Development of cardiac hypertrophy and its relationship to the cardiac baroreflex deficit in hypertension.
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A total of 105 patients with suspected sick sinus syndrome were examined. All of them underwent transesophageal pacing and endoscopical investigation. A relationship is shown between lesions of the gastrointestinal tract and emergence of the sinus vagal depression leading to various disturbances of cardiac rhythm.
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Blockade of biosynthesis of prostaglandins (indomethacin) was shown to decrease significantly disorders of cardio- and hemodynamics after immune heart damages (intracoronary anticardiac serum injections) in experimental anesthetized dogs. A positive effect of indomethacin was produced by blockade of the first part (0-15 min) of capacity vessels dilation reaction (blood deposition), subsequent decrease of venous return limit and fall of heart output. Indomethacin potentiated constriction of coronary vessels.
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Ethanol was administrated intragastrically (25%, w/v) to Wistar male rats. They received 7-10 g ethanol/kg b.wt. daily in 2 fractional doses for 6 days. In 20-24 hours after the last ethanol administration behavioral and neurological signs of withdrawal syndrome and pain latent period were measured. Analgesia was determined using the tail flick and hot plate tests. Two days later systolic function of the isolated perfusing heart and creatine phosphokinase outflow were examined. Rats had longer latent pain period than in control. Heart perfusion revealed a decrease of systolic pressure, dp/dt of systolic and diastolic pressure, increase of enzyme outflow. Kendall's correlation analysis revealed a positive relationship between intensity of withdrawal symptoms and analgesia index in the hot plate test (tau = +0.343, p. 0.01) and a lack of relationship in the tail flick test. There was negative relationship between the analgesia index and the indices of heart disorders. It is proposed that analgesia index can be used as a predictor of the cardiac muscle injury caused by the alcoholic abstinent syndrome.
In 1951 in our laboratory in Stockholm, we successfully used our experimental pump oxygenator: the first dogs survived 40 minutes of total cardiopulmonary bypass with right ventricular cardiotomy. In the same year extracorporeal circulation was combined with hypothermia (26 degrees to 28 degrees C) to allow lower perfusion flows, thus diminishing blood trauma and the risk of perfusion complications. To avoid air emboli during cardiotomies, the heart was "arrested" with electrically induced ventricular fibrillation (1952). Our standard perfusion technique used cooling and rewarming with left ventricular bypass, the oxygenator was used only during intracardiac manipulations and when the right ventricle was unable to maintain a sufficient pulmonary circulation. Left ventricular bypass was continued until normal body temperature was reached and the heart could be weaned off the pump. In July 1954 we successfully extirpated a left atrial myxoma in our first patient undergoing open heart surgery, a 40-year-old woman, who is still alive today. Other successful applications of open heart surgery involved resection of a huge left ventricular aneurysm after infarction in 1955, correction of supracardiac total anomalous venous return in 1956, and the first hemodynamic correction of transposition of the great arteries by atrial switch method in 1958. Also in 1958, the first totally implantable pacemaker was inserted in a patient with total atrioventricular block to eliminate the infections that occurred along the percutaneous pacemaker leads. In October 1958, we also operated on a patient with severe angina pectoris with stenosis of the left anterior descending and circumflexed arteries and occluded right coronary artery. Endarterectomy of the left coronary arteries was performed, and the arteriotomies were repaired with saphenous vein patches.
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The chronic treatment of rats with the beta-adrenergic antagonist propranolol causes a double increase in the amount of beta-adrenergic receptors in the cardiac membranes. The purpose of the paper is to investigate the effect of propranolol on the activity and regulatory properties of rat heart adenylate cyclase. Propranolol injections to rats for 3 weeks (10-20 mg/l kg bw) did not influence the enzyme basal activity but caused a rise of a degree of myocardial adenylate cyclase activation by isoproterenol and glucagon.
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The clinical course and biochemical, radioimmune and electrophysiologic findings were assessed in 421 patients with acute myocardial infarction involving heart rhythm and conductivity disorders and 49 patients with acute myocardial infarction, free of cardiac electrical instability. The studies were carried out during arrhythmias and after they were controlled, prior to treatment, at the peak of antiarrhythmic effect of medication, and after a continuous treatment course. Heart rhythm disorders related to acute myocardial infarction were accompanied with a marked response on the part of blood free fatty acids, sympatho-adrenal and kallikrein-kinin activity and carboxycathepsin. Metabolic and neurohumoral changes were eventually reversed and tended to normalize as soon as the sinus rhythm was restored by treatment.
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Malonic dialdehyde content was increased by 53% in the myocardium of male Wistar rats (250-300 g) devoid of vitamin E for 2 months, as compared to the control rats (animals receiving an optimal amount of vitamin E). Transitory ischemia (10 min) with subsequent reoxygenation (5 min) was induced during open heart surgery under urethan anesthesia. Ischemia was induced by the occlusion of the descending branch of the left coronary artery. In ischemic rats with vitamin E deficiency the incidence of ventricular fibrillation, tachycardia, extrasystoles and the additive duration of arrhythmias were significantly increased as compared to the control.
Using ultrafiltration and subsequent gel filtration a fraction of middle mass peptides (MMP) possesing cardiodeppressing activity, has been isolated from the blood plasma of dogs exposed to burn injury. In contrast to the corresponding MMP fraction from healthy animal blood, this fraction suppressed contractility of the isolated rat's papillary muscle. Moreover, the active MMP fraction caused an appreciable bradycardia when administered subarachnoidally. The same phenomenon is typical of the corresponding MMP fraction from intact dog's blood, but the rate of bradycardia is significantly lower than that obtained for the fraction from the blood of injured animals. The possibility of local and central-mediated influence of the active fraction on heart functions is discussed. Central-mediated action of the active MMP fraction is confirmed by the ability of other MMP fractions from the blood of injured animals to enhance the blood-brain barrier permeability.
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