00 in the USA, whereas all forms of cancers and infections together, killed only 400,000 in the year, in that country" Physiological basis of treatinent of angina pectons. Aims of the traetment include. (A) Long term and (B) Short term projects. Short term projects are: (1) Use of amylnitrite or its pharmacological relatives during an attack. It relaxes vascular smooth muscles of the systemic arteries (e.g. arterioles) therefore produces fail of BP — reduces work of heart - pain relieved. Other vasodilators are also in vogue. (ii) Use of Ca++ channel blocker like ve However, in the USA, today (in 1991) most people have given up smoking, vegetarianism is popular intake of animal fat is down, obesity is rare and physical exercise is universal CHD, today is not the number one killer, rapamil and nifedipine. These drugs reduce the contractility of heart and lower the myocardial work done and their mode of action has been described in an earlier chapter, (chap: 2. sec V). Verapamil and nifedipine, however also cause coronary vasodilatation. (iii) B blockers like propranolol. which by inhibiting the sympathetic, reduces the cardiac metabolisin and 02 requireinent are lowered. The bradycardia induced by, propranolol also helps the coronary flow. Long term projects include: (i) development of collaterals. The subject (provided there is no infarction) is encouraged to mild but sustained exercise like walking on the level. Question is whether the collaterals grow with physical exercise ? The overall picture is given below, Experiments on the animals have yielded conflicting reports. The clinical experiences however, suggest that physical exercise does help in the growth of collaterals. (ii) Coronary 'by pass surgery', 'where the area of occlusion is by passed by a graft, has been very popular. It greatly improves anginal attacks but it is 19 questionable whether it can prolong the life of the patient. It is also not clear whether it can protect against myocardial infarction Coronary
angiopiatty, where a catheter is introduced into the affected coronary artery and dilated, is also very popular [it should be understood clearly, that the best treatinent at present, when the patient has developed a frank myocardial infarction is to dissolve the clot immediately, say. within aboul 1/2 hr of onset of the chest pain. This is done by urokinase or streptokinase injection which aids powerfully the fibrinolytic mechanism (for details, see chap 5 sec II, plasina fibnnolytic mechanism) (ii) methods to reduce the hyperlipidemia and hypercholesteremia must also be concomit antly tried i(see lipid metabolism chap 10. sec vll. atherosclerosis) (4) Reactrve hyperemia When there is a temporary occlusion of a branch of coronary artery, the part distal to the occlusion suffers from anoxia as usual. But when the occlusion is removed, a marked vasodilatation occurs in the anoxic part (fig. 5.10. 3). Fig. 5 .10.3 To illustrate the phenomenon of reactive hyperemia. This hyperemia which fallows a temporary occlusion is called reactive hyperemia. During occlusion, a 'debt of blood flow' occurred, as shown in fig. 5.10. 3. which is now repaid by the reactive in.peremia Reactive hyperamia occurs in other tissues also, when they are temporarily hypoxic Cause of reactive hyperemia is not very definitely known. It is not due to neural activity. During occlusion, some metabolites accumulate in the rschemic area which produce the hyperemia But the identification of the metabolite(s) is yet to be made with certainty it may be 02 lack, adenosine accumulation or others (like K+ accumulation, lactate accumulation) [Exercise hyparemia which is seen in skeletal muscles is remarkably similar to the reactive hyperamia] NUTRITION OF THE HEART, SUBSTRATE UTILIZATION The heart utilizes tally acids, glucose and lactate principally. small amounts of amino acids and pyruvate are also used. In presence of ketone bodies (acetoacetate, hy-droxy butyrate) in the blood (e.g. in starvation, diabetic ketosis) the heart can vigorosly utilize the ketone bodies, this ineans, although other organs suffer due to lack of nutrients in starvation or diabetic ketosis, the heart has no such problem. Under normal conditions about 60% of the energy is obtained from the fatty acids, About 35% of the energy comes from glucose. II. PULMONARY CIRCULATION 1. Functional anatomy 2. Factors deter-mining pulmonary blood flow. 3. Distribution of the blood, 4. The question of tissue fluid in the lungs. 5 Values, measurement 6. Special functions of pulmonary circulation 7 Applied physiology FUNCTIONAL AWATOMY The pulmonary trunk (also called. the main pulmonary artery',) anses from the right ventricle divides into right and left branches (pulmonary artery) each branch accompanying the main bronchurs, 'enters the lung divides repeatedly ultimately form the capillaries. True arterioles. ie. fine blood vessels with heavy muscu-lature, are not present in the lungs. Recall (fig.5.7.4), in the systemic circulation vene cave, arterioles are present and the main drop of pressure occurs in the arterioles. But in the pulmonary circulation (pulmonary trunk end of pulmonary veins, in man there are four pulinonary veins opening into the left atrium) there is no true artenoles and therefore the pressure drop occurs mainly in the capillaries. Features of pulmonary circulation: 1. The musculature of pulmonary vessels (eg, pulmonary 'trunk, main arteries) are thin BP in pulmonary artery is very low (systolic 20 mm Hg, diastolic about 10 mm Hg ) Pulmonary circulation, therefore , is also called low pressure circulation. 2. The capillary walls of course.
angiopiatty, where a catheter is introduced into the affected coronary artery and dilated, is also very popular [it should be understood clearly, that the best treatinent at present, when the patient has developed a frank myocardial infarction is to dissolve the clot immediately, say. within aboul 1/2 hr of onset of the chest pain. This is done by urokinase or streptokinase injection which aids powerfully the fibrinolytic mechanism (for details, see chap 5 sec II, plasina fibnnolytic mechanism) (ii) methods to reduce the hyperlipidemia and hypercholesteremia must also be concomit antly tried i(see lipid metabolism chap 10. sec vll. atherosclerosis) (4) Reactrve hyperemia When there is a temporary occlusion of a branch of coronary artery, the part distal to the occlusion suffers from anoxia as usual. But when the occlusion is removed, a marked vasodilatation occurs in the anoxic part (fig. 5.10. 3). Fig. 5 .10.3 To illustrate the phenomenon of reactive hyperemia. This hyperemia which fallows a temporary occlusion is called reactive hyperemia. During occlusion, a 'debt of blood flow' occurred, as shown in fig. 5.10. 3. which is now repaid by the reactive in.peremia Reactive hyperamia occurs in other tissues also, when they are temporarily hypoxic Cause of reactive hyperemia is not very definitely known. It is not due to neural activity. During occlusion, some metabolites accumulate in the rschemic area which produce the hyperemia But the identification of the metabolite(s) is yet to be made with certainty it may be 02 lack, adenosine accumulation or others (like K+ accumulation, lactate accumulation) [Exercise hyparemia which is seen in skeletal muscles is remarkably similar to the reactive hyperamia] NUTRITION OF THE HEART, SUBSTRATE UTILIZATION The heart utilizes tally acids, glucose and lactate principally. small amounts of amino acids and pyruvate are also used. In presence of ketone bodies (acetoacetate, hy-droxy butyrate) in the blood (e.g. in starvation, diabetic ketosis) the heart can vigorosly utilize the ketone bodies, this ineans, although other organs suffer due to lack of nutrients in starvation or diabetic ketosis, the heart has no such problem. Under normal conditions about 60% of the energy is obtained from the fatty acids, About 35% of the energy comes from glucose. II. PULMONARY CIRCULATION 1. Functional anatomy 2. Factors deter-mining pulmonary blood flow. 3. Distribution of the blood, 4. The question of tissue fluid in the lungs. 5 Values, measurement 6. Special functions of pulmonary circulation 7 Applied physiology FUNCTIONAL AWATOMY The pulmonary trunk (also called. the main pulmonary artery',) anses from the right ventricle divides into right and left branches (pulmonary artery) each branch accompanying the main bronchurs, 'enters the lung divides repeatedly ultimately form the capillaries. True arterioles. ie. fine blood vessels with heavy muscu-lature, are not present in the lungs. Recall (fig.5.7.4), in the systemic circulation vene cave, arterioles are present and the main drop of pressure occurs in the arterioles. But in the pulmonary circulation (pulmonary trunk end of pulmonary veins, in man there are four pulinonary veins opening into the left atrium) there is no true artenoles and therefore the pressure drop occurs mainly in the capillaries. Features of pulmonary circulation: 1. The musculature of pulmonary vessels (eg, pulmonary 'trunk, main arteries) are thin BP in pulmonary artery is very low (systolic 20 mm Hg, diastolic about 10 mm Hg ) Pulmonary circulation, therefore , is also called low pressure circulation. 2. The capillary walls of course.
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