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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Calcium antagonists are now widely used for the treatment of clinical hypertension and angina pectoris. They are efficacious for the treatment of vasospastic, fixed atherosclerotic and mixed angina; they reduce the incidence of silent ischemia; and they have been shown to reduce postmyocardial infarct angina. Experimental data suggest that they may have certain cardioprotective properties in cases of acute myocardial ischemia and infarction, stunned myocardium, diastolic dysfunction, left ventricular hypertrophy and atherosclerosis. Moreover, they have been shown to improve exercise performance, as well as the diastolic abnormalities in patients with hypertrophic cardiomyopathy. In animals, they may delay or reduce the extent of myocardial necrosis after coronary occlusion or coronary occlusion followed by reperfusion, and in low doses that do not alter the hemodynamic profile, they have been shown to enhance the return of ventricular function in animals with stunned myocardium. However, the early first-generation calcium antagonists (nifedipine, verapamil, diltiazem) have not been shown to reduce myocardial infarct size or to enhance survival in patients with acute myocardial infarction. There now are clinical studies that suggest that, unlike beta blockers or nitrates, nifedipine may slow the development of atherosclerotic progression in humans over a 2-year period, and it seems likely that in the 1990s there will be further expansion of the use of calcium antagonists for not only angina and hypertension but also for aspects of cardioprotection. That calcium antagonists may delay, prevent or possibly regress atherosclerotic lesions is an exciting possibility.
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PMID:Progress in cardioprotection: the role of calcium antagonists. 214 58

Between 1974 and 1988, 7 myocardial infarctions occurred in 6 (4 men, 2 women) out of 400 systemic lupus erythematosus patients. Their ages at the onset of lupus ranged from 13 to 44 years (m = 26). Four had renal involvement. Control of lupus in all 6 patients required high-dose steroids (at least 1 mg/kg/d of prednisone). Myocardial infarction occurred 4 to 19 years after the onset of lupus (m = 13). One patient died of cardiogenic shock. When the infarction occurred, only one patient was undergoing a lupus flare, while the disease was quiescent or slightly active in the 5 others. One patient had no risk factors for atheroma but had been taking steroids for 10 years. Among the other 4, one had hypertension, another had hyperlipidemia and 3 were smokers; they had been on steroids for 2, 4, 11 and 13 years. Coronary angiogram showed occlusion in all 4, but atheroma in only 2 patients. Lupus anticoagulant was present in 3 of these 4 patients. The mechanisms responsible for coronary occlusion in lupus patients are probably complex and interwoven. In addition to "classical" factors (i.e., vasculitis or steroid-induced atheroma), other factors, such as antiphospholipid antibodies and/or smoking, may play an important thrombogenic role.
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PMID:[Myocardial infarction in systemic lupus erythematosus. 7 cases in 6 patients]. 228 5

We used the technique of high-performance liquid chromatography combined with radioimmunoassay to establish the profile of angiotensin peptides in the periphery and across the circulation of the dog's heart. Data were obtained before and after blockade of angiotensin converting enzyme, and after acute myocardial ischemia produced by occlusion of the left anterior descending coronary artery. Baseline values of plasma renin activity and immunoreactive angiotensin II were higher in the aortic root than in the coronary sinus but concentrations of angiotensin I and angiotensin-(1-7) were similar. In untreated animals, coronary occlusion produced significant increases in renin activity and arterial and venous levels of angiotensin I and angiotensin II. Inhibition of converting enzyme with benazeprilat (CGS-14,831) increased baseline circulating levels of angiotensin I, whereas angiotensin II and its carboxyl terminal fragments were reduced markedly. Baseline plasma levels of angiotensin-(1-7) and its fragments did not change. Myocardial ischemia in benazeprilat-treated dogs increased plasma renin activity and circulating levels of angiotensin I. Concentrations of angiotensin II and angiotensin-(1-7) did not change either in peripheral blood or across the coronary circulation. These results indicate that angiotensin peptides can be formed endogenously by enzymatic pathways alternate to converting enzyme. Furthermore, these data provide the basis for a further understanding of the role of the renin-angiotensin system after myocardial ischemia.
Hypertension 1990 Feb
PMID:The renin-angiotensin system during acute myocardial ischemia in dogs. 240 54

Cicletanine is a new antihypertensive agent. In view of its various pharmacological properties and of the different factors involved in sudden death, cicletanine was tested on an ischaemia-reperfusion model in anaesthesized dogs. In these experiments myocardial reperfusion induced ventricular fibrillation in 87 p. 100 of the cases, where as only 20% of those animals who received cicletanine 20 mg/kg intravenously 15 minutes before the 30 minute coronary occlusion developed ventricular disorders (p less than 0.001 vs controls). Moreover, cicletanine showed good antiarrhythmic activity during occlusion (total number of arrhythmias: 73.0 +/- 23.15 in treated animals, as against 293.4 +/- 40.03 in controls; p less than 0.05). Thus, antihypertensive treatment with cicletanine may prevent some of the cardiovascular risks associated with arterial hypertension.
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PMID:[Effect of cicletanine on a sudden death model in dogs]. 251 57

The presence of a lupus anticoagulant (LA) is paradoxically associated with a high incidence of arterial and venous thrombosis. In a patient with a lupus-like systemic disease, having received phenindione for 11 years, LA was discovered in association with recurrent deep venous thrombosis, a right atrial thrombus, coronary occlusion, arterial hypertension, thrombopenia, and anticardiolipin antibodies without anti-DNA antibodies. Renal cortical ischemia was detected by a tomographic scan. Renal biopsy showed glomerular ischemia and diffuse interstitial fibrosis. After a one-year anticoagulant and steroid therapy, LA has disappeared despite a high level of anticardiolipin antibodies, and renal function remains normal.
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PMID:[Renal cortex ischemia, right atrial thrombosis and coronary occlusion in anti-phospholipid antibody syndrome]. 251 17

Open chest anesthetized dogs were given dopamine (DA) in intravenous (i.v., 2-16 micrograms.kg-1.min-1) and intracoronary (i.c., 10-40 micrograms.min-1) infusions. The drug effect was analyzed using the nonselective beta-adrenoceptor antagonist oxprenolol (0.5 mg.kg, i.v.) and the nonselective alpha-adrenoceptor antagonist phentolamine (1.0 mg.kg-1, i.v.). Coronary blood flow (CBF, electromagnetic flowmeter), arterial pressure and left ventricular contractile force (strain gauge) were measured. Coronary vascular responses were characterized by changes of CBF and calculated coronary vascular resistance (CVR). In the control state, DA-induced arterial hypertension (i.v. administration) and augmented inotropism (i.v. and i.c. administration) were accompanied by a dose-dependent coronary vasodilatation (increase of CBF and decrease of CVR). Oxprenolol converted coronary vasodilatation to vasoconstriction during DA infusions and blocked the inotropic action; the hypertensive DA effect remained unaffected. Similar alterations were observed after a transitory (45 min) regional myocardial ischemia, elicited by coronary occlusion. On the other hand, phentolamine-pretreatment potentiated the DA-induced coronary vasodilatation and converted hypertension to hypotension; the inotropic component of the DA action was not affected. After combined beta- and alpha-blockade, DA failed to increase CBF and decrease CVR during the infusion periods. Instead, the drug elicited a very slight coronary vasoconstriction. I.c. (but not i.v.) infusions of DA were regularly followed by a rebound-like, transient CBF increase, even after combined beta- and alpha-blockade. These results show that all of the multifactorial determinants of the direct, steady state coronary effects of DA can be ascribed to alpha- and beta-adrenoceptor stimulation, whereas the hypothetical dopaminergic coronary vascular receptors do not seem to play a decisive role in these responses. However, undefined after-effects provoked by i.c. DA, may be connected with specific dopaminergic effects.
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PMID:Dopamine-induced coronary effects in the dog heart attributed to beta- and alpha-adrenergic mechanisms. 284 27

The effects of physiological left ventricular hypertrophy on coronary reactivity and reserve were examined by comparing greyhounds with their remarkable myocardial hypertrophy with mongrel dogs (left ventricular body weight ratios 7.7(0.1) and 4.4(0.1) g X kg-1 respectively). Peak reactive hyperaemia and flow debt repayment after 15 s coronary occlusions were virtually identical in both groups at baseline heart rates and paced atrial rates up to 270 beats X min-1. Furthermore, the changes in myocardial blood flow and its transmural distribution after release of a 45 s coronary occlusion both at baseline heart rate and during atrial pacing at 210 beats X min-1 were similar in both greyhounds and mongrel dogs. Collateral flow during a 1 min coronary occlusion in conscious animals and myocardial flows and distribution during treadmill exercise were also similar. To determine minimal coronary vascular resistance intracoronary adenosine (400-600 micrograms X min-1) was infused to dilate maximally the coronary vasculature without having appreciable systemic effects. In both groups of dogs adenosine increased coronary flow six to seven fold. Coronary vascular resistance per gram of left ventricle decreased equally, and the minimal resistance was 2200(147) kPa X litre-1 X min X g (RU X g-1) in greyhounds and 2360(453) RU X g-1 in mongrels, thus indicating similar maximal vascularity in each gram of the hypertrophied and mongrel left ventricles. Because of the larger greyhound heart, the minimal coronary vascular resistance for the entire left ventricle (11.7(0.7)RU) was 50% of that in mongrel dogs (24.1(0.7)RU). Thus all forms of left ventricular hypertrophy cannot be assumed to have similar effects on the coronary vasculature. Whereas the pathological hypertrophy associated with renovascular hypertension and aortic banding is accompanied by decreased coronary vascularity, the myocardial hypertrophy of the greyhound is accompanied by increased total vascularity and preserved coronary reserve.
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PMID:Coronary vascular reserve in the greyhound with left ventricular hypertrophy. 293 56

We have shown that there was a 50% increase in infarct size and a threefold increase in the incidence of sudden death following coronary occlusion in dogs with hypertension and left ventricular hypertrophy (LVH). To further investigate this problem, we separated the effects of hypertension from those of LVH by decreasing arterial pressure either by renal anastomosis or intravenous administration of nitroprusside in dogs with chronic renal hypertension and LVH. In 123 conscious dogs, the circumflex coronary artery was acutely occluded. Hemodynamics were monitored, myocardial perfusion was measured with labeled microspheres, the risk area was defined by postmortem angiography, and infarct size was determined pathologically 48 h after occlusion. The incidence of sudden death following acute coronary occlusion decreased dramatically in dogs with LVH if the arterial pressure was decreased with either nitroprusside or renal anastomosis. In addition, if arterial pressure was decreased with nitroprusside or renal anastomosis, infarct size in dogs with LVH was not augmented. In conclusion, normotension induced by renal anastomosis or nitroprusside returned infarct size and the incidence of sudden death in dogs with chronic hypertension and LVH toward control values. Thus it is likely that hypertension, as opposed to LVH, is the critical factor responsible for the increase in infarct size and the high incidence of sudden death observed in dogs with hypertension and LVH following sudden coronary occlusion.
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PMID:Relative importance of hypertension after coronary occlusion in chronic hypertensive dogs with LVH. 296 Dec 80

Previous studies have shown that hypertension and left ventricular hypertrophy (HT-LVH) increase completed infarct size. Myocardial infarction progresses in a wavefront of myocardial necrosis from the subendocardium to the subepicardium. We tested two hypotheses: First, HT-LVH accelerates the wavefront of myocardial necrosis when compared with normotensive animals; and second, lowering of arterial pressure by infusing nitroprusside 1 hour after coronary artery occlusion exerts a salutary effect on infarct size. To test these hypotheses, systemic hypertension (mean aortic pressure = 141 +/- 3 mm Hg) and left ventricular hypertrophy (18% increase in left ventricular mass) were induced in dogs using a single-kidney, single-clip model. Seventeen adult mongrel dogs were used as controls. We measured mean aortic pressure, heart rate, left atrial pressure, and myocardial perfusion (microspheres) in several groups of normal and HT-LVH awake dogs. In two groups (normal and HT-LVH), 1 hour of circumflex coronary artery occlusion was followed by 4 hours of reperfusion. In two additional groups (normal and HT-LVH), 3 hours of circumflex coronary artery occlusion was followed by 90 minutes of reperfusion. In another group with HT-LVH, nitroprusside was infused to reduce mean arterial pressure to 100 mm Hg beginning 1 hour after occlusion and was continued for the duration of reperfusion period (HT-LVH + N). Infarct size was assessed using triphenyltetrazolium chloride stain and risk area was determined using postmortem barium angiography. Fifteen of 17 (88%) control animals survived coronary artery occlusion, whereas only 17 of 42 (40%) dogs with HT-LVH survived coronary occlusion (p less than 0.05). Infarct-to-risk ratios in the various layers of the left ventricular wall were determined for survivors in all groups. After 1 hour of coronary occlusion more than twice as much mid-wall and epicardium was infarcted in the HT-LVH group compared with the control group. After 3 hours of coronary occlusion significantly more endocardium, mid-wall, and epicardium was infarcted in the dogs with HT-LVH. In the nitroprusside-treated HT-LVH dogs, the infarct sizes were similar to control animals. From these data we conclude: 1) the rate of infarction is accelerated in animals with HT-LVH; 2) nitroprusside infused 1 hour after coronary artery occlusion and continued throughout the reperfusion period exerts beneficial effect on infarct size when compared with control animals; and 3) acute coronary artery occlusion in animals with HT-LVH is associated with significantly greater mortality when compared with control animals.
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PMID:Acceleration of the wavefront of myocardial necrosis by chronic hypertension and left ventricular hypertrophy in dogs. 296 95

Pressure-induced cardiac hypertrophy has many effects on the functional capacity of the coronary circulation. Many studies have been performed in both animal and humans and the major findings are as follows: 1. Most types of myocardial hypertrophy are associated with the decrement in coronary vasodilator reserve; 2. The magnitude of the decrement in coronary reserve in myocardial hypertrophy is usually much more prominent in patients with myocardial hypertrophy than in animal models; 3. Left ventricular hypertrophy secondary to systemic hypertension is associated with altered autoregulation of myocardial perfusion; 4. The perfusion abnormalities associated with hypertension and left ventricular hypertrophy are affected by various factors such as age of onset, ventricular involvement, and the stimulus for hypertrophy; 5. Left ventricular hypertrophy secondary to renal hypertension markedly augments the adverse effects of coronary occlusion. In this setting, coronary occlusion is associated with a three-fold increase in the incidence of lethal ventricular arrhythmias and a 35% increase in infarct size. Thus, pressure-induced hypertrophy profoundly alters the coronary circulation.
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PMID:The effects of pressure-induced cardiac hypertrophy on the functional capacity of the coronary circulation. 296 42


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