16
Experiment 5 Levels of Anesthesia Reaction Level 1: Analgesia o Patient is conscious but has little to no pain o I.e. local anesthetic Level 2: Excitement/Delirium o Patient is unconscious but may still thrash Level 3: Surgical Anesthesia o Patient is breathing normally, relaxed o Check pedal/corneal reflexes o Proper stage to perform surgery Level 4: Respiratory, Circulatory paralysis o Patient dies Types of Anesthesia Gaseous – inhalable, rapid action o Few side effects o Potent and flammable o Easy to administer o Ex. Nitrous oxide, ethylene Volatile – inhalable o Liquid at room temperature but easily evaporates o Lipid soluble o Tied up in fat cells slow action o Ex. Ether, halothane Injectable – useful and rapid acting o Cant remove once injected o Dosage levels has to be carefully computed o Ex. Barbituates, ketamine, carbamate (carbamate urethane in this lab) o Types (slowest to fastest): Subcutaneously (SC): under skin Intramusculary (IM): in the muscle Intraperitonealy (IP): in the gut Intravenously (IV): in the vein How to calculate drug amount to give: (Weight of animal)*(1kg/1000g)*(dose)*(concentration of drug/1kg) Experiment 6: Blood Pressure Physiology Blood pressure is the force of blood against the artery walls o Measured: Blood Pressure = Cardiac Output (CO) * Total Peripheral Resistance (TPR) o CO = Heart Rate (HR) * Stroke Volume (SV) Stroke volume: amount of blood pumped by heart per beat CO: amount of blood pumped by each ventricle/minute TPR: blood viscosity; radius of blood vessels Medullary Centers Vasomotor Center o Sympathetic (excitatory) o Via nerves T1-T12 and L1-L4 o Epinephrine binds to beta1 on the heart, which causes an increase in heart rate. o Adrenal Medulla stimulation releases epinephrine into blood stimulates alpha1 receptors on vasculature causes vasoconstriction causes increase in TPR and HR, so increases BP o Negative feedback loop = activation of VMC inhibits VC Vagal Center o Decrease in HR plus vasodilation causes a decrease in BP o Parasympathetic (inhibitory) o Via the vagus nerve o Acetylcholine binds to M receptors on the heart decrease HR o Activation of the VC inhibits the VMC causing vasodilation Control of Blood Pressure: Hormonal: Long Term o Via the kidney, adrenal cortex, right atrium Neural Control: Short term o Via sympathetic and parasympathetic pathways o Neural reflexes use baroreceptors At the arch of aorta and bifurcation of the common carotid artery Respond to stretch of blood vessels, only stimulated by an increase in blood pressure Afferent signal from aorta travel via Vagus (nerve X) and signals from carotids travel via glossopharyngeal nerve (nerve IX) High BP increases firing of baroreceptors Signals to medulla inhibits the Vasomotor center (VMC) which stimulates the vagal center (VC) yields lower BP (slows heart rate, decreases CO) Low BP decreases firing of baroreceptors VMC is no longer inhibited inhibits VC yields higher BP o Chemoreceptors Located in bifurcation of common carotid artery and arch of aorta When BP is low, a build up of waste products such as carbon dioxide (CO2) and H+ ions occurs. Chemoreceptors then inadvertently stimulate the VMC Chemoreceptors signals have a direct effect on respiratory centers which are in close proximity to VMC Part A: Normal EKG and Arterial Blood Pressure Systolic = contracting; diastolic = relaxed *know the material above about controls of BP, definition of BP, how to calculate BP, brain centers, neurotransmitters, and receptors Part B: Carotid Sinus Reflex Pulling a suture at the carotid artery will tell you where the bifurcation is at depending on the change in HR If the suture is below the bifurcation, there will be an increase in BP o Blood flow to the carotid is cut off stimulates the baroreceptors body will assume that blood pressure has fallen VMC is activated and VC is inhibited will cause blood pressure to rise If suture is above the bifurcation, there will be a drop in BP o Blood will pool increases the pressure near the baroreceptors activating the VC and inhibiting the VMC Part C: Effect of Acetylcholine and Atropine followed by ACH Ach will stimulate all nicotinic and muscarinic receptors There are more muscarinic receptors in the body than nicotinic so parasympathetic effect happens (lowers BP) M2 receptors lower HR, cause vasodilation and decrease TPR. Atropine blocks M2 receptors o Ach stimulates nicotinic receptors on sympathetic pathway, epinephrine is released and so blood pressure increases. o Parasympathetic is stimulated but halted at muscarinic receptors because blocked. Part D: Effect of Epinephrine Sympathetic neurotransmitter Binds to B1 receptor to increase HR; binds to alpha1 to increase BP (vasoconstriction) Experiment 7: Cardiac Physiology Cardiac Tissue Myogenic 2 types of cells within the sinous venosus (SV) o Round Cells = pacemaker Cells o Elongated Cells = propagate the rhythmic action potentials to atria and ventricle Nervous System involvement Parasympathetic o Ach is main NT bind to muscarinic receptors open potassium channels hyperpolarize the cell (make it more difficult to have an action potential) Sympathetic o Norepinephrine/Epinephrine are the two main NT bind to B1 receptors on the ventricle open calcium channels (make it easier for an action potential) Part A: Frank-Starling Law Law = the more a muscle is stretched, the more forceful a subsequent contraction will be o Occurs when venous return increases Heart muscles are myogenic, cardiac cells initiate and propagate action potentials Frog heart is 3 chambered (2 atrial, 1 ventricle) Pace maker is the sinus venous (evolved to mammalian SA node) Stimulation of venous return is by an increase of ventricle stretch via manipulation of Myograph position. When tension was added to the heart, the Force of Contraction should have risen. Part B: Effect of Temperature When temperature decreases, it effects the enzyme efficiency by decreasing it Enzymes involved in contraction o Acetylcholinesterase: when temperature falls, causes an increase in contraction duration (Achase cannot take up Ach as fast so contraction time lasts longer) o Myosin ATPase: when temp falls, causes increase in contraction duration and contraction force (causes enzyme to cleave ATP slower than normal so longer time between think and thin filament detachment. o Calcium ATPase: when temp falls, causes an increase in relaxation duration (ATP cleavage powers Calcium from sarcomere, allowing troponin and tropomyosin to recover myosin head on actin There is a possible initial increase in force of contraction is possible causes a slower heart rate increases fill time More blood means more stretch which stimulate receptors increase force of contraction Part C1: Effect of Epinephrine Sympathetic NT (epi) is added to the ventricle to stimulate B1 receptors o Increases rate of depolarization increases heart contraction Heart rate should increase and so should force of contraction due to sympathetic input Part C2: Effect of Pilocarpine Pilocarpine is an Ach mimic (parasympathomimetic) Mimics the effect of Ach in the parasympathetic pathway binds to M receptors M receptors are at the SV Pilocarpine decreases the rate of depolarization D1: Effect of Acetylcholine Ach is part of the parasympathetic response Stimulates parasympathetic nicotinic and muscarinic receptors. Potassium leaves the cell decreases the rate of depolarization decreases heart rate and force of contraction D2: Effect of Atropine followed by Ach Atropine is a M receptor blocker Because Ach cannot bind to M receptors increased force of contraction (due to Ach stimulating N1 receptors of sympathetic pathway) Ach has no effect on the parasympathetic pathway when atropine is added Experiment 8: Ventilation Respiration Regulation Neural control o Ventral respiratory group (VRG): located in the pons/medulla junction Autonomous depolarization – rhythm generating and integrative center Pre-Botzinger Complex (part of VRG): has spontaneously firing neurons; thought to be the potential pacemaker (hypothesis) Has two subnuclei Subnucleus 1: excitatory neurons; spontaneously send action potentials at increasing frequencies; causes inspiration Subnucleus 2: spontaneous depolarizing action potentials; inhibitory neurons o Dorsal respiratory group (DRG): located in the nucleus tractus solitaries of the medulla; near cranial nerve IX, X (receives input from these) Integrates input from peripheral stretch and chemoreceptors Communicates information to the VRG will send impulses to modify autonomous breathing cycle. May also have effect on breathing depth o Pontine Respiratory Centers: modify activity of medullary neurons Smooths out transition from inspiratory to expiratory set by basic rhythm of VRG Formally pneumotaxic and apneustic Transmit impulses to VRG/DRG fine tunes breathing depth/rhythms during sleep, vocalization, and exercise. Humoral/chemical control o Central chemoreceptors – in the medulla Respond to increase H+ ions derived from CO2 CO2 + H2O H2CO3H+ + HCO3- CO2 derived H+ ions must cross the blood brain barrier to stimulate central chemoreceptors, which then stimulate respiratory centers Respiration rate and depth will increase to rid excess CO2 decrease H+ ions to restore pH back to normal. o Peripheral Chemoreceptors – in the aortic arch and bifurcation of the carotid arteries Respond to increase arterial CO2, increase in arterial CO2 derived H+ ions, and a SEVERE decrease in arterial O2 If blood levels of CO2 or H+ rise, these receptors send afferent messages to the DRG, signaling an increase in repiration to blow off excess CO2 Effect of declining O2 is slight but enhances sensitivity of CO2 receptors Normal breathing – Eupena Cyclic on/off excitation constantly repeats Produces a rate of 12-15 breaths/minute Subnuclei 1: fire impuslses to phrenic and intercostal nerves to diaphragm and external intercostals thorax expands, burst of air rushing in lasts ~2sec Subnuclei 2: inhibit inspiratory signals so excitation output stops; does not cause expiration expiration occurs passively diaphragm relaxes and external intercostals relax ~3sec Part A1: Effect of Hypercapnia Simulating asphyxia causes an increase in CO2 in the brain o Increases the H+ concentration in the blood stimulates both central and peripheral receptors o There should be an increase in both rate and depth of ventilation to compensate for increase CO2 and H+ Part A2: Effect of Sodium Phosphate Sodium Phosphate = NaH2PO4 Dissociates into Na+, H+, and PO4(-2) Dissociation causes an increase in H+ ions in the blood stimulates peripheral chemoreceptors, which modify breathing rate and depth o Breathing rate is increased to decrease H+ ions o As breathing brings levels back to normal, breathing rate slowly decreases back to normal with it. Part B: Effect of Epinephrine Binds to B1 receptors on the heart (increase HR) and bind to alpha1 receptors on vasculature (increase BP- vasoconstriction; increase TPR) Baroreceptors send inhibitory signals to VMC Inhibitory signals spill over to DRG bc it is located close to VMC The DRG then modulates the VRG causing a decrease in rate and depth of breathing Epi is not directly stimulating VRG or DRG indirect Part C: Hering-Breuer Response Reflex in newborns retained though out adulthood When lungs are over-inflated, the stretch receptors inhibit inspiratory neurons to a greater extent than normal. Breathing rate slows to compensate for over inflation. Protective rather than regulatory Stretch receptors send signals up vagus nerves, so when we stimulate the vagus nerves, we are simulating signals from stretch receptors in bronchioles. After cutting vagus nerve, no afferent signals at all being sent to respiratory centers respiration increases Slight stimulation when nerve is cut so will increase than decrease Part D: Cord Facilitation When thigh is stimulated at high intensity many impulses rush up the spinal cord impulses spill over to DRG modulate VRG Increase in respiration or a temporary stop in respiration occurs. Experiment 9: Renal Physiology Three phases of Urine Formation: Filtration: o Occurs in the glomerulus and bowman’s capsule o Any solute that can pass enters Bowman’s (positive and small) o Three pressures: Blood pressure – driving force; pushes fluid into Bowman’s capsule Bowman’s capsule pressure (BCP) – pressure of fluid in capsule; pushes fluid back into glomerulus Plasma colloid osmotic pressure (PCOP) – due to plasma proteins; too large to pass; causes osmotic movement of fluid towards glomerulus o Glomerular filtration rate (GFR): GFP = BP – (BCP + PCOP) Reabsorption o Transfer of substances from filtrate into tubular portion back into peritubular capillary Secretion o Transfer of substances from peritubular back into filtrate (H+, HCO3-, NH4+, K+) Specific Gravity Density of fluid relative to pure water Influenced by number of mols + their molecular weight and size Measuring osmolality = approximate solute concentration Part A: Normal 750 ml of distilled water was taken in (hypotonic) Large volume decreases the osmolality of blood Increase blood pressure because increasing volume; decrease PCOP bc blood is diluted Increase filtration rate, increase urine output Less water reabsorbed at proximal convoluted tubule and distal convoluted tubule Part B: Effect of Saline Increase BP by increasing the amount of fluid Increase blood volume Decrease PCOP because blood is diluted Increase filtration rate, increase urine output Not as great as part A because no pressure changes in filtrate Part C: 5% NaCl solution Increases osmolality of blood When sodium accumulates in circulatory system, the posterior pituitary is stimulated and produces ADH triggers kidneys to reduce production of urine and reabsorb water Excess sodium and chloride in tubules make filtrate more concentrated increases specific gravity (osmolality) Part D: 3% NaHCO3 Dissociate into sodium and HCO3- increase blood pH HCO3- will be secreted from peritubule capsule into collecting duct increasing pH of urine also decreasing H+ secreted and more reabsorbed from tubular system Excessive sodium in tubules more concentrated filtrate Higher retension of water in tubules Decrease urine production
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