Invited Guest Speaker: Dr. Tim Gilbertson Nov. 11 Thursday 11 AM Olin Theater Sensory Cues for Fat...
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Transcript of Invited Guest Speaker: Dr. Tim Gilbertson Nov. 11 Thursday 11 AM Olin Theater Sensory Cues for Fat...
![Page 1: Invited Guest Speaker: Dr. Tim Gilbertson Nov. 11 Thursday 11 AM Olin Theater Sensory Cues for Fat and their Role in Fat Intake Dr. Gilbertson is Professor.](https://reader035.fdocuments.net/reader035/viewer/2022062314/56649dfe5503460f94ae6b06/html5/thumbnails/1.jpg)
Invited Guest Speaker: Dr. Tim Gilbertson Nov. 11Thursday11 AMOlin Theater
Sensory Cues for Fat and their Role in Fat Intake
Dr. Gilbertson is Professor & Associate Department Head of Biology and serves as the Associate Director of the Center for Advanced Nutrition at Utah State University. Dr. Gilbertson's research is focused on the investigation of the mechanisms the body uses to recognize nutrients & how this process is regulated by nutritional need. His lab studies the way nutrients including fats, carbohydrates and minerals are detected by chemosensory cells in the oral cavity and in several nutrient-sensitive, post-ingestive organs. The research spans from genes through behavior with expertise in molecular biology, proteomics, electrophysiology, imaging, biochemistry and analysis of behavior.
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10 November 2010Cardiovascular Physiology
The Cardiac Cycle
Control of HR and SV
MAP and TPR
Blood Vessels
Lab this week: Frog Heart PhysiologyArrive early if you want to pith.
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1QQ # 26 for 8:30 am1.How do action potentials in cardiac myofibers
differ from action potentials in skeletal myofibers?a) Cardiac APs are shorterb) Cardiac APs involve Ca++ influxc) Cardiac APs permit summationd) Cardiac APs do not rely on Na+ influxe) Cardiac APs are conducted from myofiber to myofiber via gap junctions of intercalated disks.
2.As blood passes from the left atrium to the left ventricle, it passes througha) the tricuspid valveb) an atrioventricular valvec) a semilunar valve
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1QQ # 26 for 9:30 am1.How do action potentials in cardiac myofibers
differ from action potentials in skeletal myofibers?a) Cardiac APs are longerb) Cardiac APs involve Ca++ influxc) Cardiac APs prevent summationd) Cardiac APs do not rely on Na+ influxe) Cardiac APs are conducted from cell to cell via gap junctions of intercalated disks.
2.As blood passes from the right atrium to the right ventricle, it passes througha) the tricuspid valveb) an atrioventricular valvec) a semilunar valve
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Figure 12.14
Pacemaker Cells in
Conducting System:
SA Node andBundle of His
Ectopic Pacemaker
Locations other than SA Node
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Figure 12.22Intrinsic Rate = 100 beat/min
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Figure 12.23
Effect of “Beta blockers”
NE EPI ACh
mAChR
Effect of atropine
Beta-adrenergic receptors
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Figure 12.181st Heart Sound = Closure of Atrioventricular (AV) valves at beginning of Ventricular Systole
2nd Heart Sound = Closure of Semilunar valves at beginning of Ventricular Diastole
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Figure 12.20Systolic
Diastolic
Ejection Fraction = SV/EDV
Atrial Fibrillation
Ventricular Fibrillation & Defibrillation
Stroke Volume
Animation
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Events are same for Cardiac Cycle for Right Side of Heart; only difference is lower systolic pressures in right atrium and right ventricle.
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Frank-Starling Law of the Heart
FS LoH = SV is proportional to EDV
Ventricular Function Curve
Does not depend on hormones or nerves
Assures that the heart adjusts its output based on VENOUS RETURN
Ways to enhance Venous Return:1) muscle contractions2) “respiratory pump”3) venoconstriction
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Who Cares?Heart transplant patients
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Fig. 09.21
Low EDV
High EDV
Length-tension “curve” for Cardiac muscle
Overinflation of ventricles leads to less effective pumping
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Overinflation of ventricles results in reduction in stroke volume
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Treatments?…..diuretics
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Figure 12.25Contractility
NE from Symp postganglionics & EPI from Adrenal medulla
Note: cardiac myofibers NOT innervated by parasympathetic division
Increase Ejection Fraction
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3 Effects of SympatheticStimulation
1: Increase rate of contraction2: Increase peak tension3: Decrease twitch duration
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Why does this happen?
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Control of Stroke Volume
• End diastolic volume (preload)
• Contractility (strength of ventricular contraction due to adrenergic stimulation)
• Pressure in arteries that must be overcome = Afterload
FS LoH
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Afterload is analogous to trying to pump more air into a tire that is already fully inflated (heart contracting to overcome diastolic pressure.)
High blood pressure increases the workload of the heart….. Cardiac hypertrophy….increase chance of irregular conduction of AP through heart
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Hypertrophic cardiomyopathy