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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The blood pressure is not a fixed entity but rather a parameter subject to substantial situational fluctuations. Studies based on ambulatory blood pressure measurement as well as exercise testing have shown that the highest blood pressure values in an individual can be recorded during physical exercise. During exercise in healthy subjects, in association with an increase in cardiac output and decrease in peripheral resistance, there is an increase in systolic arterial pressure with nearly constant diastolic pressure. In contrast to normotensive individuals, during dynamic exercise hypertensive patients demonstrate excessive pressure increases due to impaired vasodilatation. The mechanism responsible may be structural changes in the arteriolar walls but age is also an important determinant. The extent of blood pressure increase is more dependent on the mass of contracting muscle than on the mode of contraction. During isometric exercise, there is an increase in both systolic and diastolic blood pressure, predominantly reflex-induced, which is more marked in patients with manifest hypertension at rest than in those with borderline hypertension or in normotensive subjects. During dynamic exercise in a subgroup of patients with coronary artery disease, in contrast to normal subjects in whom the diastolic pressure remains constant, an increase in up to 15 mm Hg in this parameter may be found as a result of ischemia induction with left ventricular dysfunction, inadequately increased cardiac output and reflex vasoconstriction. During dynamic exercise, there is an increase in norepinephrine, more marked in hypertensive than normotensive subjects together with an increase in plasma renin activity; plasma aldosterone changes are in parallel with those of renin activity.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Pathophysiology of exercise hypertension. 295 61

Nineteen mongrel dogs had 30 minutes of thoracic aortic occlusion to determine the effects that blockade of the renin-angiotensin system may have on preserving spinal cord blood flow and function during a period of temporary spinal cord ischemia. Cross-clamping of the thoracic aorta causes renal ischemia and activates the renin-angiotensin system with resulting increased production of angiotensin II. Angiotensin II is a potent peripheral constrictor and elevated levels may constrict collateral spinal cord circulation. At the time of aortic cross-clamping, 10 dogs received 100 mg/kg of MK422 (intravenous enalapril maleate), a converting enzyme inhibitor, and nine animals served as controls. The blockade of the renin-angiotensin system had no preserving effects on spinal cord flow as measured by microspheres and on spinal cord function as graded with the Tarlov scale. However, the paraplegic animals all had significantly increased lower thoracic and lumbar spinal cord flows 30 minutes after clamp release when compared with those animals that remained neurologically intact. In conclusion, marked hyperemia occurring after a period of hypoperfusion may lead to spinal cord edema and compartment syndrome with resulting paraplegia.
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PMID:The effect of hyperemia on spinal cord function after temporary thoracic aortic occlusion. 317 89

Current data support the existence of an endogenous renin-angiotensin system in the heart. Vascular angiotensin may contribute to the regulation of coronary vascular tone. Enhanced local angiotensin production in areas of vascular injury or inflammation may result in increased vasoconstriction or vasospasm. Cardiac angiotensin may adversely influence myocardial metabolism and provoke ventricular arrhythmia during ischemia and reperfusion-induced myocardial injury. Local angiotensin may stimulate cardiac contractility. In addition, angiotensin may influence cardiac myocyte growth and may contribute to the development of cardiac hypertrophy in hypertension. Recent data show that the pharmacologic inhibition of cardiac angiotensin converting enzyme may have important therapeutic consequences for the ischemic, hypertrophic, or failing heart.
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PMID:Cardiac renin-angiotensin system. Molecular and functional aspects. 321 53

Studies have shown that in comparison to rapid occlusion of a vessel, gradual occlusion produces less severe tissue ischemia due to a more effective development of collateral circulation. As other studies have shown that collateral circulation can be enhanced by stimulation of the endogenous renin-angiotensin II system, it was hypothesized that this system is involved in the mechanism of protection against ischemia that obtains during gradual vascular occlusion. To test this hypothesis, mortality rates were evaluated in gerbils subjected to gradual vascular occlusion by means of progressive carotid ligation while simultaneously infused with inhibitors of the renin-angiotensin II cascade--enalaprilat or saralasin. Groups of animals with either abrupt or progressive carotid ligation infused with saline served as controls. Results showed that (1) in saline-infused animals, there was a significant decrease in the mortality rate of progressive-ligated animals when compared to abrupt-ligated animals, and (2) administration of either enalaprilat or saralasin to progressive-ligated animals resulted in mortality rates that were indistinguishable from those of saline-infused abrupt-ligated animals. These results suggest that the endogenous renin-angiotensin system is indeed involved in an adaptive mechanism that occurs during progressive ligation of the carotid artery, and more specifically, that the relatively benign effect of progressive carotid ligation may be due to the action of angiotensin II to stimulate the development of collateral circulation and reduce the severity of focal brain ischemia.
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PMID:Differences in mortality rate between abrupt and progressive carotid ligation in the gerbil: role of endogenous angiotensin II. 334 89

Visual disturbance after marked and/or recurrent blood loss has been known for at least 25 centuries, since Hippocrates; however, so far its clinical features have been controversial and its pathogenesis enigmatic. The author studied seven patients, four of whom were seen soon after the visual loss and followed prospectively. A detailed review of the extensive literature and analysis of the cases provide relevant information on the subject. The blood loss is usually from the gastrointestinal (GI) tract, less often from other sites. There is typically a time lag between the bleeding and the onset of visual loss--usually up to 10 days, less often even 2 to 3 weeks. The ocular findings are typically those of anterior ischemic optic neuropathy (AION) and are usually bilateral. Considerable evidence has accumulated that blood loss, with or without arterial hypotension, causes increase in release of renin and endogenous vasoconstrictor agents (e.g., angiotensin, epinephrine, and vasopressin) because of activation of the sympathoadrenergic system and vasomotor center. Our experimental studies on renovascular malignant hypertension indicate that endogenous vasoconstrictor agents produce choroidal ischemia and AION. In view of all the evidence, it is postulated that in the production of AION after blood loss, release of endogenous vasoconstrictor agents is probably a very important factor, with arterial hypotension an additional factor; increased platelet aggregation may also play a role.
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PMID:Anterior ischemic optic neuropathy. VIII. Clinical features and pathogenesis of post-hemorrhagic amaurosis. 350 Apr 45

The hepatic hemodynamic response to cardiogenic shock was investigated in a porcine model produced by pericardial tamponade to better understand the pathophysiology of postshock hepatic insufficiency. Reductions of cardiac output to 50 percent of baseline levels produced marked hepatic ischemia by causing disproportionate reductions in blood flow through the celiac and hepatic arteries and portal vein. These were due to selective vasoconstriction of the splanchnic resistance vessels that was mimicked without tamponade by the infusion of angiotensin II, ablated by angiotensin-converting enzyme blockade, unaffected by alpha-adrenergic ablation, and correlated closely with levels of plasma renin activity. The ischemic liver injury of cardiogenic shock appears to be largely due to an exquisite responsiveness of the splanchnic vascular smooth muscle to endogenously released angiotensin II.
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PMID:Pathophysiology of hepatic ischemia in cardiogenic shock. 351 57

The acute effect of T-2 toxemia on local blood flow and vascular resistance in hindquarter, mesenteric, and renal vascular beds was continuously measured by the directional pulsed Doppler technique in conscious, male Sprague-Dawley rats. Intravenous injection of T-2 toxin (1 mg/kg) in the conscious rat reduced blood flow and increased vascular resistance in all blood vessels studied but had no significant effect on mean arterial pressure or heart rate. The blood flow in hindquarters gradually decreased to a minimum of -77 +/- 9% (mean +/- SE) 6 hr after the toxin injection. The hindquarter vascular resistance concomitantly increased to a maximum value of +323 +/- 69% above the resistance before toxin administration. Mesenteric and renal blood flow initially increased (slightly) and then gradually decreased. The maximum drop of blood flow, -90 +/- 13% and -76 +/- 13% for the mesenteric and renal vascular beds, respectively, was achieved 4 hr after T-2 toxin injection and the blood flow values remained low for up to 6 hr. Simultaneously with the impairment of blood flow the mesenteric and renal vascular resistance increased to reach the maximal values of +404 +/- 99% and +556 +/- 15%, respectively. In addition, plasma renin activity was markedly elevated (+653 +/- 160%) at the time of reduced renal blood flow. Intravenous injection of the same value of vehicle (10% ethanol in saline) had no significant effect on any of the cardiovascular variables studied. Two of five rats in the T-2 toxin-treated group died within 5 hr after the T-2 toxin injection and only one animal survived 24 hr while all the control animals survived over 24 hr. The results suggest that strong vasoconstriction in skeletal muscle, mesenteric, and renal vascular beds leads to impairment of local blood flow. The ischemia in vital organs together with the earlier reported decrease in cardiac output by T-2 toxin might then be the cause of rapid death in acute T-2 toxemia.
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PMID:Effect of T-2 toxin on regional blood flow and vascular resistance in the conscious rat. 351 54

There is little, if any, good evidence in the literature to indicate a role for cardiovascular PG in congestive heart failure, either in its pathogenesis or as a consequence of and defense against its manifestations. Usually congestive heart failure is considered to develop as a vicious cycle in which impaired cardiac output, increased peripheral resistance, decreased renal blood flow, increased renin release and further increased peripheral resistance and decreased cardiac output are important constituents. Increased sympathetic activity may promote cardiovascular PG formation through the sympathetic neurotransmitter noradrenaline; such an action has, however, not been documented hitherto. Furthermore, increased plasma renin activity may promote PG formation via increased circulating levels of angiotensin; even such an action remains, however, to be demonstrated. If the heart failure leads to local tissue ischemia the hypoxia as such, or the subsequent increase in adenosine production, may also facilitate cardiovascular PG formation. All these mechanisms, if operative, would counteract the increased peripheral resistance, by promoting the formation of vasodilator PG. On the other hand PGI2 stimulates renal formation of renin, which would act to elevate the peripheral resistance. These contradictory effects of endogenously formed PG focus on the need for more careful studies on their involvement in the hemodynamic consequences of congestive heart failure: until more data are available it is impossible to know whether an activated synthesis of PG should be regarded as advantageous and worth therapeutical support, or negative and subject to inhibition.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cardiovascular prostaglandins: some comments on their involvement in circulatory physiology and pathophysiology. 352 21

Hypertension and simple renal cysts are frequent clinical diagnoses. With the widespread use of new non-invasive diagnostic technics such as abdominal ultrasound and computer-assisted tomography renal cysts are diagnosed with increasing frequency. In patients 50 years or older renal cysts of various size may be found in nearly one third. Similarly, the incidence of hypertension increases with age. Thus, the coexistence of a simple renal cyst and hypertension in a patient may represent a pure coincidence or be a cause of high blood pressure. The effect of cyst removal upon hypertension has been documented in 22 patients in the literature. Surgical cyst removal or percutaneous cyst aspiration caused a significant fall in blood pressure in most patients. The drop in blood pressure was closely related to an activation of the renin angiotensin system in the involved kidney. Fifteen patients (68%) were considered cured and 2 improved after the intervention. All patients had large cysts. It is suggested that in patients with large renal cysts the lesion may, through local tissue and/or renal arterial compression, cause ischemia and in turn activate the renin angiotensin system. Since most of the renal cysts are 2 cm or less in diameter this may represent a very rare event. In patients with large renal cysts and hypertension percutaneous needle aspiration of the cyst and/or renal venous renin determination may be useful tools to determine a causal rather than a coincidental relation between the 2 lesions.
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PMID:Simple renal cyst and hypertension: cause or coincidence? 353 May 68

We studied renal venous blood after renal infection for its concentrations of leukocytes, complement and renin. In addition, we evaluated this blood for granulocytic aggregation and chemiluminescence of granulocytes. We found that very rapid activation of serum complement occurred with associated granulocytic aggregation and evident vascular occlusion and ischemia since renin rose rapidly. It appears that this early sequence of events will cause renal damage by ischemic change, as well as that known to occur from the inflammatory reaction.
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PMID:Immunology of pyelonephritis. VIII. E. coli causes granulocytic aggregation and renal ischemia. 353 7


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