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Generic Isordil sublingual (Isosorbide dinitrate 5mg)
- Denomination
Isordil, Sorbitrate
- Active Substance
Isosorbide Dinitrate
- Indications for Use.
Stenocardia (cessation and preventive measures of attacks), acute myocardial infarction, acute left ventricular failure, hypertension, backward heart failure.
- Action
Under the influence of Isosorbide Dinitrate there comes relaxation of smooth muscles, arteries and veins. From the other hand, the drug has an obvious capacity to dilate coronary vessels and, thus, it increases the oxygen delivery to heart muscle.
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Posology and Administration
Isosorbide Dinitrate should be taken orally, sublingually, intravenously, with inhalation, with skin application. In stenocardia: capsules and tablets — 5–20 mg each every 6 hours(if needed it may be taken up to 20–40 mg 4 times daily); dosage forms of durable action should be taken 40–80 mg every 8–12 hours (should be swallowed in whole); chewing tablets should be taken 5 mg each every 2–3 hours.
Sublingually it should be taken 2,5–5 mg each, if needed - every 2–3 hours.
In acute myocardial infarction and acute left ventricular failure the drug should be used intravenously: the starting dose is 1–2 mg/hour, the maximal dose is 8–10 mg/hour.
With inhalation in order to stop stenocardia attacks: it is necessary to spray 1–3 doses on the mouth cavity mucus coating with an interval of 30 seconds in a breath-holding spell.
Skin application - 1 g of cream/2 doses are to be applied on the skin surface.
- Counterindications
Hypersensitivity, anemia, insult to the brain or recently had head injury, glaucoma, compromised function of thyroid gland, hypotension, pregnancy, breastfeeding (breastfeeding should be stopped), childhood.
- Should Be Taken with Precautions, if…
With caution Isosorbide Dinitrate is administered to stroke patients; to high intracranial pressure patients, to hypotension-prone patients; to elderly people; to pregnant and breastfeeding women. In the period of treatment, especially in cases of gradual increase of a dose, control of arterial tension and frequency of heart beats is needed.
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Interface with Other Medications
If there is a need of combination of drugs - approach your attending doctor on the matter of compatibility of medications.
- Overdosing
Symptoms: cyanosis of lips and nails, severe dizziness or fainting fit, pressure sense in the head, weakness, labored breath, weak heartbeat and rapid heart, elevated temperature of the body, convulsions.
- Side Effects
Flush, headache, dizziness, nausea, vomiting, heat sensation on the tip of the tongue, orthostatic hypotension, collapse, motor anxiety, stiffness, disorder of attention, tachycardia, withdrawal syndrome.
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Pregnancy and Lactation
The use in the I-st trimester of pregnancy is counterindicated. Administration in the II-nd-III-d trimester of pregnancy is possible only on strict indications and under permanent medical control. During treatment breastfeeding should be stopped.
- Driving
In the beginning of the treatment the people whose activity requires quick psychic and motion reactions should take a special care.
DYSLIPIDEMIA AND PHYSICAL ACTIVITY
Epidemiology
Physical inactivity in 51 studies involving 4700 subjects showed the following patterns:
• Decreased plasma HDL-C by 4.4%, which represents an approximate increase in coronary heart disease risk of 4% in me and 6% in women.
• Increased plasma triglycerides, LDL-C, and total cholesterol b 3.8%, 5.3%, and 1.0%, respectively.
The effect of physical activity is most pronounced postprandially, but the effect is missed clinically. Blood lipids must be measured in the fasting state so that the results can be compared to population norms. Otherwise, patients would present with huge postprandial variations in lipid levels related to the timing and content of their last meal, and meaningful diagnosis would be impossible. Note, however, that fasting is not a natural condition for most individuals in the U.S. On a population basis, repeated elevations of postprandial triglyceride-rich lipoproteins do contribute to the development of atherosclerosis/CHD. Unfortunately, the role of physical activity on blood lipids is underestimated due to the testing procedures.
Biochemical and Cellular Mechanisms
A single preceding bout of exercise decreases the rise in post-me; blood lipids (i.e., diminishes postprandial hyperlipidemia). The rise in blood triglycerides is attenuated after a high-fat, high-carbohydrate me if an aerobic (treadmill run or walk) bout of exercise preceded the meal by 16-18 hours in untrained women.
In another report, reductions of 28%, 42%, and 45% in the post-meal rise in blood total triglycerides, VLDL-triglycerides, and chylomicron-triglycerides, respectively, were produced by physical activity (2 hrs at 60% of maximal effort running on a motor-driven treadmill) that had been performed 16 hours prior to eating a fatty meal at time zero in men. The clinical significance of post-exercise-induced reductions in plasma triglycerides is that most sedentary individuals in the U.S. are likely "persistently" hyperlipidemic, considering the relatively brief, perhaps even nonexistent periods of true fasting during a 24-hour period. As the exercise-induced reduction in plasma triglycerides is greater after a meal than in a fast, the true significance of the exercise-induced reduction of plasma lipids is likely underestimated. There are two mechanisms by which physical activity attenuates the rise in blood triglycerides after a fatty meal:
1. Increased clearance of triglycerides from the blood by the previously exercised skeletal muscle.
2. Increased lipoprotein lipase (LPL) activity in exercising skeletal muscles
• LPL activity in the blood and skeletal muscle peaks about 4 to 18 hours post-exercise as it takes this long for LPL to increase in the capillaries of the exercised muscles. Postprandial plasma triglycerides peak about 4 hours after a meal.
• Individuals with the lowest LPL activity in skeletal muscles after exercise also had the highest increases in postprandial hyperlipidemia.
Blood HDL-C increased the most after exercise if the exercise bout had been performed 12 hours prior to the meal. The increase in HDL-C was associated with an increase in LPL activity. Increased levels of HDL-C are seen in the venous blood from exercising skeletal muscles,
The effect of a single bout of physical activity in lowering the post-meal hyperlipidemia is short-lived, and thus is of clinical significance. Persistent, routine physical activity is required to obtain and maintain the benefits of the lipid-lowering effects of physical activity.
Physical activity increases LPL activity in skeletal muscle, allowing the muscle to take up and replenish its stores of triglycerides. Initial changes in LPL levels in fat and skeletal muscle are mediated via post-translational mechanisms. Concurrently, the transcription rate of the LPL gene has been reported to be lower in the non-exercising leg muscle as compared to muscle recovering from 60-90 minutes of exhaustive one-legged knee extensor exercises. The signaling mechanisms by which physical inactivity keeps skeletal muscle LPL low are unknown. However, it is known that physical activity increases skeletal muscle LPL protein content via alterations in local cellular homeostasis, rather than by adrenergic-receptor stimulation.
Physical inactivity (sedentary state) results in a preferential uptake of fat or sugar into adipose tissues, rather than skeletal muscle. The preferential upregulation of LPL protein in fat cells by physical inactivity causes the breakdown of triglycerides in capillaries around fat cells, which directs blood fat into fat cells. Furthermore, physical inactivity decreases the expression of LPL protein in skeletal muscles. Consequently, triglyceride breakdown is minimized in capillaries supplying skeletal muscle.
*10/282/5*
CARDIO & BLOOD
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