History
Extracts of the adrenal gland were first obtained by Polish physiologist Napoleon Cybulski in 1895. These extracts, which he called nadnerczyna ("adrenalin"), contained adrenaline and other catecholamines. American ophthalmologist William H. Bates discovered adrenalines usage for eye surgeries prior to 20 April 1896. In 1897, John Jacob Abel (1857–1938), the father of modern pharmacology, found a natural substance produced by the adrenal glands that he named epinephrine. The first hormone to be identified, it remains a crucial, first-line treatment for cardiac arrests, severe allergic reactions, and other conditions. Japanese chemist Jōkichi Takamine and his assistant Keizo Uenaka independently discovered adrenaline in 1900. In 1901, Takamine successfully isolated and purified the hormone from the adrenal glands of sheep and oxen. Adrenaline was first synthesized in the laboratory by Friedrich Stolz and Henry Drysdale Dakin, independently, in 1904.Although secretin is mentioned as the first hormone, adrenaline is the first hormone since the discovery of the activity of adrenal extract on blood pressure was observed in 1895 before that of secretin in 1902. In 1895, George Oliver (1841–1915), a general practitioner in North Yorkshire, and Edward Albert Schäfer (1850–1935), a physiologist at University College of London published a paper about the active component of adrenal gland extract causing the increase in blood pressure and heart rate was from the medulla, but not the cortex of the adrenal gland. In 1897, John Jacob Abel (1857–1938) of Johns Hopkins University, the first chairman of the first US department of pharmacology, found a compound called epinephrine with the molecular formula of C17H15NO4.
Some people have cilioretinal arterial branches, which may or may not be included in the blocked portion. Treatment
While no treatment has been clearly demonstrated to be benefit for CRAO in large systematic reviews of randomized clinical trials, many of the following are frequently used:
Lowering intraocular pressure;
Dilating the CRA;
Increasing oxygenation;
Isovolemic hemodilution;
Anticoagulation;
Dislodging or fragmenting thrombus or embolus;
Thrombolysis; and
Hyperbaric oxygen.To achieve the best outcome for a person with CRAO, it is important to identify the condition in a timely manner and to refer to the appropriate specialist. Prognosis
The artery can re-canalize over time and the edema can clear. However, optic atrophy leads to permanent loss of vision. Irreversible damage to neural tissue can occur after approximately 15 minutes of complete blockage to the central retinal artery, but this time may vary between people. Two thirds of people experience 20/400 vision while only one in six will experience 20/40 vision or better. Epidemiology
The incidence of CRAO is approximately 1 in 100,000 people in the general population. Risk factors for CRAO include the following: being over 50 years of age, male gender, smoking, hypertension, tranexamic acid, diabetes mellitus, dyslipidemia, angina, valvular disease, transient hemiparesis, cancer, hypercoagulable blood conditions, lupus, or a family history of cerebrovascular or cardiovascular issues. Additional risk factors include endocarditis, atrial myxoma, inflammatory diseases of the blood vessels, and predisposition to forming blood clots. See also
Central retinal vein occlusion
Branch retinal artery occlusion
Branch retinal vein occlusion
Amaurosis fugax
Ocular ischemic syndrome

References


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