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)

A congestive cardiomyopathy (CCM) model occurs in inbred broad-breasted turkeys and is manifested by reduced hatchability and a high mortality within a week of hatching. In the survivors, cardiac dilation begins by 3-4 weeks of age and further mortality occurs from chronic congestive heart failure. The mechanisms behind these changes is unknown, and, therefore, we investigated what role, if any, myocardial energy metabolism might play in these events. Ventricular myocardial samples were obtained for analysis of adenine nucleotides (ATP, ADP, AMP) and creatine phosphate (CP) in control and CCM turkeys, 1-31 days old. The adenine nucleotide energy charge (EC) was calculated using the formula EC = ATP + 1/2ADP/(ATP + ADP + AMP). We found the myocardial ATP levels and EC in CCM hearts at 1-2 days were reduced. In control turkeys, no significant age-related differences were found in myocardial high-energy phosphate compounds or in the EC. This depression in the energy metabolism of CCM turkeys may also be reflected in their poor hatchability. By 6-10 days, however, ATP levels had recovered and remained normal despite the onset of cardiac dilation and failure at 3-4 weeks of age in CCM turkeys. Because CP levels in control and CCM turkey hearts were similar in all age groups, significant ischemia did not appear to be present after hatching in CCM turkeys. Our results suggest, therefore, that an insult probably prior to hatching produced depressed myocardial energy levels in CCM turkeys and led to reduced hatchability. This early insult appears to be significant, in that late cardiac dysfunction resulted despite the recovery of myocardial ATP levels.
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PMID:Myocardial high-energy phosphate levels in cardiomyopathic turkeys. 376 30

The administration of digitalis glycosides causes a variety of extracardiac effects. In both normal human subjects and in other species, digitalis increases smooth muscle tone of resistance and capacitance vessels. The vasoconstriction is mediated, in part, by a direct action of these glycosides on smooth muscle and, in part, by an increase in alpha-adrenergic tone. Constriction of coronary and splanchnic vessels may lead to myocardial or mesenteric ischemia. In contrast to normal subjects, patients with congestive heart failure demonstrate arteriolar and venodilation in response to these glycosides, possibly because the myocardial effect, to increase cardiac output and peripheral blood flow, overcomes the vasoconstrictor properties of these drugs. Other important actions of digitalis glycosides occur in the central and peripheral nervous systems. Their effects on the area postrema of the medulla oblongata are largely responsible for the alpha-adrenergic-mediated peripheral vasoconstriction, as well as the nausea and vomiting that frequently accompany digitalis intoxication. Actions of glycosides on the cerebral cortex are responsible for the wide range of neurotoxic effects that range from visual disturbances and headaches to seizures and coma. Finally, peripheral neurologic effects of digitalis glycosides on baroreceptor and cardiac afferent fibers may: improve the depressed function of these receptors in the situation of heart failure, and reflexly lower peripheral vascular resistance, thereby partially preventing the vascular constrictor action of these glycosides.
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PMID:Extracardiac and coronary vascular effects of digitalis. 388 56

It has long been thought that the symptomatology and prognosis of coronary events in patients with diabetes may differ from those in nondiabetic persons. A review of recent data demonstrates a higher mortality during the acute phase of myocardial infarction for diabetic patients than for their nondiabetic counterparts, possibly related to a higher incidence of congestive heart failure and cardiogenic shock. The clinical course of diabetic patients with infarction and the role of insulin in myocardial adaptation to ischemia are both reviewed. Diabetic patients surviving the acute phase of myocardial infarction have a lower survival in follow-up than nondiabetic survivors, although some improvement in survival has been noted following beta-adrenergic-blocker therapy.
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PMID:Myocardial infarction in the diabetic patient. 389 1

During the past ten years, we have surgically managed seven neonates who developed total occlusion of the distal aorta due to umbilical artery catheters. All patients experienced symptoms of congestive heart failure. Five patients presented with severe hypertension, and all of these had aortorenal involvement: three infants had aortorenal thrombosis and two infants had infrarenal aortoiliac thrombosis with suprarenal extension of thrombus. Two infants had aortoiliac thrombosis with clot confined to the infrarenal aorta. Aortic thrombosis imposes an additional severe hemodynamic insult in these already seriously ill infants. Survival in this group of patients depends upon prompt recognition of this problem, effective surgical correction, and careful perioperative management. Our experience suggests that this diagnosis should be entertained in the infant presenting suddenly with congestive heart failure, hypertension, or lower limb ischemia after umbilical artery catheterization. The diagnosis is preferably confirmed by real-time ultrasound and/or radionuclide flow scan, although aortography may sometimes be necessary. Surgical management includes early transabdominal aortotomy with thrombectomy. Prompt thrombectomy resulted in the survival of six patients. One infant died in acute renal failure. Renal function and leg perfusion is satisfactory in the remaining patients, although one child required later operative correction of renovascular hypertension. Two additional patients needed prolonged postoperative antihypertensive therapy for 14 to 34 months before this problem resolved. Long-term follow-up is necessary for managing renovascular hypertension and monitoring lower extremity perfusion.
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PMID:Management of aortic thrombosis secondary to umbilical artery catheters in neonates. 390 Mar 26

Nitroglycerin (NTG) and isosorbide dinitrate (ISDN) are potent dilators of vascular smooth muscle. The organic nitrates produce venodilation at very low doses, with little additional vasodilation of the venous circulation with increasing dosage. Nitrates increase arterial diameter and improve arterial conductance at low to moderate doses, and at high doses these agents produce dilation of the arteriolar or resistance vessels of the body. The overall hemodynamic response to nitrate administration will be modulated by the degree of sympathetic reflex discharge, the presence or absence of congestive heart failure, the dosage of administered nitrate, and the presence or absence of nitrate tolerance. Regional circulatory effects of the organic nitrates include a decrease in vascular resistance and an increase in arterial blood flow to the arms and legs. Venodilation also occurs in the extremities. In the splanchnic and mesenteric circulations, nitrates induce an initial vasodilative response followed by reflex vasoconstriction. Hepatic blood flow changes little in the normal state. Pulmonary blood flow decreases and pulmonary artery and venous pressures fall after nitrate administration. Renal blood flow remains essentially unchanged or decreases slightly after NTG administration, although reflex sympathetic activity may cause secondary vasoconstriction. The antianginal effects of nitrates have long been thought to be related to their systemic or peripheral actions, which reduce myocardial oxygen requirements through decreases in left ventricular preload and afterload. There is, however, considerable evidence that nitrates have important direct effects on the coronary circulation in both the normal and the ischemic heart. Such actions include coronary artery dilation, increased collateral blood flow, and enhanced oxygenation and nutrient perfusion to zones of ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hemodynamic effects of nitroglycerin and long-acting nitrates. 392 41

Nitroglycerin and other organic nitrates exert a number of favorable effects on the circulation of patients with severe congestive heart failure, and these effects mediate the short- and long-term hemodynamic and clinical improvement that follows treatment with these drugs. Although these agents are potent dilators of systemic venous capacitance vessels, present evidence indicates that they do not exert their beneficial hemodynamic and clinical effects by decreasing venous return to the heart. Rather, their ability to dilate pulmonary and systemic resistance vessels offsets any decrease in cardiac output that might be expected to occur from a decrease in venous return. Of equal importance, the increase in output of the left side of the heart that results from drug-induced pulmonary and systemic vasodilation prevents any decrease in venous return to the right side of the heart that might be expected to accompany an increase in systemic venous capacitance. The net effect of these two interacting forces is not only to keep cardiac output and venous return constant but also to translocate blood volume from the pulmonary circulation and left ventricle to the systemic vessels. In addition, nitrates also relieve subendocardial ischemia and favorably alter pressure-volume relationships in the left ventricle. These observations support the conclusion that the complex cardiovascular responses to organic nitrates in patients with congestive heart failure cannot be adequately summarized by the single concept of preload reduction.
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PMID:Mechanisms of nitrate action in patients with severe left ventricular failure: conceptual problems with the theory of venosequestration. 392 45

Patients with chronic renal failure requiring dialysis and in whom multiple attempts at vascular access have previously failed represent a challenge to vascular surgeons. In these difficult patients the arm offers an excellent site for either an autogenous fistula or a prosthetic shunt because of the relatively unharmed portion of the upper cephalic vein or the protected location of the brachial vein in most individuals. (The anatomic region of the arm by definition is the area between the shoulder and the elbow.) Over the last two years we have studied 15 patients with a mean of 2.5 previously failed shunts or fistulas who subsequently had vascular access procedures in the arm, with the brachial artery as the inflow and the cephalic vein or brachial vein as the outflow. The first choice was the cephalic vein transposition to the brachial artery because it involved only one anastomosis and is autogenous vein. The alternative was a prosthetic graft of polytetrafluoroethylene (PTEE) between the brachial artery and the cephalic vein or brachial vein in the arm. The patency rate of these arm access procedures has been 75%. None of these patients had had congestive heart failure, distal ischemia, or excessive hematoma formation. The arm represents an excellent source for fistula or shunt construction in those difficult patients in whom previous vascular access sites have already failed.
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PMID:The arm as an alternative site for vascular access for dialysis in patients with recurrent access failure. 396 71

A 31-yr-old Japanese woman who was on chronic hemodialysis for 3 yr died of intractable congestive heart failure. Three years before death, the patient was in a state of shock for 48 h due to ventricular tachycardia and gastrointestinal bleeding, which was followed by marked elevation of serum transaminase. Four months later, abdominal plain radiography demonstrated diffuse hepatic calcification. At autopsy, microscopic examination of the liver revealed parenchymal necrosis and tiny calcifications in the central to midzonal area of the lobule. Calcification in the degenerative area of the hepatic lobule occurred subsequent to parenchymal ischemia after overt shock that lasted for 2 days. Although a definitive explanation for the calcification was not obtained, it may be related to the disturbances of intracellular Ca2+ homeostasis as a result of ischemic liver injury or it may be related to an elevated calcium-phosphorus product in the uremic state.
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PMID:Diffuse hepatic calcification as a sequela to shock liver. 400 4

Based on the concept of the "primary lobule" as the microcirculatory unit of human pancreas that we previously established (Yaginuma et al., submitted to Path Res Pract), ischemic injuries of this organ were microscopically screened over many autopsy cases and were classified according to the zone of the unit involved. The primary lobule was defined as a small parenchymal region, supplied by a centrally placed arteriole and drained by flanking venules, often with an islet at the center because of its close relation with arteriole. The screening disclosed twenty out of 221 autopsy cases to be harboring some ischemic injury. In a 3-D reconstruction study performed on these pancreases to correlate the injured areas with performed architecture, three types of injuries were established as comprising different categories; 1) peripheral and 2) central necroses, both presenting as multiple small foci, the distribution of which in the former exactly coinciding with the central, and that in the latter with the peripheral zone of primary lobules, and 3) peripheral atrophy, uniformly affecting the peripheral acini. The first type tended to coexist with malignant hypertension, the second type was mostly found in shock cases and the third type exclusively in those with congestive heart failure. The pathogenesis of peripheral and central necroses was explained by a working hypothesis that correlates these categories with different impediments of microcirculation, assuming that in the former, blood flow was severely impeded by constriction of relatively proximal arteries, while in the latter, sporadic occlusion at terminal arterioles was responsible for peripheral ischemia.
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PMID:Ischemic injury of the human pancreas. Its basic patterns correlated with the pancreatic microvasculature. 402 41

Nitrates, betablockers an calcium antagonists are the major drugs for treating angina pectoris. Therapeutic efficacy and incidence of unwanted reactions depend on the proper choice and dosage of these agents. The type of ischemic symptoms, cardiac function, presence of sinoatrial or atrioventricular conduction anomalies, and coexistent non-cardiac disorders should be taken into account when a particular drug is selected. In patients with angina at rest a calcium antagonist is indicated in the first place, while in exercise-induced ischemia betablockers and calcium antagonists are equally effective. With regard to antianginal efficacy there are no important differences between various representatives of these drug groups, but their tolerance may markedly vary in individual patients. Combination of betablockers, calcium antagonists and/or nitrates is often required in cases with severe limitation of exercise capacity. Therapeutic guidelines for patient groups with and without congestive heart failure are suggested.
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PMID:[The choice of drugs and dosage for angina pectoris]. 614 1


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