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

We measured indices of the renin-aldosterone system and body-fluid spaces in 11 adolescents who had received a renal transplant after removal of their own diseased kidneys. None had hypervolemia but 6 had hypertension. Renal angiography revealed greater than 50% luminal occlusion by allograft renal-artery stenosis (RAS) in only the 3 patients who had severe hypertension refractory to conventional medical therapy. Excessive peripheral plasma renin activity (PRA) distinguished these patients from those who had less severe stenosis or normal angiogram, and diuretic stimulation heightened the PRA differences. We conclude that significant allograft RAS does not necessarily act like a typical single-kidney Goldblatt model until after volume depletion. Our findings indicate that peripheral PRA values can be used to assess the degree of graft ischemia clinically. This permits early identification of patients who have severe RAS that probably will be difficult to control medically, and, therefore, should be followed closely with a view of reconstructive vascular surgery before further deterioration of renal function.
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PMID:Allograft renal-artery stenosis: increased peripheral plasma renin activity as an early indicator of uncontrollable hypertension. 36 8

Examination of patients with acute embologenic arterial occlusion yielded data testifying to activation of the renin-angiotensin-aldosterone system both in the ischemic and in the postischemic periods. Direct dependence of the activation of the renin-angiotensin-aldosterone system on the degree of tissue ischemia and duration of the ischemic period of up to 2 days was revealed. The development of secondary hyperaldosteronism in patients with embolism of the major vessels stipulated the expediency of using aldosterone antagonists in patients with most marked ischemic changes in the tissues as well as when the ischemic period lasted more than 6 hours.
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PMID:[Renin-angiotensin-aldosterone system in acute embologenic arterial obstruction]. 43 Sep 58

The role of rat adrenal mineralocorticoid function in the development of experimental reno-vascular hypertension was studied. Na-retention action of aldosterone was blocked by means of verospiron. Daily excretion of aldosterone proved to be significantly increased in rats with unilateral stenosis of the renal artery (the contralateral kidney was intact). In ischemia of the only kidney there was seen no change in the activation of adrenal mineralocorticoid function. Administration of verospiron strongly suppressed the development of the first form of reno-vascular hypertension and had no effect on the blood pressure in rats with stenosis of the only kidney.
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PMID:[Role of aldosterone in the initial stage of 2 forms of experimental vasorenal hypertension]. 122 11

Eleven patients with uncomplicated mild-to-moderate hypertension (diastolic pressure 95-115 mmHg) were treated for four weeks with daily single quinapril doses of 20-40 mg. Already during the second week a significant reduction in blood pressure was observed without increase of heart rate; 27.3% of patients responded to the lower dose (diastolic blood pressure [90 mmHg], and 54.6% responded to the higher dose. Drug treatment led to reduced pressure increase in response to cold stimulation without influencing the adrenergic response both in basal conditions and after cold pressor test. The drug brought about peripheral vasodilatation as shown by increased perfusion index during Doppler ultrasound examination, and improved arterial reactivity with increased perfusion index and reduced recovery time after ischemia. The reduction of angiotensin and aldosterone plasma levels during treatment was not correlated to diminished blood pressure values, indicating that the antihypertensive effect can occur via pathways different from ACE inhibition. Tolerance was excellent as shown both by clinical and laboratory evidence.
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PMID:[Clinical-instrumental evaluation of the effects of quinapril treatment in mild-to-moderate hypertension]. 214 11

The effects of 1-year antihypertensive treatment with the diuretic fenquizone were evaluated in 16 patients with mild essential hypertension. During treatment with placebo, after 2, 4, 24, and 52 weeks of treatment we measured blood pressure, heart rate, forearm blood flow (FBF) and vascular resistance (FVR) at rest and after 10 minutes ischemia, and forearm venous distensibility. Subjects whose diastolic blood pressure after fenquizone was reduced at least 10% were classified as responders. On this basis, 56% of patients after 1 month and 68% after 1 year responded to fenquizone. Responders, in comparison to nonresponders, were characterized by a greater increase in FBF and a greater decrease in FVR. The reduction in diastolic blood pressure was significantly related to the fall in FVR whereas no correlation was found between blood pressure and venous compliance changes. Nonresponders had a PRA increase similar to that observed in responders but they showed a much greater increase in aldosterone, whose changes were inversely related to modifications of both FVR and blood pressure. Our results demonstrate that chronic therapy with fenquizone causes a reduction of FVR, and that nonresponders have an exaggerated rise in aldosterone. This observation further reinforces the hypothesis that factors influencing the secretion of aldosterone are important determinants of the antihypertensive mechanism of diuretics.
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PMID:Hemodynamic and humoral effects of chronic antihypertensive treatment with fenquizone: importance of aldosterone response. 217 89

The effects of angiotensin converting enzyme inhibitors (ACEIs), CGS 14831 (CAS 86541-78-8) and captopril, on the mechanical function and energy metabolism were studied in isolated rat hearts using global ischemia-reperfusion model. The myocardial tissue levels of ATP, creatine phosphate (CP) and pH were determined with 31P-nuclear magnetic resonance (31P-NMR). Global ischemia was induced by cross-clamping of the inflow line for 40 min. While thiol containing ACEI, captopril, significantly inhibited the ATP depletion and pH fall produced by ischemia, non-thiol compound, CGS 14831, did not have any influence on the ATP degradation and pH fall during ischemia. Both CGS 14831 (20 micrograms/ml) and captopril (80 micrograms/ml) have little influence on the mechanical function during the ischemia-reperfusion period. L-Cysteine (44.6 micrograms/ml) inhibited the pH fall significantly during the ischemia without exerting influence on the ATP degradation. These data suggest that local renin-angiotensin-aldosterone system does not play an important role in maintenance of the myocardial mechanical function during ischemia-reperfusion. The thiol residue of captopril is not responsible for the inhibitory effect of this compound on ischemia-induced ATP degradation. Some specific effect of captopril may play a role in the protective effect.
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PMID:Effects of two angiotensin converting enzyme inhibitors on the mechanical function and energy metabolism of isolated rat hearts. A nuclear magnetic resonance study with an active form of benazeprilat and captopril. 229 44

This experimental study in dogs was designed to investigate whether maximal loading produces atrial natriuretic factor (ANF) release and whether this physiological peptide is involved in the improvement of the early renal function recovery after acute ischemia. The experimental protocol included a renal artery occlusion for 45 min in uninephrectomized dogs and the measurement of various parameters of renal function over 2-hr period after declamping. There were 3 experimental groups. In the control group (I) (n = 10), the dogs received, after ischemia, an isotonic saline solution infusion at a rate of 0.2 ml/kg/min. In group II, (n = 10) the animals underwent acute volemic expansion (1 ml/kg/min) with whole blood (hematocrit approximately equal to 25%) during the ischemic period, and after declamping, an isotonic saline infusion (NaCl 0.9%) infusion at the same rate as in the control group. In group III, (n = 8) the dogs only received NaCl 0.9% (0.2 ml/kg/min) before ischemia and alpha human ANF (3.6 ng/kg/min) dissolved in saline after ischemia and during the 2 hr of the renal recovery period. Volemic expansion induced a highly significant increase of the cardiac filling pressures concomitant with a prompt but transient 5-6-fold increase in ANF levels (357 +/- 92 pg/ml versus 60 +/- 4.1 pg/ml in controls at the time of declamping [P less than 0.05]). With these higher plasma ANF levels in overloaded animals, we observed, 2 hr after declamping, considerably improved renal function recovery in terms of glomerular filtration rate--37.5% +/- 8.7 versus 11.8 +/- 3.9%; urinary sodium excretion rate--53.89 mu eq/min versus 5.36 +/- 1.2 mu eq/min (P less than 0.01); total Na reabsorption rate--1.2 +/- 0.23 meq/min versus 0.28 +/- 0.09 meq/min (P less than 0.01) (group II vs. controls, respectively). A 1-28 alpha ANF infusion after the ischemic insult allowed a comparable but more significant improved recovery of renal function--indeed, 2 hr after declamping, the GFR reached 73.7 +/- 14% of the preoperative GFR values. The urinary sodium excretion rate was 15-fold higher than in controls, and the total and fractional sodium reabsorption rates followed a similar increase. These beneficial effects of ANF were obtained with low doses of synthetic ANF (3.6 ng/kg/min) inducing plasma levels slightly higher (120 pg/ml) than in controls and comparable to the levels reached in the overloading group. In addition, maximal loading or ANF infusion produces an inhibition of the aldosterone rise occurring after the ischemic insult.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Evidence that atrial natriuretic factor is the humoral factor by which volume loading or mannitol infusion produces an improved renal function after acute ischemia. An experimental study in dogs. 252 2

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

Myocardial interstitium plays an important role in the regulation of cardiac function compared with myocytes and it is actively involved in ischemia-reperfusion damage and in the acute and chronic remodelling during ischemic heart diseases. Myocardial post-ischemic oedema seems to interfere in this process. Myocardial oedema is able to induce structural alterations, to reduce myocardial function and to activate the renin-angiotensin-aldosterone system. Angiotensin II and aldosterone seem to be the cause of myocardial fibrosis that is detected during ischemic heart disease. Post-ischemic vascular permeability alterations have a similar role. In clinical conditions, ACE-inhibitors have important effects on cardioreparation and are able to improve cardiac function and reduce early and late mortality. The effects of myocardial oedema reduction (i.e. hypertonic reperfusion) on ischemia-reperfusion damage and myocardial fibrosis are still to clarify. A reduction in myocardial fibrosis may improve cardioreparation and prevent congestive heart failure, following ischemic heart disease.
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PMID:[Role of interstitial myocardium in ischemia-reperfusion injury: experimental data and clinical implications]. 763

Endothelin-1 may function pathophysiologically as a counterregulatory vasoconstrictor peptide that is modified in its activity by the opposing action of endothelium-derived relaxing factor(s) (EDRF). The present study determined in part the integrated cardiorenal and endocrine actions of pathophysiologic plasma concentrations of endothelin in the anesthetized dog. In addition, nitroglycerin, which inhibits vascular smooth muscle contraction by increasing cGMP in a mechanism similar to EDRF, acts like an endogenous nitrovasodilator. Therefore, we tested the hypothesis that nitroglycerin would effectively antagonize the cardiac and renal actions of exogenous endothelin. The results confirm that endothelin-1-mediated vasoconstriction in vivo is heterogenous with a greater renal than coronary action. Further, nitroglycerin effectively blocked endothelin-1-mediated coronary flow reductions, but only partially antagonized reductions in renal blood flow. Endothelin-1-induced reduction in cardiac output also was not antagonized by nitroglycerin despite its effects to preserve coronary blood flow. Nitroglycerin did, however, antagonize endothelin-induced elevations in plasma epinephrine, norepinephrine, and aldosterone. These results would suggest that in pathophysiologic states where endothelin-1 is elevated, such as hypertension or congestive heart failure, there is a major compromising of renal function, and also the production of cardiac ischemia. Since exogenous nitroglycerin is relatively ineffective in antagonizing the renal vasoconstrictive effects of endothelin, it may be that the endogenous vasodilating systems, such as ERDF and prostacyclin, are inadequate in such pathologic states to counter the vasoconstrictor effects of endothelin.
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PMID:Endothelin-mediated cardiorenal hemodynamic and neuroendocrine effects are attenuated by nitroglycerin in vivo. 838 58


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