Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Guancydine (1-cyano-3-tert-amylguanidine) lowered within normal limits the tensional values in an interval of four hours after its administration in eight out of nine hypertensive patients under experiment. The hypotensive effect of a single oral dose of 500-750 mg persists for about 6-7 hours after its administration. Guancydine does not impair the vasopressor response to angiotensin II but reduces the action of this peptide on the excretion of water, Na, K and Ca through urine. The hypotensive effect of Guancydine is associated with a decrease of platelet adhesiveness and an activation of fibrinolysis. In view of this fact, Guancydine might play a role in the prophylaxis of complications of arterial hypertension - atherosclerosis and trombosis. The increase of venous blood oxygenation after Guancydine could be attributed to the opening of arterio-venous shunts or to the reduction of tissular extraction of oxygen. Guancydine does not seem to be toxic. It produced, in some patients, slight headache and orthostatic hypotension, especially during the first hours after administration.
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PMID:Guancydine, a new hypotensive agent with complex action. 56 30

Horses clinically affected with chronic obstructive pulmonary disease (COPD) were found to have pulmonary artery hypertension which was associated with systemic arterial hypoxia. The pulmonary hypertension in symptomatic COPD-affected horses was partially reversible upon remission of clinical signs or by oxygen administration. The induction of acute hypoxaemia caused an increase in pulmonary artery pressure in both normal and COPD-affected horses.
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PMID:Pulmonary artery pressures in normal horses and in horses affected with chronic obstructive pulmonary disease. 56 82

A patient with intractable congestive cardiac failure secondary to renovascular hypertension and severe coronary artery disease was infused with the competitive antagonist of angiotensin II, saralasin acetate. The infusion produced an impressive increase in cardiac output and left ventricular stroke work index in parallel with a striking decrease in the systemic and pulmonary vascular resistance, the coronary resistance, and the myocardial oxygen consumption. It is suggested that angiotensin inhibition may present advantages over other forms of treatment of congestive cardiac failure in selected cases.
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PMID:Angiotensin II inhibition. Treatment of congestive cardiac failure in a high-renin hypertension. 57 78

The role of physiological changes occurring during prolonged seizures in the causation of epileptic brain damage has been investigated experimentally in baboons and rats. Prolonged drug-induced myoclonic seizure activity is associated with initial arterial hypertension and subsequent hypotension, increased venous pressure, early hyperglycaemia and subsequent hypoglycaemia, variable arterial hypoxia and lactacidosis, and hyperpyrexia. Cerebral metabolic rate for oxygen and glucose is increased 2--3 fold throughout prolonged seizures provided the physiological status of the animal is well maintained. Ischaemic neuronal change is found after seizures lasting 1.5--7 hours, involving the small neurones of the third cortical lamina, Purkinje and basket cells in the cerebellum, and pyramidal neurons in the endfolium and Sommer sector of the hippocampus. Muscular paralysis and artificial ventilation minimise late physiological changes such as arterial hypotension and hyperpyrexia, and protect against cerebellar damage, but only slightly against neocortical and hippocampal damage. When arterial hypotension, hypoxia or hypoglycaemia lead to a reduction in the intensity of seizure discharge in paralysed, ventilated rats, there is also a reduction in hippocampal and neocortical damage. Factors intimately related to the intensity and duration of the neuronal discharge are responsible for neocortical and hippocampal lesions.
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PMID:Physiological changes during prolonged seizures and epileptic brain damage. 58 96

Intact anesthetized dogs were exposed for 75 min to either 5.75, 9.0, or 12.0% oxygen in nitrogen. Although pulmonary artery pressures were significantly elevated in all hypoxic exposures, systemic hypertension occurred only at the onset of severe hypoxia(5.75% O2). Coronary blood flow increased from an average of 130 during normoxia to a peak of 400 ml/100 g per min during inhalation of 5.75% O2, and coronary sinus oxygen tensions of 8 Torr and oxygen contents of 1.1 ml/100 ml were sustained for 75 min without biochemical, functional, or electrophysiological evidence of myocardial ischemia. Cardiac index (CI) increased significantly only during severe hypoxia (5.75% O2) with the greatest elevation after 30 min. Subsequently, CI decreased concomitantly with a 27% elevation in arterial hemoglobin concentration and oxygen-carrying capacity. It is concluded that the hypoxic threshold for significant elevations of cardiac output is between 6.0 and 9.0% O2.
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PMID:Effects of acute prolonged hypoxia on cardiovascular dynamics in dogs. 59 70

Cardiovascular, aerobic, and ventilatory responses to a multistage treadmill test of near-maximal exercise were determined in 208 middle-aged Chinese men to provide standards in health, and to identify differences in relation to hypertension, coronary heart disease, chronic pulmonary disease and stroke. Except in patients with hypertension, exercise duration was shortened and symptom-limited oxygen uptake was reduced in all disease groups. Unexpectedly, stroke patients exhibited lower heart rate responses to exercise than did patients with coronary heart disease.
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PMID:Near-maximal exercise responses in health and disease in middle-aged Chinese men. 59 76

In tests conducted on anesthetized cats it was shown that imipramine used in doses of 1 and 3 mg/kg causes hypertension, increases the vascular tone in the kidneys and limbs. In doses of 5 and 10 mg/kg the drug provokes a short-lived (1--3 minutes) hypertension with a subsequent prolonged drop of the arterial pressure. The tonicity of the kidney and limb arteries changes in the same way as the arterial pressure, but the vascular tone in the heart only falls. In these doses imipramine blocks the adrenergic transmission of the excitation from the sympathetic nerve to the effector, e. g. produces a sympatholytic effect. Imipramine in a dose of 1 mg/kg intensifies the coronary circulation and then the oxygen absorption by the heart increases to a still greater degree. This is attended by the development of tachycardia, a greater cardiac output and an intensified contractility of the myocardium. In doses of 5 and 10 mg/kg imipramine protractedly reduces the cardiac ejection, coronary blood flow and significantly lowers the contractile function of the heart muscle.
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PMID:[Effect of imipramine on the vasomotor tone, blood supply and activity of the heart]. 59 97

Cerebral blood flow autoregulation (CBFA) to changes in perfusion pressure has not been previously reported in the rat. A modification of the Kety and Schmidt technique employing 133Xenon was used to measure cerebral blood flow (CBF) in paralyzed adult Sprague Dawley rats passively ventilated with 70% nitrous oxide and 30% oxygen. At a mean arterial blood pressure (MABP) of 121 +/- 19 mm Hg, and a mean arterial PCO2 of 36.2 +/- 2.9 mm Hg, mean CBF was 103 +/- 22 ml/min/100 gm of brain. CBF responses to hypercarbia were 4.9 ml/min/100 gm per mm Hg change in arterial PCO2. CBF was measured during steady state levels of hypo- and hypertension induced by phlebotomy, or by intravenous metaraminol, over the MABP range of 48-205 mm Hg. From a MABP of 80 to 160 mm Hg. CBF remained nearly constant, indicating the presence of CBFA. However, when MABP exceeded 160 mm Hg, CBF became pressure dependent, indicating a "breakthrough" of autoregulation in acute severe hypertension.
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PMID:Cerebral blood flow autoregulation in the rat. 64 8

A 20 year old woman with tetralogy of Fallot and an associated atrial septal defect presented with severe hypertension and congestive heart failure. She had been acyanotic for several years. An acute trial of antihypertensive therapy during cardiac catheterization resulted in severe systemic oxygen desaturation and loss of consciousness. Since surgical correction, antihypertensive therapy has been well tolerated. This case demonstrates the hemodynamic importance of systemic vascular resistance in tetralogy of Fallot and the need for extreme caution if aggressive antihypertensive therapy is attempted before surgical correction.
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PMID:Systemic hypertension complicating tetralogy of Fallot: effects of antihypertensive therapy. 68 43

A cardiac catheter enclosing an extensible blade was used to enlarge the interatrial opening in seven patients. Two patients with transposition of the great arteries who had balloon atrial septostomy as newborns subsequently presented with clinical evidence of a restrictive interatrial opening at 1 and 4 months of age. Cardiac catheterization confirmed restenosis of the interatrial opening and inadequate intracardiac mixing. After blade atrial septostomy the systemic arterial oxygen saturation increased by 20% and 30%, respectively. Five patients with mitral atresia complex, ages 2 months-9 1/2 years, had a restrictive interatrial communication and severe pulmonary venous hypertension (mean left atrial pressures ranged from 20-38 mm Hg). Following blade atrial septostomy, the pressure gradient between the atria was almost completely abolished and prompt clinical improvement was observed in each patient. All patients tolerated the procedure without complications. Blade atrial septostomy was a safe, effective procedure for enlarging the interatrial communication in this limited series of patients with an interatrial septum too thick to permit adequate rupture by conventional balloon atrial septostomy.
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PMID:Clinical use of blade atrial septostomy. 68 69


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