Brinzolamid - new inhibitor karboanhydrazy
P ervichnaya vidkrytovuhilna glaucoma (Pogue) - one of the most frequent causes of irreversible blindness. It should be noted that the incidence of blindness from glaucoma in the world for the past 30 years has not changed and is 14-15% of the total number of blind [1]. In our country, according to ES Liebman, there is a sharp increase in the role of glaucoma among the primary reasons invadilizatsyi share in nosological structure has increased over the past decade from 12 to 20%, and the prevalence of 0.1 to 0.8 per 10 thousand adults [4].
AP Nesterov in the book "Glaucoma" notes that the pathogenesis of glaucoma regardless of the kind comprising two mechanisms, separated by a space and part time. One operates in the anterior eye and eventually leads to elevated intraocular pressure (IOP). Another mechanism that is localized in the posterior part of the eyeball, is the cause of optic nerve atrophy. Glaucomatous process begins in the anterior part of the eye, changes in the optic nerve is the result bunzi of increased IOP at him.
The leading pathogenetic factor bunzi that causes damage to the optic nerve and the deterioration of visual function is increasing oftalmotonusa. Increased IOP causes mechanical deformation of the lattice plate sclera, anguish in her tubule bundles of nerve fibers and blood microcirculation disturbances in the area. In this regard, the main treatment POUG (medical, laser and surgical action) aimed at lowering IOP to a level that prevents further atrophy of optic nerve fibers [1,2].
Drug antihypertensive therapy is most important in the treatment of glaucoma. Scale the means includes a variety of drugs with different mechanisms of antihypertensive action. At the same time, according to the literature, in 27-33% of patients suffering from glaucoma and oftalmohypertenziyey and receiving bunzi monotherapy antihypertensive agents was identified need for the appointment of additional antihypertensive drugs to normalize IOP [2].
Many patients with glaucoma as an additional therapy is often prescribed oral inhibitors karboanhydrazy (HCA), which play an important role in the secretion of aqueous humor. The medicinal effect of HCA is associated with selective ability to oppress karboanhydrazy activity - an enzyme involved in the process of hydration and dehydration of carbonic acid.
Karboanhydraza - enzyme tsynkoprotyeyidom that is. The content of zinc 0,33-0,34%. Karboanhydraza was first isolated bunzi from red blood cells. In 1 liter of blood of mammals - approximately 1 g karboanhydrazy. bunzi The presence of this enzyme gives the body a chance to rid of excess CO2. Typically, but concentrated in the cellular elements, it is not found in the tissue fluids. bunzi
In humans, this enzyme, which is represented by two isoenzymes KAI and KAII, found in red blood cells, cells of the pancreas, stomach mucosa, parotid gland, kidney, eye ciliary body.
Karboanhydraza catalyzes the conversion karboksyda to carbonic acid (CO2 + H2O = H2CO3). Carbonic acid dissociates later (H + + HCO3-). This reaction - the key to secretory physiological processes in many tissues, including the eye.
As a result of inhibition of activity karboanhydrazy kidney decreases the formation of carbonic acid and bicarbonate reabsorption and decrease Na + tubular epithelium, and therefore bunzi significantly increases the excretion of water. This observed increase in urine pH and loss of potassium ions.
In the formation bunzi of aqueous bunzi humor of the eye bicarbonate ions are actively transported into the back of the camera bespihmentnyh cytoplasm of cells to compensate gradient of positive ions due to active transport bunzi of ions Na +. HO inhibitors block the formation of carbonic acid, thus lowering bunzi production HCO3-. In the absence of sufficient bunzi HCO3- ions increases bunzi positive ion gradient that causes a decrease in the secretion of aqueous humor. This is probably the mechanism by which HCA reduce IOP.
The first drug inhibitor of HO - acetazolamide - was developed half a century ago. In 1954 it was used as a diuretic agent. In the same year was set acetazolamide ability to reduce IOP glaucoma patients.
However, the use of oral HCA such as acetazolamide and metazolamid accompanied by side effects. Side effects include symptoms of malaise, paresthesias, gastrointestinal disturbances (nausea, vomiting and other symptoms), weight loss, depression, anorexia and loss of libido. Also included is information on the occurrence of fever, rash (including erythema polymorphous bunzi and Stevens-Johnson syndrome), kristallouriyi, hematopoiesis disorders, including thrombocytopenia, hemolytic bunzi anemia, leukopenia and agranulocytosis [3, 6, 11].
The emergence of side effects limit the systemic nature of oral inhibitors karboanhydrazy for long-term treatment of glaucoma. They are mainly used for the treatment of acute attack
P ervichnaya vidkrytovuhilna glaucoma (Pogue) - one of the most frequent causes of irreversible blindness. It should be noted that the incidence of blindness from glaucoma in the world for the past 30 years has not changed and is 14-15% of the total number of blind [1]. In our country, according to ES Liebman, there is a sharp increase in the role of glaucoma among the primary reasons invadilizatsyi share in nosological structure has increased over the past decade from 12 to 20%, and the prevalence of 0.1 to 0.8 per 10 thousand adults [4].
AP Nesterov in the book "Glaucoma" notes that the pathogenesis of glaucoma regardless of the kind comprising two mechanisms, separated by a space and part time. One operates in the anterior eye and eventually leads to elevated intraocular pressure (IOP). Another mechanism that is localized in the posterior part of the eyeball, is the cause of optic nerve atrophy. Glaucomatous process begins in the anterior part of the eye, changes in the optic nerve is the result bunzi of increased IOP at him.
The leading pathogenetic factor bunzi that causes damage to the optic nerve and the deterioration of visual function is increasing oftalmotonusa. Increased IOP causes mechanical deformation of the lattice plate sclera, anguish in her tubule bundles of nerve fibers and blood microcirculation disturbances in the area. In this regard, the main treatment POUG (medical, laser and surgical action) aimed at lowering IOP to a level that prevents further atrophy of optic nerve fibers [1,2].
Drug antihypertensive therapy is most important in the treatment of glaucoma. Scale the means includes a variety of drugs with different mechanisms of antihypertensive action. At the same time, according to the literature, in 27-33% of patients suffering from glaucoma and oftalmohypertenziyey and receiving bunzi monotherapy antihypertensive agents was identified need for the appointment of additional antihypertensive drugs to normalize IOP [2].
Many patients with glaucoma as an additional therapy is often prescribed oral inhibitors karboanhydrazy (HCA), which play an important role in the secretion of aqueous humor. The medicinal effect of HCA is associated with selective ability to oppress karboanhydrazy activity - an enzyme involved in the process of hydration and dehydration of carbonic acid.
Karboanhydraza - enzyme tsynkoprotyeyidom that is. The content of zinc 0,33-0,34%. Karboanhydraza was first isolated bunzi from red blood cells. In 1 liter of blood of mammals - approximately 1 g karboanhydrazy. bunzi The presence of this enzyme gives the body a chance to rid of excess CO2. Typically, but concentrated in the cellular elements, it is not found in the tissue fluids. bunzi
In humans, this enzyme, which is represented by two isoenzymes KAI and KAII, found in red blood cells, cells of the pancreas, stomach mucosa, parotid gland, kidney, eye ciliary body.
Karboanhydraza catalyzes the conversion karboksyda to carbonic acid (CO2 + H2O = H2CO3). Carbonic acid dissociates later (H + + HCO3-). This reaction - the key to secretory physiological processes in many tissues, including the eye.
As a result of inhibition of activity karboanhydrazy kidney decreases the formation of carbonic acid and bicarbonate reabsorption and decrease Na + tubular epithelium, and therefore bunzi significantly increases the excretion of water. This observed increase in urine pH and loss of potassium ions.
In the formation bunzi of aqueous bunzi humor of the eye bicarbonate ions are actively transported into the back of the camera bespihmentnyh cytoplasm of cells to compensate gradient of positive ions due to active transport bunzi of ions Na +. HO inhibitors block the formation of carbonic acid, thus lowering bunzi production HCO3-. In the absence of sufficient bunzi HCO3- ions increases bunzi positive ion gradient that causes a decrease in the secretion of aqueous humor. This is probably the mechanism by which HCA reduce IOP.
The first drug inhibitor of HO - acetazolamide - was developed half a century ago. In 1954 it was used as a diuretic agent. In the same year was set acetazolamide ability to reduce IOP glaucoma patients.
However, the use of oral HCA such as acetazolamide and metazolamid accompanied by side effects. Side effects include symptoms of malaise, paresthesias, gastrointestinal disturbances (nausea, vomiting and other symptoms), weight loss, depression, anorexia and loss of libido. Also included is information on the occurrence of fever, rash (including erythema polymorphous bunzi and Stevens-Johnson syndrome), kristallouriyi, hematopoiesis disorders, including thrombocytopenia, hemolytic bunzi anemia, leukopenia and agranulocytosis [3, 6, 11].
The emergence of side effects limit the systemic nature of oral inhibitors karboanhydrazy for long-term treatment of glaucoma. They are mainly used for the treatment of acute attack
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