Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To study the effects of myocardial ischemia on plasma atrial natriuretic peptide (ANP) levels, immunoreactive ANP levels in the pulmonary artery (ANP-PA) and femoral vein (ANP-V) were measured before and during percutaneous transluminal coronary angioplasty (PTCA). Ten patients (group 1), seven of whom had no symptoms during PTCA, maintained a normal mean pulmonary capillary wedge pressure (PCWP) of less than or equal to 13 mm Hg during PTCA, whereas five patients (group 2), all of whom had symptoms and signs of ischemia during PTCA, had an increased PCWP of greater than or equal to 20 mm Hg. ANP levels did not differ significantly between the two groups before PTCA, but ANP-PA (p less than 0.02) and ANP-V (p less than 0.01) during PTCA were higher in group 2 than in group 1. ANP-V at rest and during exercise was measured in 11 patients with and 14 patients without anginal symptoms and ischemic ST changes on the ECG during exercise. The values did not change significantly in either group, and there were no difference between the groups. Thus myocardial ischemia during PTCA may lead to left ventricular dysfunction serious enough to increase PCWP and subsequently plasma ANP levels in some patients. Myocardial ischemia induced by dynamic exercise seems to be unrelated to significant changes in the plasma ANP level.
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PMID:Plasma levels of atrial natriuretic peptide during myocardial ischemia induced by percutaneous transluminal coronary angioplasty or dynamic exercise. 252 19

In previous studies in humans, mannitol (20%, 250 ml) has been shown to reduce the incidence of acute renal failure (ARF) after transplantation from 54% to 19%. In rats, atrial natriuretic peptide appears to prevent ischemia-induced ARF. We therefore decided to evaluate the effects of alpha-human atrial natriuretic peptide (alpha-h-ANP) both alone and combined with mannitol during transplantation in humans. First, we demonstrated that systemic alpha-h-ANP infusion during kidney transplantation was safe in dosages up to 0.08 micrograms/kg per minute. In these patients the calculated metabolic clearance rate of alpha-h-ANP was relatively low ranging from 0.68 to 1.80 l/min. In a second study of 11 renal graft recipients, no mannitol was used and alpha-h-ANP (0.05 micrograms/kg per minute) was infused into the donor kidney artery during transplantation for 46 +/- 2 min, followed by IV administration for 71 +/- 2 min. Our aim was to reduce the incidence of ARF. Nevertheless, ARF occurred immediately after surgery in four of the patients (36%) in this group and, as a result, mannitol was reintroduced. A third group of nine renal graft recipients received alpha-h-ANP (total dose 400 micrograms) as five IV injections within 90 min after transplantation. ARF occurred in four of these patients (44%). We conclude that alpha-h-ANP, administered according to the aforementioned protocols in such small groups of patients, does not seem to be of value in the prevention of ARF after transplantation.
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PMID:The effect of alpha-human atrial natriuretic peptide on the incidence of acute renal failure in cadaveric kidney transplantation. 214 26

The effects of the synthetic 28-amino-acid alpha-human atrial natriuretic peptide (ANP) on the proximal coronary arteries and coronary blood flow were evaluated in 17 patients. Proximal coronary dimension was quantitated by digital angiography, and coronary flow was quantitated with 3F Doppler flow catheters. ANP, when given as a 2.5-micrograms/kg bolus in the left ventricle, caused sustained significant proximal coronary dilations from 3.49 +/- 0.57 to 4.09 +/- 0.76 mm, lasting more than 30 minutes. The proximal coronary diameter did not increase further after intracoronary injection of 0.3 mg nitroglycerin (4.08 +/- 0.79 mm). Coronary flow (resistance coronary dilation) was not significantly increased at 5 minutes after ANP (87 +/- 55 to 102 +/- 54 vol flow units), indicating that the proximal coronary dilations were not flow dependent. The persistent proximal coronary dilations were associated with minor and transient decreases in aortic pressure and left ventricular end-diastolic pressure and with minor and transient increases in heart rate, cardiac output, and left ventricular contractility. Plasma ANP level increased significantly by more than sixfold from 39.8 +/- 8.8 to 245.8 +/- 168.5 pg/ml. The time course of proximal coronary dilations was related more closely to the time course of increase in plasma cyclic guanosine monophosphate than that of plasma ANP. This study demonstrates that bolus injection of ANP (2.5 micrograms/kg), an endogenous vasodilator, caused marked sustained preferential proximal coronary dilations and brief minor changes in cardiac and systemic hemodynamics. Although additional studies are needed to assess its clinical efficacy as a coronary dilator in the treatment of coronary artery disease, these data suggest a potential of ANP in the therapy of ischemia.
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PMID:Effects of atrial natriuretic peptide on the coronary arterial vasculature in humans. 255 73

Because of its ability to increase glomerular filtration, antagonize the actions of vasoconstrictors, and produce vasodilation, alpha human atrial natriuretic peptide (alpha-hANP) was evaluated for its potentially beneficial effects in experimental ischemic renal failure induced by 45-60 min of renal artery occlusion in bilaterally or unilaterally renally intact Sprague-Dawley rats. After ischemia, a 4-h intrarenal infusion of alpha-hANP restored 14C-inulin clearances in bilaterally and unilaterally intact animals from 0.05 +/- 0.006 and 0.05 +/- 0.01 ml/min per 100 g to 0.314 +/- 0.04 and 0.25 +/- 0.01 ml/min per 100 g, respectively (P less than 0.001, n = 8), compared with normal values of 0.49 +/- 0.023 ml/min per 100 g. Histologically, there was a progressive decrease in medullary hyperemia and prevention of intratubular cell shedding and granulocyte margination as a result of the 4-h alpha-hANP infusion such that after 24 and 48 h the histological appearance of the tissue was essentially normal. The results show that a 4-h intrarenal infusion of alpha-hANP after renal ischemia can preserve glomerular filtration rate and reduce renal tissue damage.
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PMID:Atrial natriuretic peptide protects against acute ischemic renal failure in the rat. 296 Jun 93

In a rat experimental study we investigated whether the atrial natriuretic peptide by itself is able to improve early renal function after an ischemic injury. Two groups of Wistar male rats underwent a right nephrectomy and a left renal artery occlusion for 30 min and were infused for 2 hr after ischemia with isotonic saline or rat atrial natriuretic peptides (alpha ANF: 28 amino acids (AP 28) and atriopeptin III (AP 24): 24 amino acids). ANF infusion increased the urinary flow (P less than 0.001), the urinary sodium concentration (P less than 0.001), the sodium excretion rate (P less than 0.0001), and improved the glomerular filtration rate (GFR) recovery (P less than 0.02) determined at the end of the 2-hr infusion period. AP 24 exhibited higher natriuretics activities than AP 28. The effect of both peptides upon GFR recovery was equivalent. These effects of ANF observed after acute ischemia suggest that this peptide may be beneficial on the resumption of renal function in the early phases following transplantation.
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PMID:Beneficial effect of atrial natriuretic factor on ischemically injured kidneys in the rat. A new approach to improve early renal function. 296 98

The elevation of cardiac filling pressure induces the release of atrial natriuretic peptide into the circulation. Ischemia during exercise in patients with coronary artery disease may manifest itself with elevation of cardiac filling pressure before the onset of electrocardiographic changes or chest pain. Thus, patients with ischemic heart disease might have an elevated circulating atrial natriuretic peptide after exercise. The present study investigated the effect of exercise on circulating atrial natriuretic peptide in patients with and without ischemic heart diseases. Group 1 was composed of five patients who had ischemic heart disease by clinical history, previous myocardial infarction, angina or angiographically proven coronary artery disease and positive electrocardiogram during exercise. Group 2 was composed of five patients without ischemic heart disease and negative electrocardiogram response. Heart rate, blood pressure, and atrial natriuretic peptide were measured during routine treadmill exercise testing using the Bruce protocol. Our results indicate that the rate of rise of heart rate (12.3 +/- 1.8 vs. 8.5 +/- 0.7 beats/min/min), blood pressure (7.1 +/- 1 vs. 4.2 +/- 0.8 mm Hg/minute), and atrial natriuretic peptide (4.1 +/- 1 vs. 1.4 +/- 0.3 pg/ml/min) was significantly elevated in patients with ischemic heart disease compared to the group 2 patients. These findings suggest that the disproportionate elevation of atrial natriuretic peptide after exercise in ischemia may be caused by elevation of cardiac filling pressure, which may provide a noninvasive method for the diagnosis of ischemic heart disease.
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PMID:The differential response in atrial natriuretic peptide release during exercise in patients with and without ischemic heart disease. 296 77

The separate effects of hypoxia and ischemia on atrial natriuretic peptide (ANP) release were evaluated in Langendorff-perfused rabbit hearts. Heart rate, coronary flow, and atrial and ventricular volumes were kept constant. Hypoxia was induced for 20 min at room temperature in seven hearts and at 37 degrees C in a second group of seven hearts. A third group of eight hearts was subjected to global ischemia for 20 min by reducing coronary flow to 1 ml/min at room temperature. All hearts were reoxygenated/reperfused at 37 degrees C for 30 min. Hypoxia at 37 degrees C induced a significant increase in ANP release. In contrast, both room temperature hypoxia and ischemia were characterized by a significant decrease in ANP release, despite hemodynamic alterations similar to those recorded during hypoxia at 37 degrees C. Both reoxygenation and reperfusion induced a prompt reversal of the changes of ANP release observed during the period of oxygen deprivation. These data demonstrate that decreased oxygen availability and reduced coronary flow are not the primary factors affecting release of ANP during ischemia and that alterations of myocardial temperature may play a major role in this phenomenon.
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PMID:Influence of O2 deprivation, reduced flow, and temperature on release of ANP from rabbit hearts. 761 87

We studied the effects of short-term global ischemia and reperfusion on ANP secretion from Langendorff-perfused rat hearts compared with isolated ventricles. Effects of regional ischemia, with or without increased atrial pressure, were examined in Langendorff-perfused and working heart models. Five minutes of global ischemia were associated with elevated levels of atrial natriuretic peptide (ANP) in the coronary effluent immediately and for approximately 10 min after resumption of reperfusion, resulting in a net hormone excess of 23 +/- 5 ng/g wet wt. The ventricles produced on the average 11% ANP compared with the whole heart, and their contribution of to postischemic ANP overflow was approximately proportional to their basal production. In Langendorff-perfused hearts, regional ischemia increased the concentration of ANP in the coronary effluent 51 +/- 11%, whereas the secretion rate (per minute) decreased 18 +/- 5%. In the presence of atrial distension in the working heart model, a trend for increase in ANP secretion was apparent. We conclude that global ischemia, even of brief duration, has an independent stimulatory effect on ANP release, the ischemic atrium being responsible for most of the excess. Regional ischemia, when not accompanied by atrial distention, reduces the ANP secretion rate during the ischemic period. Heart failure secondary to ischemia stimulates ANP secretion, but this response seems to be both delayed and attenuated compared with atrial stretch alone.
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PMID:Release of atrial natriuretic peptide in brief ischemia-reperfusion in isolated rat hearts. 820 96

Bicaval anastomoses in orthotopic cardiac transplantation offer the advantage of preserving the right atrial geometry. To elucidate the impact of this anastomotic technique on atrial natriuretic peptide plasma levels at rest and with exercise, nine patients were submitted to a symptom-limited supine exercise test. Atrial natriuretic peptide plasma levels in samples obtained from the right atrium were elevated at rest (274.4 +/- 60.4 pg/ml), at peak exercise (438.1 +/- 71.7 pg/ml), and thereafter (328.1 +/- 71.2 pg/ml) with respect to normal reference values of 21 +/- 1 pg/ml at rest and 92 +/- 14 at peak exercise. Renin, angiotensin, and aldosterone plasma levels were almost normal and did not indicate any pathologic processes in volume homeoostasis. Right-sided hemodynamic parameters were not correlated with atrial natriuretic peptide secretion. An adverse relationship between cold ischemic time of the donor organ and atrial natriuretic peptide release was found (r = 0.88, p < 0.0008), indicating that endocrine cardiocytes are sensitive to prolonged ischemia. Atrial natriuretic peptide release may thus be independent of the surgical approach, and other unique characteristics of the transplanted heart, such as denervation, are more likely to be responsible for elevated atrial natriuretic peptide plasma concentrations after orthotopic heart transplantation.
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PMID:Atrial natriuretic peptide release at rest and with exercise after cardiac transplantation with bicaval anastomoses. 852 69

Left ventricular hypertrophy is considered to be an independent risk factor giving rise to ischemia, arrhythmias, and left ventricular dysfunction. Slow movement of intracellular calcium contributes to the impaired contraction and relaxation function of hypertrophied myocardium. Myofibril content may also be shifted to fetal-type isoforms with decreased contraction and relaxation properties in left ventricular hypertrophy. Myocyte hypertrophy and interstitial fibrosis are regulated independently by mechanical and neurohumoral mechanisms. In severely hypertrophied myocardium, capillary density is reduced, the diffusion distance for oxygen, nutrients, and metabolites is increased, and the ratio of energy-production sites to energy-consumption sites is decreased. The metabolic state of severely hypertrophied myocardium is anaerobic, as indicated by the shift of lactate dehydrogenase marker enzymes. Therefore, the hypertrophied myocardium is more vulnerable to ischemic events. As a compensatory response to severe cardiac hypertrophy and congestive heart failure, the ADP/ATP carrier is activated and atrial natriuretic peptide is released to increase high-energy phosphate production and reduce cardiac energy consumption by vasodilation and sodium and fluid elimination. However, in severely hypertrophied and failing myocardium, vasoconstrictor and sodium- and fluid-retaining factors, such as the renin-angiotensin system, aldosterone, and sympathetic nerve activity, play an overwhelming role. Angiotensin-converting enzyme inhibitors (ACEIs) are able to prevent cardiac hypertrophy and improve cardiac function and metabolism. Under experimental conditions, these beneficial effects can be ascribed mainly to bradykinin potentiation, although a contribution of the ACEI-induced angiotensin II reduction cannot be excluded.
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PMID:Substrate metabolism, hormone interaction, and angiotensin-converting enzyme inhibitors in left ventricular hypertrophy. 852 2


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