Wondershare EdrawMind
EdrawMindPharmacology - Adrenaline Drugs
MindMap Gallery Pharmacology - Adrenaline Drugs
- 14
Pharmacology - Adrenaline Drugs
This is a mind map about Chapter 10. Adrenaline drugs, and its main contents include: overview, classification, α, β-R agonist, α-R agonist, β-R agonist.
Edited at 2025-03-10 15:18:47- Rumi 10 spiritual high-dimensional awakenings
Rumi: 10 dimensions of spiritual awakening. When you stop looking for yourself, you will find the entire universe because what you are looking for is also looking for you. Anything you do persevere every day can open a door to the depths of your spirit. In silence, I slipped into the secret realm, and I enjoyed everything to observe the magic around me, and didn't make any noise. Why do you like to crawl when you are born with wings? The soul has its own ears and can hear things that the mind cannot understand. Seek inward for the answer to everything, everything in the universe is in you. Lovers do not end up meeting somewhere, and there is no parting in this world. A wound is where light enters your heart.
- Pathophysiology - Heart failure
Chronic heart failure is not just a problem of the speed of heart rate! It is caused by the decrease in myocardial contraction and diastolic function, which leads to insufficient cardiac output, which in turn causes congestion in the pulmonary circulation and congestion in the systemic circulation. From causes, inducement to compensation mechanisms, the pathophysiological processes of heart failure are complex and diverse. By controlling edema, reducing the heart's front and afterload, improving cardiac comfort function, and preventing and treating basic causes, we can effectively respond to this challenge. Only by understanding the mechanisms and clinical manifestations of heart failure and mastering prevention and treatment strategies can we better protect heart health.
- Pathophysiology - ischemia - reperfusion injury
Ischemia-reperfusion injury is a phenomenon that cellular function and metabolic disorders and structural damage will worsen after organs or tissues restore blood supply. Its main mechanisms include increased free radical generation, calcium overload, and the role of microvascular and leukocytes. The heart and brain are common damaged organs, manifested as changes in myocardial metabolism and ultrastructural changes, decreased cardiac function, etc. Prevention and control measures include removing free radicals, reducing calcium overload, improving metabolism and controlling reperfusion conditions, such as low sodium, low temperature, low pressure, etc. Understanding these mechanisms can help develop effective treatment options and alleviate ischemic injury.
Pharmacology - Adrenaline Drugs
- Rumi 10 spiritual high-dimensional awakenings
Rumi: 10 dimensions of spiritual awakening. When you stop looking for yourself, you will find the entire universe because what you are looking for is also looking for you. Anything you do persevere every day can open a door to the depths of your spirit. In silence, I slipped into the secret realm, and I enjoyed everything to observe the magic around me, and didn't make any noise. Why do you like to crawl when you are born with wings? The soul has its own ears and can hear things that the mind cannot understand. Seek inward for the answer to everything, everything in the universe is in you. Lovers do not end up meeting somewhere, and there is no parting in this world. A wound is where light enters your heart.
- Pathophysiology - Heart failure
Chronic heart failure is not just a problem of the speed of heart rate! It is caused by the decrease in myocardial contraction and diastolic function, which leads to insufficient cardiac output, which in turn causes congestion in the pulmonary circulation and congestion in the systemic circulation. From causes, inducement to compensation mechanisms, the pathophysiological processes of heart failure are complex and diverse. By controlling edema, reducing the heart's front and afterload, improving cardiac comfort function, and preventing and treating basic causes, we can effectively respond to this challenge. Only by understanding the mechanisms and clinical manifestations of heart failure and mastering prevention and treatment strategies can we better protect heart health.
- Pathophysiology - ischemia - reperfusion injury
Ischemia-reperfusion injury is a phenomenon that cellular function and metabolic disorders and structural damage will worsen after organs or tissues restore blood supply. Its main mechanisms include increased free radical generation, calcium overload, and the role of microvascular and leukocytes. The heart and brain are common damaged organs, manifested as changes in myocardial metabolism and ultrastructural changes, decreased cardiac function, etc. Prevention and control measures include removing free radicals, reducing calcium overload, improving metabolism and controlling reperfusion conditions, such as low sodium, low temperature, low pressure, etc. Understanding these mechanisms can help develop effective treatment options and alleviate ischemic injury.
- Recommended to you
- Outline
No relevant template
Chapter 10. Adrenaline-modified medicine
Overview
Adrenaline receptor agonist
Chemical structure and pharmacological effects are similar to sympathetic amines → also known as sympathetic amines
Classification
Catecholamines
Benzene ring 3 and 4 positions C with -OH
include
Adrenaline
Norepinephrine
Isoproterenol
Dopamine
Non-catecholamines
Benzene ring 3 and 4 positions C without -OH, without catecholamine structure
include
Metahydroxyamine
Phenylene epinephrine
Methoxyamine
Ephedrine
Albutamol
Not easily destroyed by catechol-o-methyltransferase
Longer working time
Weaker effect intensity
α,β-R agonist
Adrenaline
Physiological reasons are secreted by adrenal medulla pheochromocytic cells, which activate α and β receptors
The structure is unstable and it is prone to failure when exposed to light. It is prone to failure in alkaline environments. Can't take oral, only injectable
Pharmacological effects
heart
Adr agonizes β1 receptor (the heart mainly contains β1-R)
It has an excitatory effect on myocardial contractility, excitability, conductivity and self-discipline
Myocardial contraction force↑, heart rate↑, conduction speed↑, metabolism↑
Myocardial oxygen consumption↑
Blood vessel
The density of α and β distributions on vascular smooth muscle is very different, so there are differences in the effect on it
R
Main α-contraction
Arterioles, cap. anterior sphincter
Skin, mucous membrane blood vessels
Kidney, mesenteric blood vessels
Major β-dilation
Coronary blood vessels
Skeletal muscle blood vessels
blood pressure
Small doses and treatment doses
Positive effects on the heart → Systolic blood pressure↑
Diastolic pressure
Expansion offset contraction→unchange
Expansion exceeds contraction→Decrease
Pulse pressure↑
Large doses
Systolic blood pressure↑
Diastolic blood pressure↑
α dominant → all blood vessels contract
Pulse pressure↓
"Biphase Reaction"
Alpha receptors of paraglomerular cells
Renin secretion↑
Blood pressure↑
smooth muscle
trachea
Diastolic effect
reason
Agitate β2 receptors, especially when smooth muscle spasms
Inhibiting the release of allergic reaction substances in tissues and mast cells
These substances can shrink blood vessels
Constricting bronchial mucosal blood vessels (α receptors) to reduce airway edema and exudation
Eye
Aroused iris open myometrium alpha receptor → dilated myocardial
metabolism
β2 receptor excitation → insulin secretion ↓ → promote glycogen decomposition
Activate triglycerase → accelerate lipid metabolism
......
Enhanced
Clinical application
Powerful cardiac stimulant → for cardiac arrest
Sudden suspension caused by electric shocks and other factors are prone to ventricular fibrillation, and defibrillator is required at the same time.
Allergic shock
Performance
Small blood vessels expand in large quantities, cap. Permeability↑→BP↓
Bronchial smooth muscle spasm, etc.
mechanism
Contracts arteries and cap. anterior blood vessels, reduces vascular permeability → reduces airway exudation and edema
Relieve bronchial smooth muscle spasm
Improve heart function and strengthen heart
Acute attacks of bronchial asthma and other rapid hairstyle allergies
Diastolic bronchial smooth muscle
Inhibiting the release of allergic substances in tissues and mast cells
Reduce airway edema and exudation
Contract blood vessels → reduce exudation
Local application
Combined with local anesthetics
Contracts blood vessels around the injection site and reduces bleeding
e.g. Reduce bleeding during tooth extraction
Delay the absorption of local anesthetics
Avoid local anesthetic poisoning reactions
Prolong the time of local anesthetic action
Enhance local anesthesia effect
For bleeding from the nasal mucosa and gingival
Agitate alpha receptor → contraction of blood vessels
Contraindications
Hypertension, cerebral arteriosclerosis, ischemic heart disease, heart failure, hyperthyroidism and diabetes
Dopamine
Agitate α, β, DA receptors
Unstable - cannot be taken orally, should be given intravenously
Exogenous DA cannot pass through the blood-brain barrier → no central effect
Pharmacological effects
Blood vessel
Skin mucosa alpha receptor → Vascular contraction, blood pressure↑
DA receptors of kidney and mesenteric vascular → diastolic, vascular resistance↓→ increase kidney blood flow and increase glomerular filtration rate
Large doses
Excite the heart, contract blood vessels → boost pressure
heart
DA at high concentrations
Agitation of the heart β1 receptor
Promote NA Release
→Strong positive muscle strength effect
kidney
Low concentration DA
Agitate the kidney DA1 receptor → dilate the renal blood vessels, glomerular filtration rate ↑→ Urination
Directly inhibit reabsorption of renal tubular sodium → sodium excretion and urination
Clinical application
shock
Such as cardiogenic shock, septic shock and hemorrhagic shock, etc., especially hypovolemic shock accompanied by renal dysfunction, especially hypovolemic shock.
Acute renal failure
Use with diuretics
Ephedrine
Directly agonize α and β receptors; it can also promote the release of NA
More stable, easy to take oral
Pharmacological effects
heart
Positive
Blood vessel
Vascular contraction of skin mucosa
Skeletal muscle/coronary vasodilation
BP↑
Bronchial
Smooth muscle β receptor → diastolic
Vascular alpha receptor → Vascular contraction, reduced exudation, and reduced edema
The same effect, but weaker than NE and lasts longer
CNS
Passing the blood-brain barrier
Excitement effect
application
Hypotension
e.g. BP reduction caused by improper epidural/sarachnoid anaesthesia
Congestive nasal congestion
Contracts the nasal mucosa blood vessels to smooth ventilation
Bronchial asthma
Adverse reactions
Central excitation → anxiety, insomnia
Confront with barbiturates
Rapid tolerance
Mechanism: Promote the release of Adr nerve endings to reduce or even exhaust
Contraindications
Same as Adr
α-R agonist
Norepinephrine NA
Agitated α-R＞＞β1-R＞＞β2-R
Oral structure is easily destroyed, and intramuscular injection can easily contract blood vessels and cause local necrosis → Intravenous drip
Pharmacological effects
Blood vessel
Strong contraction effect, skin and mucosal blood vessels > kidney, mesenteria, liver and cerebrovascular → obvious peripheral resistance↑
Coronary dilation
reason
Metabolites (such as adenosine)↑
BP↑→Perfusing pressure↑
heart
Positive stimulation effect
That is, "contraction force, output volume, heart rate, and accelerated conduction"
Weaker effect strength than Adr
However, under the overall effect, the heart rate is unchanged or slightly
Reason: Total peripheral resistance↑→Vagus N activity reflexivity is enhanced
Large doses → obvious self-discipline ↑ and even arrhythmia
blood pressure
When the effect of small doses of NA blood vessel shrinkage is not obvious, due to heart excitation → systolic blood pressure ↑, pulse pressure ↑
At large doses, vasoconstriction is obvious → systolic blood pressure and diastolic blood pressure are obvious ↑, pulse pressure ↓ → tissue blood perfusion ↓ ↓
application
shock
Drug-induced shock
Talking agents and general anesthetic poisoning
Neurogenic shock
Upper gastrointestinal bleeding
No absorption after oral administration → local vasoconstriction of gastrointestinal mucosa
Cardiac arrest
Adverse reactions
Acute renal failure
Severe contraction of kidney blood vessels causes kidney damage
When long-term intravenous drip, excessive concentration or leaking of the medicine liquid, local blood vessels at the injection site may be severely contracted.
In severe cases, local tissue ischemia and necrosis
Treatment - Local infiltration injection
Procaine-blocking nerve conduction
α receptor blocker
Contraindications
Same as Adr
Metahydroxyamine
It can also promote NA release
Features
Weak renal blood vessels and are not prone to renal failure and arrhythmia
Therefore, NA has been replaced for anti-shock
Methoxylate
Features
Reflective vagus N is strong
The heart rate is significantly slowed down
Directly inhibit sinus nodes
For the treatment of paroxysmal supraventricular tachycardia
Phenylene epinephrine
Features
Excited iris opening the large muscle alpha receptor → enlarged pupil (weaker than atropine) → do not cause intraocular pressure ↑ and regulate paralysis
Quick short-acting pupil shrinkage agent
More suitable for ophthalmic examination
β-R agonist
β1/β2-R agonist
Isoproterenol
Oral administration is ineffective, generally intravenous injection/drip, also used as a spray
Pharmacological effects
heart
β1 receptor, obvious excitation effect
Mainly excited sinoatrial nodes
Fewer ventricular arrhythmias
Blood vessel
Skeletal muscle blood vessels and coronary vasodilation → diastolic blood pressure ↓; excitement of the heart → systolic blood pressure ↑
Pulse pressure↑
Bronchial
Agitated β2-R
Inhibit the release of allergic active substances
Diastolic bronchial smooth muscle
Relieve bronchospasm and obvious effect
metabolism
Agitate beta receptors → promote glycogen and fat decomposition → enhance
application
Various types of cardiac arrest
Direct effect on sinoatrial nodes → pacing effect
Not easy to induce ventricular fibrillation/arrhythmia (adrenergic induces)
Atrioventricular block
Strong effect on sinoatrial node excitation
Bronchial asthma
Sublingually take or spray
shock
Cannot significantly improve tissue microcirculation disorders → not commonly used
β1-R agonist
dobutylamine
effect
Selective agonizing β1 receptors, stimulating the heart
Heart contraction force↑
Cardiac output↑
No significant change in heart rate
Two isomers
S
Weaker effect on β receptors
Mainly agonizing alpha receptors
R
Agitation effect on β receptor > S about 10 times
No agonism effect on renal DA receptors
Clinical application
Mainly treats myocardial ridge blockage and heart failure
β2-R agonist
Albutamol
Tebutalin
Make bronchial dilation
Prevent and treat bronchial asthma