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)

Perioperative coronary spasm after coronary bypass surgery is increasingly recognized as a possible cause of circulatory collapse. Most of the reported cases involved the right coronary artery (RCA). A case where transient right coronary spasm provoked right ventricular ischemia and collapse is described.
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PMID:Perioperative coronary spasm and right ventricular ischemia. 348 66

The revival of the concept of coronary spasm has stimulated research into coronary artery disease. Observations in patients with variant angina have substantially contributed to the appreciation of painless myocardial ischemia. However, the presence or absence of pain during ischemic episodes is not related to the cause of ischemia, because painless ischemia can be observed in variant angina (caused by spasm), in effort-induced angina (caused by increased myocardial demand) and in myocardial infarction (caused by thrombosis). Continuous monitoring initially of patients with variant angina and subsequently of patients with unstable and stable angina proved that often painful and painless ischemic episodes are caused by a transient impairment of regional coronary blood flow rather than by an excessive increase of myocardial demand. The transient impairment of coronary flow appears to be caused by dynamic stenosis of epicardial coronary arteries. This most often occurs at the site of atherosclerotic plaques encroaching on the lumen to a variable extent. Dynamic stenosis can be caused by 1) "physiologic" increase of coronary tone, as in stable angina, 2) spasm, as in variant angina, and 3) thrombosis, usually in combination with "physiologic" changes in tone or with spasm, or both, as in unstable angina. The mechanisms of spasm, as typically observed in variant angina, are different from those of "physiologic" increase of tone; they appear to be related to a local alteration that makes a segment of coronary artery hyperreactive to a variety of constrictor stimuli causing only minor degrees of constriction in other coronary arteries. The nature of this abnormality, which may remain stable for months and years, is yet unknown.
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PMID:Louis F. Bishop lecture. Role of coronary artery spasm in symptomatic and silent myocardial ischemia. 354 91

Research during the last ten years into the pathophysiology of acute myocardial infarction (AMI) has made it gradually clearer that this is a phasic event. A number of independent authors have made this conclusion quite obvious. The authors of this review suggest that the alternating sequence of coronary spasm and dilatation should be described as the "thromboischemic reentry mechanism," which itself leads to waves of reperfusion, producing characteristic episodic changes in some of the parameters of AMI. The spasms are brought about by substances let loose from aggregating platelets. Metabolites released during the concomitant ischemia lead the vessel from spasm to dilatation. Following thrombolytic treatment, the 'staccato' signs of myoglobinemia disappear, because of the withdrawal of the spasmogenic products of the platelets. It could also be shown that the concentration of myoglobin in the serum as a result of the dilating effect of calcium antagonists is twice the mean maximum value that the myoglobin time curve would show without such treatment.
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PMID:New perspectives on the function of coronary artery spasm in acute myocardial infarction: the thromboischemic reentry mechanism. A review of 10 years research on the pathophysiology of AMI. 354 66

The long-acting antianginal drug molsidomine has been shown experimentally to reduce myocardial infarct size when administered prior to or after cardiac insult. This is due to several drug actions. Dilation of postcapillary capacitance vessels diminishes venous return, preload, heart dimensions, and myocardial oxygen consumption. Relaxation of stenosed conductive coronary arteries increases the perfusion of myocardial areas at risk of infarction due to enhanced collateral circulation. Increased regional blood supply nourishes predominantly subendocardial cardiac muscles as a result of reduction of extravascular coronary pressure, and resistance. The stable heart rate and cardiac contractility favor improved heart performance. The inhibition of platelet aggregation in vivo by molsidomine or its active metabolites, SIN-1 and SIN-1A, is linked to the stimulation of prostacyclin synthesis, inhibition of thromboxane release with induction of thrombosis and vasoconstriction, and enhanced concentrations of cyclic guanosine monophosphate. Dilation of coronary arteries after intracoronary administration of SIN-1, with inhibition of platelet aggregation by restrained release of adenosine diphosphate and stabilization of platelet membranes, facilitates the recanalization of stenosed arteries and reduces coronary muscle tone at the site of thrombosis. Activation of the human fibrinolytic system and drug-induced release of a plasminogen activator favor dysaggregatory effects. The drug's inhibiting actions on lipoxygenase products of arachidonate (e.g., 12-hydroperoxy-eicosatetraenoic acid and leukotrienes) may shift prostaglandin catabolism to cyclooxygenase products (e.g., prostacyclin) that protect against the expansion of ischemia and the induction of coronary spasm. Experimentally, the hemodynamic effectiveness of molsidomine can be antagonized by catecholamines (afterload effects) and dihydroergotamine (preload and afterload effects) respectively. Further clinical investigations will clarify the application of these mechanisms for the therapeutic success of the drug in human myocardial infarction.
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PMID:Molsidomine: alternative approaches to treat myocardial ischemia. 355 58

Influence of helium-neon laser lg-75 rays on the microcirculatory bed and neurocytes of the small intestine after its experimental ischemia has been studied. When a normal small intestine is radiated, dilatation of the luminal diameter is observed in all links of the microcirculatory bed (MCB) and also hypertrophy of neurocytes, when phenomena of distrophic processes are absent. In 30 days after 3-hours' ischemia of the intestinal loop and its successive radiation, spasm of arterial and dilatation of the venous link of MCB is registered; they normalize by the 45th day. In the control, after ischemia (without radiation) in 45 days venous plethora of the vessels in the intermuscular plexus of the intestinal wall is kept. In the nervous elements of the muscular-intestinal plexus at early stages of the experiment against the background of ischemia reactive and distrophic changes appear. By the 30th day after radiation, the volume of neurocytic bodies increases, processes grow out, nuclear-cytoplasmic index increases. Nonspecific character of the laser rays is supposed; their effect is realised via regional microvascular and nervous formations.
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PMID:[Effect of helium-neon laser radiation on restoration of the structure of the microcirculatory bed and neurocytes of the small intestine following experimental ischemia]. 361 74

Human arteries and veins contract with hypoxia and deprivation of substrate provoked by increasing calcium inflow into the cell and reduced energy. Such spasm may be eliminated by phosphoenolpyruvate which loads up the cell's energy, blocking glycogen reduction at the same time. Reperfusion will then guarantee a sufficient energy stroke. Therapy should pursue the following steps: 1. Phosphoenolpyruvate infusion (1 X 10(-6) up to 1 X 10(-3) gm/ml in tyrodes solution pH 7.3) into the arterial branch, proximal and distal to the injury. 2. Subsequent treatment with vasodilating drugs and rheologically active substances. 3. Failed therapy after more than three hours warm ischemia could be due to autolytic processes and requires resection of the affected vessel. 4. The imbalance of the thrombolytic system with the so-called no reflow phenomenon could be due to a plasminogen activator's inhibitor released during hypoxia. Such cases may reasonably be treated by urokinase or by streptokinase plasminogen complex.
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PMID:[Vascular spasms in microsurgery]. 362 68

The effect of oral administration of 500 mg of levodopa with 50 mg of carbidopa, a peripheral dopadecarboxylase inhibitor, on coronary vasomotion during vasoconstrictor stimuli was examined in 15 patients with variant angina presenting with hyperventilation-induced myocardial ischemia. Patients were studied during 3 noninvasive sessions and 1 angiographic session. In all sessions the basic protocol consisted of provocation of coronary spasm by hyperventilation before and 2 hours after levodopa and carbidopa administration. During angiography, great cardiac vein blood flow, right atrial and aortic pressures were measured, and coronary angiograms were recorded at baseline and 1 to 4 minutes after each hyperventilation. Samples for dopamine plasma levels were drawn before and throughout the studies. In 3 selected patients, levodopa and carbidopa were associated with 30 mg of domperidone, an antagonist of dopamine peripheral receptors. Levodopa and carbidopa consistently prevented the occurrence of ischemia after hyperventilation in 6 of the 15 patients. This was due to inhibition of local coronary spasm in 2 patients and reduced coronary constriction in 4. Ischemia due to hyperventilation was still prevented despite addition of domperidone with levodopa and carbidopa. Plasma dopamine levels were 23 +/- 15 before and 739 +/- 284 pg/ml 2 hours after administration of levodopa and carbidopa. These findings are consistent with either a decreased central dopaminergic activity and associated disregulation of vasomotor tone, or a peripheral vasodilatory effect of increasing dopamine.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of oral levodopa and carbidopa on coronary spasm in variant angina pectoris. 363 Sep 30

A recent report showed that during Holter monitoring of patients with syndrome X (typical anginal pain, positive exercise test response [at least 0.1 mV of ST-segment depression], no evidence of coronary spasm and angiographically normal coronary arteries), 50% of episodes of ischemic ST-segment depression were painful. This proportion is considerably higher than that in patients with chronic stable angina, which is about 30%. A significantly lower threshold and tolerance to painful stimuli was seen in a group of patients with chronic stable angina in whom 50% of episodes were painful compared with a group in whom only 5% of episodes were silent. Hence, patients with syndrome X may have enhanced sensitivity to painful stimuli. To investigate whether this difference was due to a lower threshold for painful stimuli in general, 12 patients with syndrome X and 10 (age- and sex-matched) with chronic stable angina were studied using the same battery of painful stimuli. Patients with syndrome X had a significantly lower threshold and tolerance for forearm ischemia (-36%, p less than 0.05, and -40%, p less than 0.001) and electrical skin stimulation (-37%, p less than 0.01, and -35%, p less than 0.001); the cold pressor test did not show significant differences (-7%, p = 0.391, and -1%, p = 0.818). Thus, patients with syndrome X in this study had significantly lower threshold and tolerance values for forearm ischemia and for electrical skin stimulation. These differences in sensitivity to pain may partly explain a higher incidence of painful ischemic episodes detected by ambulatory electrocardiographic monitoring during unrestricted daily life.
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PMID:Pain threshold and tolerance in women with syndrome X and women with stable angina pectoris. 363 Sep 32

Evidence that platelet activation contributes to ischemia associated with atherosclerosis led us to examine the response of the limb collateral arterial tree to a platelet product, serotonin. In 23 anesthetized dogs we measured arterial diameter (angiography) and blood flow (133Xe transit) before or 2 weeks after superficial femoral artery ligation (SFAL). In normal hindlimbs blood flow increased after 5-hydroxytryptamine (5-HT) and there was a modest but measurable, dose dependent narrowing of 1- to 2-mm vessels, the major stem vessels for collateral blood flow. After SFAL, identical segments of these vessels responded to serotonin more: the slope relating dose and response became steeper (P less than 0.001), the threshold dose fell significantly (P less than 0.001), and calf blood flow fell. The vasodilator response to acetylcholine was reduced sharply after SFAL, but was still demonstrable. The 5-HT-2 serotonin antagonist, ketanserin, reversed serotonin induced spasm in the region served by collaterals (P less than 0.025). Responses to norepinephrine were not potentiated. A 5-HT-2 receptor dependent sensitization of collateral arterial vessels, and blunting of the normal vasodilator response, mediates a paradoxical decrease in perfusion induced by 5-HT in regions served by the collaterals.
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PMID:Specific increase in sensitivity to serotonin of the canine hindlimb collateral arterial tree via the 5-hydroxytryptamine-2 receptor. 373 44

Coronary arteriography remains the most precise clinical tool for diagnosis and therapeutical decision concerning patients with coronary artery disease; when performed during a short transient episode of myocardial ischemia, this investigation can afford interesting information. The first part of the paper describes the coronary arterial angiographic findings during ischemia related to increase in myocardial requirements. Thus, a vasoconstrictor reflex can decrease the area of narrowing during handgrip exercise. Other reports have described coronary arterial spasm during exercise in highly selected patients. Coronary arterial angiographic findings during transient decrease of coronary blood flow are described in the second part of this paper. They can rarely be detected spontaneously but most often are provoked. The results obtained with cold pressor, hyperventilation and ergonovine tests are discussed. In this latter provocative test, the incidence of spasm in a population of 2572 patients undergoing coronary angiography is described.
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PMID:Coronary arterial angiographic findings during transient myocardial ischemia. 375 89


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