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)

Forty one patients with ischaemic heart disease (IHD) of the age 60 +/- 12.3 years were hospitalized and treated two weeks with Curantyl (Dipyridamol) which was applied per os in a dose of 75 mg 3 times, and after another two weeks 34 of them wass applied Isoptin (Verapamil) in a dose of 40 mg 3 times daily. The heat conductivity (J.m-1, sec-1.degree C.10(-2), HC) and skin temperature (degree C, ST) were examined at the isothermic level 2 cm above the inner ankle by the apparatus Fluvograph 2 of Hartmann and Braun A. G. (BRD). The HC after Isoptin application above the left and right ankle was in 34 patients increased significantly (p less than 0.001). In patients with IHD after Curantyl application the HC and ST was significantly decreased above the left and right ankle in 9 (21.9%) and in 12 (30.0%), respectively. Curantyl could deteriorate HC and so to worsen legs ulceration healing and to point ap ischemia in patients with associated chronic postphlebitic syndrome with ulcera crurium.
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PMID:Heat conductivity and skin temperature at the treatment of ischemic heart disease with curantyl and isoptin. 207 72

The effect of organ flushing with the calcium entry blocker verapamil on the conversion of innocent enzyme xanthine dehydrogenase (XDH) to superoxide generating enzyme xanthine oxidase (XOD) in ischemic rat livers was studied. This enzyme conversion progressed over time in warm or cold ischemia. In non-flushed livers, the activities of XOD as percentages of XDH plus XOD after 6 h at 37 degrees C and 6 days at 4 degrees C were 80.3 +/- 5.2 and 31.6 +/- 2.1, respectively. In the livers flushed with Euro-Collins solution, the conversion was inhibited to 37.0 +/- 3.9% (P less than 0.001) after 6 h of warm ischemia, while this inhibitory effect was not found in cold ischemia. Verapamil given through the portal vein on flushing further suppressed the conversion in both warm and cold ischemia (with 5.0 microM of verapamil, 21.2 +/- 5.8% (P less than 0.001) after 6 h of warm ischemia and 25.2 +/- 3.3% (P less than 0.01) after 6 days of cold ischemia). A similar effect was also obtained with the addition of 10 or 30 mM of EGTA instead of verapamil. In contrast, no inhibitory effect on conversion was obtained in livers flushed and homogenized with 10.0 microM of verapamil followed by incubation for 6 h at 37 degrees C. In the livers that were flushed and stored at a warm temperature for 6 h, verapamil reduced the increase of tissue lipid peroxidation product (P less than 0.02) after 15 min of reperfusion. Although the precise mechanisms of these inhibitory effects of verapamil on the enzyme conversion are still uncertain, it is thought that organ flushing with verapamil might reduce the XOD-mediated postischemic reperfusion injury in livers subjected to prolonged ischemia.
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PMID:Effect of verapamil on conversion of xanthine dehydrogenase to oxidase in ischemic rat liver. 208 35

Myocardial 45Ca sequestration was studied in dogs during 60 minutes of global ischemia and 30 minutes of reperfusion using cardiopulmonary bypass (CPB) and myocardial function was studied before and after CPB. Group A (n = 5), as a control, received cold hyperkalemic cardioplegic solution, Group B (n = 5) received the same solution plus verapamil (150 micrograms/kg/L) and Group C plus specific activity (TSA = DPM x 10(4)/g) and plasma specific activity (PSA = DPM x 10(4)/ml) were determined by biopsy before and after release of the cross-clamp The results showed that myocardial function in Group B and C were better than that in Group A (P less than 0.01). It is suggested that verapamil and Salvia miltiorrhiza Bunge effectively control myocardial calcium sequestration during early reperfusion and reduce myocardial reperfusion injury As to myocardial protection, cardioplegia with verapamil and Salvia miltiorrhiza Bunge were superior to hyperkalemic alone. Verapamil cardioplegia was still better than Salvia miltiorrhiza Bunge.
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PMID:[Experimental study on myocardial protection with verapamil and salvia miltiorrhiza Bunge cardioplegia]. 216 18

Ischaemia imposes a progression of damage on the myocardium, starting with a loss of adenosine triphosphate, creatine phosphate, potassium and active tension-generating capacity. These changes progress until the tissue is incapable of maintaining ionic homeostasis, is depleted of purine precursors and shows evidence of structural disorganization. Upon reperfusion the ischaemia-induced damage is exaggerated, primarily because of the accompanying uncontrolled gain in calcium, increasing tissue osmolarity and release of endogenous noradrenaline. When used prophylactically, calcium antagonists attenuate many of the deleterious effects of ischaemia and reperfusion. We have previously shown that long-term administration of verapamil to rats (50 mg/kg daily, orally) depletes their cardiac stores of noradrenaline (NA) (3.9 +/- 0.3 micrograms/g dry wt in controls vs 0.9 +/- 0.1 micrograms/g dry wt NA after 6 weeks of therapy). This loss of NA was not accompanied by a change in beta 1-adrenoceptor density (35.5 +/- 1.9 fmol/mg protein for controls vs 31.2 +/- 2.3 fmol/mg protein after 6 weeks of therapy). Verapamil withdrawal after 6 weeks of therapy resulted in a restoration of ventricular NA levels; within 2 days they had recovered to 75% of their original values. The density of the beta 1-adrenoceptor was unaltered. Withdrawal of verapamil results in rapid repletion of cardiac NA, with an initial but transient reduction in beta 1-adrenoceptor density. The absence of beta 1-adrenoceptor "up-regulation" under these conditions probably contributes to the absence of withdrawal problems upon cessation of verapamil therapy.
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PMID:Effect of verapamil withdrawal on cardiac beta 1-adrenoceptor density. 217 7

Epicardial composite electrode and isochronal mapping were used in this study to detect ventricular late potentials and ventricular activity sequence during sinus rhythm and ventricular tachycardias. 20 dogs were studied before and during acute ischemia induced by coronary artery ligation, 11 dogs 3-7 days after two-stage ligation of the left anterior descending coronary The effect of lidocaine and verapamil on VLP and reentrant ventricular arrhythmias was studied. The results demonstrated that: (1) Ventricular arrhythmias occurred right after ligation and 3-7 days later after ligation were related to the reentry in infarct myocardia zone; (2) The inhomogeneous conduction and dispersive refractory period provided a suitable milieu for reentry; (3) Reentrant excitation always occurred in a figure 8 configuration and delayed depolarization and continuous activation were reflected as VLPs at composite electrode; (4) Lidocaine in therapeutic dose prolonged the VLPs and interval of V-VLP. The effect of lidocaine on the ischemic zone was directly related to its ability to abolish reentrant ventricular arrhythmias; (5) Verapamil shortened the VLPs and interval of V-VLP, so the action of slow-response action potentials could not be excluded. Further study should be performed in order to demonstrate the precise mechanism of VLP.
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PMID:[Electrophysiologic study of ischemic ventricular arrhythmia]. 220 3

Normal left ventricular systolic performance with impaired left ventricular diastolic filling may be present in a substantial number of patients with congestive heart failure (CHF). To evaluate the effect of oral verapamil in this subset, 20 men (mean age 68 +/- 5 years) with CHF, intact left ventricular function (ejection fraction greater than 45%) and abnormal diastolic filling (peak filling rate less than 2.5 end-diastolic volumes per second [edv/s]) were studied in a placebo-controlled, double-blind 5-week crossover trial. All patients underwent echocardiography to rule out significant valvular disease, and thallium-201 stress scintigraphy to exclude major active ischemia. Compared to baseline values, verapamil significantly improved exercise capacity by 33% (13.9 +/- 4.3 vs 10.7 +/- 3.4 minutes at baseline) and peak filling rate by 30% (2.29 +/- 0.54 vs 1.85 +/- 0.45 edv/s at baseline) (all p less than 0.05). Placebo values were 12.3 +/- 4.0 minutes and 2.16 +/- 0.48 edv/s, respectively (difference not significant for both). Improvement from baseline in an objective clinico-radiographic heart failure score (scale 0 to 13) was significantly greater with verapamil compared to placebo (median improvement in score: 3 vs 1, p less than 0.01). Mean ejection fraction and systolic blood pressure were unchanged from baseline; diastolic blood pressure and heart rate decreased to a small degree. Verapamil may have therapeutic efficacy in patients with CHF, preserved systolic function and impaired diastolic filling.
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PMID:Usefulness of verapamil for congestive heart failure associated with abnormal left ventricular diastolic filling and normal left ventricular systolic performance. 222 Jun 22

The most common cardiotoxic effects of 5-fluorouracil (5-FU) are chest pain and ischemic ECG abnormalities. Coronary vasospasm may be the underlying mechanism. If so, prophylactic treatment with calcium channel blockers might have a beneficial effect. In the present study, prophylaxis with verapamil (120 mg three times daily) was given to 58 patients with esophageal or advanced head and neck carcinoma during induction chemotherapy with cisplatin and continuous infusion with 5-FU. Signs of ischemia appeared in 12% of the patients as compared to 13% in a previously studied compatible group of patients not receiving prophylaxis. The study does not support the hypothesis that prophylactic treatment with verapamil reduces the incidence of ischemia in patients undergoing 5-FU treatment. Verapamil might, however, modify the adverse cardiac effects of 5-FU by preventing supraventricular tachyarrhythmia.
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PMID:Failure of preventing 5-fluorouracil cardiotoxicity by prophylactic treatment with verapamil. 227 19

Verapamil benefits patients with angina pectoris during exercise. The mechanism underlying this effect is controversial. A direct oxygen-sparing effect on ischemic myocardium has been proposed, but previous studies seeking to demonstrate this effect have been inconclusive because of inadequate control of systemic hemodynamics. This study has assessed the direct effects of verapamil on regional myocardial contraction during graded coronary flow reductions while blood pressure and heart rate were held constant. Verapamil caused a decrease in regional contraction at normal levels of coronary flow, a finding consistent with a negative inotropic effect. At lower coronary flows, however, ischemic dysfunction was similar in the presence and absence of verapamil. These findings fail to support the concept that verapamil either selectively depresses ischemic myocardium or enhances myocardial function during ischemia. Thus, these direct mechanisms would seem unlikely causes of the observed beneficial effect during exercise in patients with coronary artery disease.
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PMID:Effect of verapamil on regional myocardial contraction during graded ischemia in the dog. 241 97

Isolated guinea pig hearts were subjected to 40 min of low flow global ischemia followed by 30 min of reperfusion. The effects of prostacyclin (PGI2) (10 pg/ml-10 ng/ml) on the response of hearts to ischemia and reperfusion were studied. Ischemia caused a 55% decline in contractile force and the development of contracture. Sinus bradycardia and varying degrees of atrioventricular conduction block were observed. Reperfusion was associated with rapid recovery of contractile force and a gradual decline in resting tension. PGI2 (1 ng/ml) enhanced ischemic contracture significantly at 10 and 20 min (P less than .05). Hearts made ischemic in the presence of PGI2 developed higher degrees of atrioventricular conduction block when compared to controls. Reperfusion in the presence of 1 or 10 ng/ml of PGI2 caused a significant decline in recovery of force (P less than .05) and enhanced reperfusion-associated contracture. We examined the influence of verapamil (100 ng/ml) and lowering external calcium to 1.25 mM on hearts subjected to ischemia and reperfusion in the absence of presence of PGI2 (1 ng/ml). Neither verapamil nor 1.25 mM calcium exerted significant effects on the decline of contractile force during ischemia or on recovery of contractility upon reperfusion. However, verapamil did reverse the reperfusion-associated cardiodepressant effects of PGI2. Verapamil abolished contracture in control hearts after 5 and 10 min of reperfusion and prevented the enhancement of contracture in hearts reperfused in the presence of PGI2.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Concentration-dependent effects of prostacyclin on the response of the isolated guinea pig heart to ischemia and reperfusion: possible involvement of the slow inward current. 244 Oct 27

The excessive gain in Ca2+ that occurs when hearts are reperfused after prolonged periods of ischemia contributes to cell death and tissue necrosis. The following experiments were undertaken to determine whether nicotine, in a concentration equivalent to the peak concentration present in plasma after cigarette smoke inhalation, alters reperfusion-induced Ca2+ gain in isolated rat hearts. Nicotine (0.15 microgram/ml) failed to increase tissue Ca2+ during aerobic perfusion but increased Ca2+ gain during reperfusion after 30 (p less than 0.02) or 60 (p less than 0.02) min of normothermic ischemia. The increase of Ca2+ gain was independent of a nicotine-induced release of norepinephrine (NE) or an altered "reflow area", heart rate, force of contraction, or end-diastolic resting tension. Pretreatment for 3 days with anipamil (20 mg/kg), a long-acting calcium channel blocker, attenuated the reperfusion-induced Ca2+ gain after 30 min of global ischemia, and reduced (p less than 0.001) the nicotine-induced exacerbation of that gain, without altering tissue ATP or creatine phosphate (CP). Verapamil (1 X 10(-6) M) reduced (p less than 0.02) the nicotine-induced exacerbation of Ca2+ gain caused by reperfusion after 30 min of ischemia.
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PMID:Nicotine-induced calcium overload during postischemic reperfusion. 245 Feb 39


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