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Lecture 17, 28 Oct 2003 Chapter 12, Circulation (con’t) Vertebrate Physiology ECOL 437 University of Arizona Fall 2003 i

1. Lecture 17, 28 Oct 2003 Chapter 12, Circulation (con’t) Vertebrate Physiology ECOL 437 University of Arizona Fall 2003 instr: Kevin Bonine t.a.: Bret Pasch. Sherwood 1997. 2. Vertebrate Physiology 437. 1. Circulation (CH12) 2. Announcements exams Wed Seminar Assgt.

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Lecture 17, 28 Oct 2003 Chapter 12, Circulation (con’t) Vertebrate Physiology ECOL 437 University of Arizona Fall 2003 i

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  1. 1 Lecture 17, 28 Oct 2003 Chapter 12, Circulation (con’t) Vertebrate Physiology ECOL 437 University of Arizona Fall 2003 instr: Kevin Bonine t.a.: Bret Pasch

  2. Sherwood 1997 2 Vertebrate Physiology 437 1. Circulation (CH12) 2. Announcements exams Wed Seminar Assgt. 3. Slide #s

  3. 3

  4. 3b ANATOMY: The integument has a unique circulatory pattern that involves a shunting system through the reticular layer into the subcutaneous layer. This cutaneous plexus gives off tributaries to supply the adipose tissue of the subcutaneous layer and the tissues of the integument. As the cutaneous plexus approaches the papillary layer they terminate in the capillaries of the dermal papillae. These branches supply the hair follicles, sweat glands, and other structures in the dermis. The unusual thing about these capillaries is that the small arteries and arterioles that supply them are organized into another interconnecting system call the papillary plexus. The papillary plexus provides arterial blood to the capillary loops that follow the contours of the dermal papilla at the epidermal-dermal boundary to feed the structures mentioned above. The venous network returns the blood back to the body core by following the arterial pattern exactly. Once you have the anatomy under control they the physiology follows from the structure of the blood flow pattern. PHYSIOLOGY: When the skin is challenged by cold, the first thing that happens is the smooth muscle surrounding the small arteries and arterioles going from the cutaneous plexus through the reticular layer to the papillary plexus constrict to conserve body heat. This action shunts the blood away from the reticular and papillary layers and keeps it in the deeper subcutaneous layers. Just the opposite happens when a person gets over-heated, along with sweating, to reduce body heat. In that case the warm blood from the deeper layer is shunted into, rather than away from, the papillary layer so that the cooling effect of evaporating sweat will be maximized as the warm blood passes through the cooler dermal capillary loops before going into the venous tree. Something fascinating happens in the cold response, however. Since tissue will die without having oxygen and nutrients delivered and waste products removed over time, the shunting mechanism cannot shut down indefinitely. Depending on how cold the area of skin gets, the smooth muscle will reduce its contraction every so often. This will occur at 5 to 15 minute intervals, as I said depending on the degree of cold on that particular skin surface. Some people have inappropriate spasms of the smooth muscle that greatly restrict the flow to the dermis and then, after a severe cold period that can become painful, the vessels will dilate much more than normal and cause the skin to be a bright pink or red. This phenomenon is most common in the digits of hands and feet and is most frequently found in young women. The case is unknown (idiopathic). The person can actually have a triphasic color change starting with pallor (shutting down of the blood flow), moving to cyanosis (bluish color due to reduction of oxygen and build up of carbon dioxide), and then reactive hyperemia (redness). This problem was described by a doctor named Raynaud and is now referred to as Raynaud’s disease. Cold, red skin?

  5. 4 Name that student: Lauren Mashaud Cricket research Linda Webb Psychology Sarju_Govani Dines at DD

  6. 5 Recall AP and refractory period differences… (12-7)

  7. Vander 2001 (see 12-5) 6 Types of Cardiac Cells: A. Contractile B. Conducting ~ autorhythmic SA node AV node ~ fast-conducting Internodal Interatrial Bundle of His Purkinje Etc.

  8. Sherwood 1997 7

  9. 8 Types of Cardiac Cells: A. Contractile Pacemakers: B. Conducting -Normally HR driven by SA node - 1 autorhythmic SA node AV node -Others areLatent pacemakers • 1 fast-conducting Internodal Interatrial Bundle of His Purkinje Etc. -Called Ectopic pacemaker when node other than SA driving HR

  10. Sherwood 1997 Sherwood 1997 9 ~ SA node ~ latent rate

  11. Sherwood 1997 10 SA AV other The Heart Rate Train oops

  12. 9-11, Sherwood 1997 11 Which way would you alter channel permeabilities to speed or slow HR?? ~Transient Ca2+ channels K+, Na+ Autorhythmic Cardiac Muscle (e.g. SA node)

  13. Sherwood 1997 Vander 2001 12 Contractile Cardiac Muscle Ca2+ current maintains plateau

  14. 13 (12-8) (Q,R,S masks atrial repolarization)

  15. 14 (12-8)

  16. 14-25, Vander 2001 15 Wiggers Diagram 760 mmHg = 1 atm = 9.8 m blood Valves open/close where pressure curves cross 1:2 (See 12-12)

  17. Sherwood 1997 16 Atrial Kick Heart filled ~same with increased HR

  18. Sherwood 1997 Vander 2001 17 Frank-Starling Curve (p. 483) Systole = Ventricular Emptying Diastole = Ventricular Filling (rest)

  19. 18 Heart Work Loops (12-13)

  20. 18b Cardiac Output: CO = cardiac output (ml/min from 1 ventricle) SV = stroke volume (ml/beat from 1 ventricle) = EDV – ESV (end-diastolic – end-systolic volume) HR = heart rate (beats/min) MABP = CO x TPR MABP = DP + 1/3(SP-DP) CO = HR x SV - Heart can utilize different types of energy sources (unlike brain)

  21. 19 HR control Parasympathetic vs. Sympathetic (12-5)

  22. 20 (12-6)

  23. 21 Cardiac Output Control Sympatheticspeeds heart rate and increases contractility 1. Norepinephrine binds to beta1 adrenergic receptors 2. Increases cAMP levels and phosphorylation 3. Activates cation channels (Na+) and increases HR 4. Epi and Norepi activate alpha and beta1 adrenoreceptors which increase contractility and rate of signal conduction across heart

  24. Vander 2001 22 How increase contractility? More Ca2+

  25. 23 HR control Parasympatheticslows heart rate -Innervate Atria (Vagus nerve = Xth cranial nerve) -Cholinergic (ACh) -Alter SA node pacemaker potential by K+ permeability  Ca2+ permeability Parasympathetic innervation of AV node slows passage of signal between atria and ventricles

  26. 14-11, Vander 2001 Vander 2001 24 Hemodynamics in Vessels Flow depends primarily on pressure gradient and resistance

  27. 25 Hemodynamics Use to approximate flow - Poiseuille’s Law: Pressure Gradient radius4 Flow rate Q = (P1 – P2)r4 8L viscosity length Small change in radius  large change in flow rate

  28. 26 Hemodynamics - From Poiseuille’s Law: Pressure Gradient length Resistance viscosity R = (P1 – P2) = 8L r4 Q radius4 Flow rate Small change in radius  large change resistance Modifiable if vessel distensible under pressure

  29. xx End

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