This document provides an overview of coronary circulation and coronary blood flow. It discusses the anatomy of the coronary blood vessels, characteristics of coronary blood flow such as rates at rest and during exercise. It describes phasic changes in coronary blood flow during the cardiac cycle. Methods for measuring coronary blood flow are presented. The regulation of coronary blood flow through local control mechanisms like autoregulation and metabolic factors as well as neural and hormonal influences are reviewed. Finally, factors that can affect coronary blood flow such as blood pressure, exercise, and hormones are outlined.
Cardiac output (The Guyton and Hall Physiology)Maryam Fida
The volume of blood pumped by each ventricle per minute is called cardiac output
Cardiac output = Stroke Volume X Heart Rate
Normal value = 5 Liters /Minute
Cardiac output = Stroke Volume X Heart Rate
The factors which regulate stroke volume and Heart rate are basically regulating Cardiac output
Volume of blood ejected by each ventricle in single systole; Normal Value = 70 ml/beat
Stroke Volume = End diastolic Volume – End Systolic Volume
So stroke volume is mainly controlled by
EDV
ESV
VENOUS RETURN: What ever blood volume returns to the heart, same is pumped forward through the Frank’s Starlings Law. According to this law 13- 15 liters of blood volume can be pumped out without cardiac stimulation.
DURATION OF DIASTOLE OR FILLING TIME: ventricular filling occurs during diastole, so there must be adequate ventricular filling time.
DISTENSIBILITY OF THE VENTRICLES: Normally ventricles are distensible to accommodate adequate blood volume. Infarction decreases the distensibility which decreases the EDV.
ATRIAL CONTRACTION: There must be adequate atrial contraction to have adequate EDV. If atrial function is not adequate then EDV will decrease.
E.S.V is basically CONTROLLED BY MYOCARDIAL CONTRACTION
FORCE OF MYOCARDIAL CONTRACTION: It depends upon the initial length of muscle fibers according to frank’s starlings law.
PRELOAD: The effect of EDV on initial length is called preload. So EDV also effects the ESV.
AFTER LOAD: Force of contraction is also dependant upon the resistance against which the ventricles have to pump
CONDITION OF THE MYOCARDIUM : It also effects the force of contraction.
AUTONOMIC NERVES : Sympathetic stimulation increases and parasympathetic stimulation decreases force of contraction
HORMONES: Catecholamines, thyroxine, glucagon, digitalis, calcium, increased temp, caffeine, theophyline increase the force.
Force decreases by hypoxia, acidosis, barniturates, procainamide and quinidine decrease the force of contraction.
Cardiac cycle refers to a complete heartbeat from its generation to the beginning of the next beat.
Cardiac events that occur from –
beginning of one heart beat to the beginning of the next are called the cardiac cycle.
Cardiac output (The Guyton and Hall Physiology)Maryam Fida
The volume of blood pumped by each ventricle per minute is called cardiac output
Cardiac output = Stroke Volume X Heart Rate
Normal value = 5 Liters /Minute
Cardiac output = Stroke Volume X Heart Rate
The factors which regulate stroke volume and Heart rate are basically regulating Cardiac output
Volume of blood ejected by each ventricle in single systole; Normal Value = 70 ml/beat
Stroke Volume = End diastolic Volume – End Systolic Volume
So stroke volume is mainly controlled by
EDV
ESV
VENOUS RETURN: What ever blood volume returns to the heart, same is pumped forward through the Frank’s Starlings Law. According to this law 13- 15 liters of blood volume can be pumped out without cardiac stimulation.
DURATION OF DIASTOLE OR FILLING TIME: ventricular filling occurs during diastole, so there must be adequate ventricular filling time.
DISTENSIBILITY OF THE VENTRICLES: Normally ventricles are distensible to accommodate adequate blood volume. Infarction decreases the distensibility which decreases the EDV.
ATRIAL CONTRACTION: There must be adequate atrial contraction to have adequate EDV. If atrial function is not adequate then EDV will decrease.
E.S.V is basically CONTROLLED BY MYOCARDIAL CONTRACTION
FORCE OF MYOCARDIAL CONTRACTION: It depends upon the initial length of muscle fibers according to frank’s starlings law.
PRELOAD: The effect of EDV on initial length is called preload. So EDV also effects the ESV.
AFTER LOAD: Force of contraction is also dependant upon the resistance against which the ventricles have to pump
CONDITION OF THE MYOCARDIUM : It also effects the force of contraction.
AUTONOMIC NERVES : Sympathetic stimulation increases and parasympathetic stimulation decreases force of contraction
HORMONES: Catecholamines, thyroxine, glucagon, digitalis, calcium, increased temp, caffeine, theophyline increase the force.
Force decreases by hypoxia, acidosis, barniturates, procainamide and quinidine decrease the force of contraction.
Cardiac cycle refers to a complete heartbeat from its generation to the beginning of the next beat.
Cardiac events that occur from –
beginning of one heart beat to the beginning of the next are called the cardiac cycle.
THE CORONARY CIRCULATION of the heart in the bodyAsiiAyodimeji
Coronary circulation of the heart the heart is supply by two artery On the side of the heart :Right coronary artery and left coronary artery the Right coronary artery supply the Right portion of the heart the Right ventricle and Right auricle
These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
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- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
- Video recording of this lecture in Arabic language: https://youtu.be/Ve4P0COk9OI
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
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Explore natural remedies for syphilis treatment in Singapore. Discover alternative therapies, herbal remedies, and lifestyle changes that may complement conventional treatments. Learn about holistic approaches to managing syphilis symptoms and supporting overall health.
These lecture slides, by Dr Sidra Arshad, offer a quick overview of physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar leads (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
Prix Galien International 2024 Forum ProgramLevi Shapiro
June 20, 2024, Prix Galien International and Jerusalem Ethics Forum in ROME. Detailed agenda including panels:
- ADVANCES IN CARDIOLOGY: A NEW PARADIGM IS COMING
- WOMEN’S HEALTH: FERTILITY PRESERVATION
- WHAT’S NEW IN THE TREATMENT OF INFECTIOUS,
ONCOLOGICAL AND INFLAMMATORY SKIN DISEASES?
- ARTIFICIAL INTELLIGENCE AND ETHICS
- GENE THERAPY
- BEYOND BORDERS: GLOBAL INITIATIVES FOR DEMOCRATIZING LIFE SCIENCE TECHNOLOGIES AND PROMOTING ACCESS TO HEALTHCARE
- ETHICAL CHALLENGES IN LIFE SCIENCES
- Prix Galien International Awards Ceremony
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
ASA GUIDELINE
NYSORA Guideline
2 Case Reports of Gastric Ultrasound
Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
New Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...i3 Health
i3 Health is pleased to make the speaker slides from this activity available for use as a non-accredited self-study or teaching resource.
This slide deck presented by Dr. Kami Maddocks, Professor-Clinical in the Division of Hematology and
Associate Division Director for Ambulatory Operations
The Ohio State University Comprehensive Cancer Center, will provide insight into new directions in targeted therapeutic approaches for older adults with mantle cell lymphoma.
STATEMENT OF NEED
Mantle cell lymphoma (MCL) is a rare, aggressive B-cell non-Hodgkin lymphoma (NHL) accounting for 5% to 7% of all lymphomas. Its prognosis ranges from indolent disease that does not require treatment for years to very aggressive disease, which is associated with poor survival (Silkenstedt et al, 2021). Typically, MCL is diagnosed at advanced stage and in older patients who cannot tolerate intensive therapy (NCCN, 2022). Although recent advances have slightly increased remission rates, recurrence and relapse remain very common, leading to a median overall survival between 3 and 6 years (LLS, 2021). Though there are several effective options, progress is still needed towards establishing an accepted frontline approach for MCL (Castellino et al, 2022). Treatment selection and management of MCL are complicated by the heterogeneity of prognosis, advanced age and comorbidities of patients, and lack of an established standard approach for treatment, making it vital that clinicians be familiar with the latest research and advances in this area. In this activity chaired by Michael Wang, MD, Professor in the Department of Lymphoma & Myeloma at MD Anderson Cancer Center, expert faculty will discuss prognostic factors informing treatment, the promising results of recent trials in new therapeutic approaches, and the implications of treatment resistance in therapeutic selection for MCL.
Target Audience
Hematology/oncology fellows, attending faculty, and other health care professionals involved in the treatment of patients with mantle cell lymphoma (MCL).
Learning Objectives
1.) Identify clinical and biological prognostic factors that can guide treatment decision making for older adults with MCL
2.) Evaluate emerging data on targeted therapeutic approaches for treatment-naive and relapsed/refractory MCL and their applicability to older adults
3.) Assess mechanisms of resistance to targeted therapies for MCL and their implications for treatment selection
3. CORONARY BLOOD VESSELS
Coronary arteries –
arise from Root of the
Aorta
Right coronary artery
– Supplies Rt ventricle,
Rt atrium, the Posterior
part of left ventricle,
posterior part of
Interventricular
septum & SA node
Friday, November 25, 2016
4. CORONARY BLOOD VESSELS
Left coronary artery –
supplies left ventricle, left
atrium, Ant part of
Interventricular septum &
left branch of bundle of
His.
Predominant supply. –
50% by Right coronary
artery, 20% Left coronary
artery, 30% Both.
Friday, November 25, 2016
5. CORONARY BLOOD VESSELS
Major coronary arteries. –
Rt coronary artery travel in
the Epicardium of heart
( superficial vessels) &
subdivides into
Penetrating branches.
End arteries- appears to be
End arteries but shows
some Anastomosis.
Friday, November 25, 2016
6. ANASTOMOSIS
Types.
Cardiac – Between branches of
two coronary artery & between
branches of 2 coronary arteries
& Deep Venous System.
Extra cardiac –Between
coronary arteries & Vasa vasora
of aorta, Vasa vasora of
pulmonary arteries, intra
thoracic arteries , bronchial
arteries & Phrenic arteries.
Friday, November 25, 2016
7. CORONARY VEINS
Coronary sinus -- Wide
vein which drain blood
from Myocardium to
Right atrium.
Tributaries are – Great
cardiac veins, Small
cardiac vein, Posterior
vein of left ventricle &
Oblique vein of left
ventricle.
Friday, November 25, 2016
8. CORONARY VEINS
Anterior cardiac vein
– Drains from right
ventricle to right
atrium.
Thebesian vein –
coronary luminal
vessels forms Deep
Venous System.
Friday, November 25, 2016
9. CORONARY BLOOD FLOW:
CHARACTERISTIC FEATURES
Normal coronary
blood flow & oxygen
demand.
A continuous flow of
blood for supply of
oxygen & nutrients
Friday, November 25, 2016
10. CORONARY BLOOD FLOW:
CHARACTERISTIC FEATURES
Normal coronary
blood flow – at rest
250 ml (70ml/100
gm/min)
5% of cardiac output.
During exercise
increases to 3-6 fold.
Blood flow to left is
twice Rt ventricle.
Friday, November 25, 2016
11. CORONARY BLOOD FLOW:
CHARACTERISTIC FEATURES
Oxygen consumption
by the myocardium.
Very high –
8ml/min/100 gm
tissue
70-80% of oxygen
extracted from each
unit as compared to
25% in other tissue.
Friday, November 25, 2016
12. PHASIC CHANGES IN
CORONARY BLOOD FLOW
Blood flow is
determined by
Balance between
Pressure head Aortic
pressure &
Resistance by
myocardium.
Friday, November 25, 2016
13. PHASIC CHANGES IN
CORONARY BLOOD FLOW
Blood flow to left
ventricles
During systole – During
contraction myocardium
produces Throttling
effect on coronary arteries
, during Isometric
contraction phase blood
flow to heart practically
Ceases.
Friday, November 25, 2016
14. PHASIC CHANGES IN
CORONARY BLOOD FLOW
During Diastole –
Myocardium relax &
blood flow increases.
Flow Increases
maximally in
Isovolumic relaxation
phase
Friday, November 25, 2016
15. EFFECT OF HEART RATE ON
CORONARY BLOOD SUPPLY.
During Tachycardia
Duration of diastole
decreases so coronary
blood flow reduces but
due to Local
Metabolite
Regulation of blood
flow is not seriously
affected.
Friday, November 25, 2016
16. BLOOD FLOW TO RIGHT
VENTRICLE & ATRIA.
Through coronary
capillaries of right
ventricle shows
similar changes but
to Less extent.
Blood flow occurs
during Both systole &
diastole.
Friday, November 25, 2016
17. BLOOD FLOW THROUGH
CORONARY SINUS.
Inflow Rises from Iso
volumic contraction
phase reaches peak
during Protodiastole
phase & then
gradually Falls.
Friday, November 25, 2016
18. CLINICAL IMPORTANCE OF
PHASIC CORONARY BLOOD FLOW.
Sub endocardial
region of left
ventricle
In Aortic stenosis
In Congestive Heart
failure.
Friday, November 25, 2016
19. SUBENDOCARDIAL REGION OF
LEFT VENTRICLE
Most Vulnerable to
Ischemia so most
common site of
Myocardial Infarction.
As this part receives
almost No blood
supply during systole.
Friday, November 25, 2016
20. COMPENSATORY MECHANISM
Capillary Density – Much Higher (1100
capillaries /mm2
) than Epicardial region (750
capillaries/mm2
)
Minimum diffusion distance – 20% Shorter (16.5
µm) as compared to Epicardial (20.5 µm)
Myoglobin content – Higher than Epicardial
region.Friday, November 25, 2016
21. IN AORTIC STENOSIS
Pressure in Left
ventricle increases --so
severe compression of
coronary vessels during
systole & Increase
Chance Of MI.
Friday, November 25, 2016
22. IN CONGESTIVE HEART
FAILURE.
Increase in Venous
Pressure --
Decreases aortic
diastolic pressure -- so
effective coronary
perfusion falls &
Coronary Blood Flow
Decreases.
Friday, November 25, 2016
23. .
MEASUREMENT OF CORONARY
BLOOD FLOW.
Nitrous oxide method (Kety Method)
Radionuclides utilization techniques.
Coronary angiographic technique.
Electromagnetic flow meter technique.
Friday, November 25, 2016
24. NITROUS OXIDE METHOD
(KETY METHOD)
Principle – based on
Fick’s Principle.
Procedure – Inhale
mixture of NO & air for 10
min.
During inhalation serial
sample of arterial &
coronary sinus venous
blood taken at fixed
intervals
Coronary blood flow
= N2O taken up/min
-------------------------------
(A-V)
Friday, November 25, 2016
25. RADIONUCLIDES UTILIZATION
TECHNIQUES.
Radioactive Tracers
pumped into cardiac
muscle cells by Na-K
ATPase enz & equilibrate
with intracellular K pool.
Distribution of
radioactive tracers is
Directly proportional to
Myocardial blood flow.
Friday, November 25, 2016
26. PROCEDURE
Radionuclide Thallium
-201 injected IV.
After 10 min amount of
Thallium taken by
myocardial cells
measured by Gamma-
Scintillation camera
Areas of ischemia
detected by low uptake.
Friday, November 25, 2016
28. ELECTROMAGNETIC FLOW
METER TECHNIQUE.
It tells about Phasic
flow & flow per min.
Blood flow through left
ventricle determined
with the help of
Electromagnetic Flow
Meter implanted
around main left
coronary artery.
Friday, November 25, 2016
29. REGULATION OF CORONARY
BLOOD FLOW
LOCAL CONTROL MECHANISM
Auto regulation
Role of local metabolite
Role of endothelial cells.
NERVOUS CONTROL MECHANISM
Direct nervous control
Indirect nervous control
Neurohumoral control factors.
Friday, November 25, 2016
30. LOCAL CONTROL MECHANISM
AUTO REGULATION
Ability of organ or tissue to
adjust its vascular resistance
& maintain relatively constant
blood flow over a wide range
of blood pressure.
But Fails below 70 mm
Hg blood pressure.
Friday, November 25, 2016
31. ROLE OF LOCAL METABOLITE
At rest 50-70% oxygen
released to
myocardium from
Haemoglobin.
Almost direct & linear
relationship observed
between coronary
blood flow & O2
consumption.
Friday, November 25, 2016
32. ROLE OF LOCAL METABOLITE
Role of Adenosine
(Berne Hypothesis) –
increased myocardial
metabolism leads to
degradation of
Adenine nucleotide
to adenosine.
Friday, November 25, 2016
33. ROLE OF LOCAL METABOLITE
This crosses Myocardial cell
membrane , ECF, reaches
Precapillary Sphincters of
coronary system producing
strong Vasodilator
response.
Role of other metabolite –
hydrogen ions,
Bradykinins, CO2, PG are
other vasodilator
substances.
Friday, November 25, 2016
34. ROLE OF ENDOTHELIAL CELLS.
Endothelium releases
vasodilator Autacoids – EDRF,
Prostacyclin, Endothelium
Derived Hyperpolarizing Factors
(EDHF)
Also releases Vasoconstrictors
Autacoids – Endothelin-1 ,
Angiotensin II, Endothelium
Derived Contracting Factors
(EDCF)
Friday, November 25, 2016
36. DIRECT NERVOUS CONTROL
Through Sympathetic & Parasympathetic nerve
supply.
Sympathetic – Innervate Coronary vessels
Transmitters – E & NE
NE – act on α receptors - Vasoconstriction
E – act on β receptors – Vasodilation.
Net result is – Vasoconstriction.
Parasympathetic – Through Vagus very little
effect – Vasodilation.
Friday, November 25, 2016
37. INDIRECT NERVOUS CONTROL
THROUGH ACTION ON HEART.
Sympathetic stimulation – Increases heart rate &
increase force of contraction of heart – increases
conversion of ATP to ADP – Coronary Vasodilation
– Overrides direct effect of sympathetic
Friday, November 25, 2016
38. INDIRECT NERVOUS CONTROL
THROUGH ACTION ON HEART.
Parasympathetic stimulation. Decreases
coronary blood flow.
Friday, November 25, 2016
39. NEUROHUMORAL CONTROL
FACTORS.
ATP (Purine) – Released with NE causes
Vasoconstriction through P1 & Vasodilatation
through P2 receptors.
NEUROPEPTIDE Y (NPY) – Released with NE
during sympathetic stimulation causes severe
Vasoconstriction.
Friday, November 25, 2016
40. NEUROHUMORAL CONTROL
FACTORS.
CALCITONIN GENE RELATED PEPTIDE (CGRP) –
with substance P releases EDRF & Produces
maximal Dilation of Epicardial coronary arteries.
Friday, November 25, 2016
45. HYPOTENSION.
Hypotension – reflex increase in NE discharge –
coronary vasodilation – Increase CBF
Friday, November 25, 2016
46. HORMONES.
Thyroid Hormone – by increasing metabolism
Adrenaline & Non adrenaline – by acting on B receptors
Acetylcholine – Increases same as parasympathetic
stimulation
Pitressin – Decrease by decreasing coronary resistance
Nicotine – Increases by liberating NE.
Friday, November 25, 2016
48. EFFECT OF IONS
K ion in low conc – dilate coronary vessels –
Increases CBF
In Higher conc- constrict coronary vessels-
Decreases -CBF
Friday, November 25, 2016