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

Myocardial pH was measured continuously with a micro pH electrode inserted into the left ventricular wall in dogs. Anterior descending coronary flow was reduced to about 1/3 of the original flow by partial occlusion of the coronary artery. Myocardial pH decreased from 7.50--7.60 to 7.06--7.24 after partial occlusion. Drugs were injected intravenously during ischemia of the heart caused by partial occlusion. l-Propranolol (1 mg/kg) reduced heart rate and increased the pH from 7.06 +/- 0.04 to 7.48 +/- 0.04 (P less than 0.01). d-Propranolol (1 mg/kg) reduced heart non-significantly and increased the pH from 7.24 +/- 0.05 TO 7.56 +/- 0.05 significantly (P less than 0.05). In other studies, the effect of l- and d-propranolol on both heart rate and metabolic responses to isoproterenol (500 micrograms/kg i.p.) was studied. Isoproterenol increased heart rate and also elevated the blood levels of glucose and lactate. l-Propranolol inhibited these responses to isoproterenol. d-Propranolol did not inhibit the heart rate response but inhibited the blood lactate response to isoproterenol significantly. The blood glucose response to isoproterenol was inhibited by d-propranolol non-significantly. The action of both l- and d-propranolol on ischemic myocardial pH may be related to their action on cardiac metabolism as well as to their local anesthetic action.
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PMID:Increase of myocardial pH by 1- and d-propranolol during ischemia of the heart in dogs. 624 50

Exercise thallium-201 perfusion scans and gated equilibrium blood pool scans were performed in 120 catheterized patients with a chest pain syndrome. Eighty-six patients had coronary artery disease and 34 patients did not. The effects of gender, propranolol, exercise level, exercise ischemia, history of typical angina, history of previous myocardial infarction, electrocardiographic Q waves, number of diseases vessels and extent of coronary artery obstruction on diagnostic accuracy were evaluated. The overall sensitivity and specificity of thallium scans were 76 and 68%, respectively, and those of gated blood pool scans 80 and 62% (p = not significant). Propranolol decreased the specificity of thallium scans (propranolol = 42%; no propranolol = 87%, p less than 0.05). Thallium scans and anginal history were less sensitive for detecting coronary disease in women (men: thallium = 79%; angina = 77%; women: 54 and 46%, respectively; p less than 0.05). Exercise level did not significantly affect the diagnostic accuracy of either scan. Thallium and gated scans were both highly sensitive (95%) in detecting disease in 20 patients with a prior myocardial infarction, angina and a positive electrocardiogram. The sensitivity of the thallium scan significantly decreased as the number of diseased vessels decreased. Both thallium and gated scans were less frequently positive in patients with atypical angina or no Q waves, but were not significantly influenced by electrocardiographic ischemia. The sensitivity and specificity of both scans were low in 57 patients with the combination of atypical angina, no history of infarction and equivocal stress electrocardiogram thallium = 61 and 63%, respectively; gated = 61 and 67%). When stress thallium scan evaluation included the electrocardiogram and thallium scan interpretation, the diagnostic accuracy was 81%. When all the information from gated scans (wall motion, ejection fraction, pulmonary blood volume) was combined for final gated scan evaluation, the diagnostic accuracy was 83%. When electrocardiographic data were added to all three gated scan variables, diagnostic accuracy was 77%. In conclusion, thallium perfusion and gated blood pool scans have reasonable diagnostic accuracy for coronary artery disease in a group of patients with a moderately high prevalence of disease. However, combined variables from each test are needed to provide reliable diagnostic accuracy.
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PMID:Comparison of exercise perfusion and ventricular function imaging: an analysis of factors affecting the diagnostic accuracy of each technique. 631 68

The effect of beta-blockade on dipyridamole thallium-201 images was assessed in 8 patients with coronary artery disease and positive dipyridamole test. Three dipyridamole thallium-201 tests were performed, the first in basal conditions, the second 30' after propranolol and the third with propranolol and atrial pacing. After dipyridamole heart rate and double product increased respectively from 75 +/- 7 to 98 +/- 15 b/min (p less than 0.01 vs starting values) and from 10 551 +/- 1255 to 11 740 +/- 4542 mmHg X b/min (p less than 0.05 vs starting values). Propranolol reduced heart rate to 64 +/- 6 b/min (p less than 0.05 vs basal conditions), systolic blood pressure to 136 +/- 13 and double product to 8733 +/- 1248 (p less than 0.05 vs basal conditions). Dipyridamole when infused after propranolol, induced an increase in heart rate to 70 +/- 5 b/min (p less than 0.05 vs starting values) while double product was 9133 +/- 1189 mmHg X b/min (p = NS vs starting values). Atrial pacing prevented the fall in heart rate and double product induced by propranolol so during dipyridamole infusion double product increased to 13 271 +/- 1868 (p less than 0.05 vs propranolol treatment; p less than 0.05 vs starting values). Segmental score calculated after dipyridamole was 5.2 +/- 2.0 in basal conditions, 5.1 +/- 1.3 after propranolol (p = NS) and 4.8 +/- 1.3 after propranolol plus atrial pacing (p = NS). Thus the results of the study show that beta-blockade does not worsen dipyridamole thallium-201 images. Furthermore the steal phenomenon seems to be the main mechanism of the dipyridamole induced ischemia. In fact, also when the increase, oxygen consumption is blunted with beta-blockade the disparity in myocardial blood flow resulted unaffected.
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PMID:Effect of beta-blockade on thallium-201 dipyridamole myocardial scintigraphy. 633 36

Effort angina is the result of acute myocardial ischemia on exercise due to an imbalance between myocardial oxygen demand and supply. During exercise, ischemia is provoked by an increase in myocardial oxygen needs (tachycardia, increased blood pressure, etc.) which cannot be met by increased coronary blood flow. The commonest cause of insufficient flow is coronary atherosclerosis. Coronary spasm does, however, play a role, whether it occurs during exercise on normal or atheromatous coronary vessels. Classical anti-anginal therapy is directed towards a reduction in the intense adrenergic activity associated with exercise, and to the limitation of myocardial oxygen consumption. Calcium inhibitors which cause peripheral vasodilation, decrease ventricular wall tension and coronary resistance, are usually reserved for unstable or resistant angina. We studied 10 patients with stable effort angina for over 2 years with significant (greater than 70 per cent) atheromatous lesions on coronary angiography unsuitable for surgical treatment. The patients underwent a randomised double blind trial to compare the effects of propranolol, diltiazem and placebo. Exercise ECG was performed after a treatment period of one week, 3 hours after drug administration. The results showed a significant improvement of work capacity with propranolol and diltiazem as compared to placebo. Propranolol (160 mg/day) was more effective than diltiazem (180 mg/day) in 6 patients. In 4 cases, the improvement with diltiazem and propranolol was the same. The association of the two drugs in one open study in 5 patients was even more effective in 3 patients. The small number of patients studied makes it impossible to draw any firm conclusions. Although calcium inhibitors are the treatment of choice in coronary spasm and betablockers in effort angina, diltiazem exerts an anti-anginal effect by reduction of myocardial oxygen consumption without depression of myocardial contractility, as other workers have shown.
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PMID:[Are calcium inhibitors useful in the treatment of effort angina pectoris]. 640 53

The purpose of this study was to characterize left ventricular systolic elastances as derived from pressure-segment length and pressure-diameter relationships, and to compare the resulting regional and global elastances to known changes in inotropy. Left ventricular pressure-segment length and pressure-diameter were varied in a series of consecutive beats by means of a volume-loading technique, and both regional and global relationships at 20-msec intervals throughout systole were found to be nonlinear and to exhibit hysteresis. In eight animals, regional hysteresis was present after vagotomy, propranolol (1.0 mg/kg), and atropine (0.1 mg/kg), and was present no matter whether hearts were loaded by volume (45-60 ml/sec) or by pressure (partial aortic occlusion) over a similar range of left ventricular systolic pressures. Elastance was linearly approximated by the slope of the major axis of the hysteresis loops. In each instance, elastance increased to a maximum and then decreased, thus defining end-systole. In seven animals, maximum elastance-length and -diameter were compared before and after treatments with dobutamine (5-13 micrograms/kg per min) and propranolol (6-51 micrograms/kg per min), or after induction of global ischemia. Dobutamine increased maximum elastance-diameter by 37% (P less than 0.01) and maximum elastance-length by 159% (P less than 0.05). Propranolol decreased maximum elastance-diameter by 27% (P less than 0.05) and maximum elastance-length by 6% (P = NS). Global ischemia (50% reduction in coronary flow) did not significantly change either maximum elastance-diameter or -length. However, with ischemia, the diameter intercept of maximum elastance-diameter increased by 24% (P less than 0.025), and the time to maximum elastance-length decreased by 33% (P less than 0.01). Comparing all interventions, the percent changes in maximum elastance-length and -diameter related directly but with a low correlation coefficient (r = 0.49). These differences in regional and global elastance suggest a complex relationship between regional and global myocardial mechanics, and may not necessarily reflect specific changes in contractility.
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PMID:Regional end-systolic pressure-length relationships using a volume-loading technique in the intact pig heart. 646 26

Antiarrhythmic and cardioprotective effects of propranolol and sotalol were examined by studying their action on cellular electrical activity (recorded using standard microelectrode techniques) and creatine-kinase leakage (measured in the effluent from the experimental bath chamber) in the in vitro guinea-pig left ventricular myocardium exposed to conditions mimicking severe or moderate ischemia. Returning the tissue to the normal conditions was considered as equivalent to ischemic-heart reperfusion. Propranolol (2 X 4 mg/kg) was intraperitoneally administered to guinea-pigs, daily for 21 days. It was perfused in vitro (1.10(-6) M) during the whole experiments. Propranolol decreased action potential duration in control conditions (p less than 0,05), precipitated the occurrence of inexcitability during severe ischemia (p less than 0,01) and improved the recovery of cellular excitability during reperfusion. Propranolol did not significantly affect the creatine-kinase leakage during ischemia and reperfusion.
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PMID:[The effects of propranolol and sotalol on the electrophysiologic and enzymatic impact of myocardial ischemia induced in vitro in the guinea pig heart]. 649 20

Propranolol's potential as a protective agent against tissue injury has been noted in experimental myocardial, renal and early acute focal cerebral ischemia. The purpose of the present investigation was to study further the effects of racemic (d,l) propranolol on blood-brain barrier permeability, morphological changes, cortical electrical activity, and regional cerebral blood flow (rCBF) in experimental focal cerebral ischemia. Thirty adult cats, anesthetized with nitrous oxide, underwent 6 hours of right middle cerebral artery (MCA) occlusion. Fifteen cats were untreated. Fifteen cats were given a continuous infusion of racemic propranolol (1 mg/kg/hr) for 7 hours beginning 1 hour before MCA occlusion and a 4 mg/kg bolus immediately before occlusion, both directly into the right carotid artery. Right Sylvian rCBF did not significantly differ in the treated and untreated groups. Carbon filling defects and vital dye (i.e., Evans blue and fluorescein) extravasation were less severe in the propranolol treated animals. Light microscopic findings demonstrated no difference in infarct size between the two groups. The findings suggest that at doses given, racemic propranolol does not exert a protective effect upon cerebral tissue subjected to 6 hours of incomplete ischemia.
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PMID:Treatment of acute focal cerebral ischemia with propranolol. 672 77

The effect of diltiazem on the contractile and vascular responses to 2 min of total occlusion and reperfusion was investigated in isolated blood-perfused canine papillary muscle preparations. Diltiazem, in doses (3 and 10 micrograms/min) that increased coronary blood flow but did not change developed tension and maximum rate of tension development (dT/dt) in papillary muscle before occlusion, attenuated tension development between 40 and 120 sec of ischemia. At-60 sec postocclusion, developed tension was at 36 +/- 4, 37 +/- 5 and 44 +/- 4% below preocclusion levels for 3, 10 and 100 micrograms/min of diltiazem, respectively (nondiltiazem treated = 24 +/- 3%). The dT/dt increased to 22 +/- 6% above preocclusion value during ischemia in nondiltiazem-treated preparations. This was blocked by diltiazem in a dose-dependent fashion. Propranolol and nitroprusside did not modify the developed tension and the increase in dT/dt of the papillary muscle during occlusion. On reperfusion, an overshoot in developed tension to 22 +/- 4% above preocclusion level was observed. This was significantly reduced by diltiazem and propranolol but not by nitroprusside. Diltiazem inhibited the maximal peak reactive hyperemia response after 2 min of occlusion by 30 to 38%. Both propranolol and nitroprusside did not change this response. The results show that diltiazem selectively depresses the inotropic state of the ischemic myocardium and suggest that a diltiazem-induced reduction in myocardial oxygen consumption during ischemia may contribute to the protection of ischemic myocardium and the reduction in reactive hypermia response in the ischemic heart.
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PMID:Studies on mechanisms of diltiazem-induced protection of the ischemic myocardium: selective myocardial depressant action of diltiazem on an ischemic isolated blood-perfused canine papillary muscle preparation. 684 4

Both nifedipine a calcium antagonist, and propranolol a beta-adrenergic blocker, are used as protective agents of the ischemic myocardium. In the clinical setting, the combination of the two drugs is used successfully although several case reports indicate potential dangers of the combination. For this reason we decided to study the combined effect of nifedipine and DL-propranolol in the isolated rat heart made ischemic for a short period of time. Apex displacement was taken as a measure of contractility. Release of the AMP catabolites adenosine, inosine, (hypo)xanthine and uric acid was used as a marker of ATP breakdown. Contractility during ischemia was not affected by the drugs. DL-Propranolol (30 or 150 micrograms/l) had no effect on ischemic myocardial purine release, while nifedipine (15 micrograms/l) reduced purine release during ischemia by 33% (P less than 0.02). The combination of 15 micrograms/l nifedipine and 150 micrograms/l DL-propranolol decreased purine release by 53% (P less than 0.005 vs. nifedipine). We conclude from these results that propranolol has a synergistic effect, adding to the beneficial action of nifedipine on ischemic myocardium.
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PMID:Synergistic effect of nifedipine and propranolol on adenosine (catabolite) release from ischemic rat heart. 688 29

Delayed postischemic brain hypoperfusion and hypermetabolism are likely detrimental factors to neurologic recovery after transient global brain ischemia and may be mediated by catecholamines acting via adrenergic receptors. We evaluated the effects of alpha and beta receptor blockade on cerebral blood flow (CBF) and metabolism after 16 min transient global brain ischemia. Ischemia was induced by arterial hypotension and a high pressure neck tourniquet in 13 anesthetized cats. Six cats were untreated, 4 received propranolol 1 mg/kg, IV and 3 a combination of propranolol and phentolamine, one mg/kg injected one min before recirculation. Total CBF was measured by continuous monitoring of cerebral venous 133Xe clearance after bolus intra-arterial injection. Arterial and cerebral venous oxygen, glucose and lactate were measured. Cerebral cortex glucose and lactate were measured 3 hours post-ischemia after in situ freezing with liquid N2. The cerebral cortex of 3 cats anesthetized, but not subjected to ischemia, was similarly frozen and analyzed for glucose and lactate. Total CBF was relatively constant for up to 3 h post-ischemia in all groups, but significant changes in fast and slow-flow rates and compartment sizes were observed. In untreated cats, the normal 60/40 percent relative weight of the fast and slow-flow compartments was reversed to 30/70 percent by 1 hr post-ischemia. Propranolol attenuated the size of the fast-flow compartment in the first 30 min post-ischemia which was partially restored by phentolamine. Brain oxygen consumption increased 2 to 3-fold by 1 h post-ischemia in all groups. Propranolol compromised CBF and impaired glucose and lactate oxidation which was partly reversed by phentolamine. We concluded that within the first 30 min post-ischemia, beta, and to a lesser extent, alpha receptors predominate in the modulation of cerebrovascular tone. By 1 h post-ischemia, however, adrenergic modulation of cerebrovascular tone is lost. Delayed post-ischemic hypermetabolism unlike stress-induced, but like hypoxia-induced hypermetabolism is only partially affected by beta blockade. Propranolol apparently compromises brain oxygen consumption secondary to a reduction in brain O2 supply while phentolamine improves perfusion and oxygen consumption.
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PMID:Post-ischemic hypermetabolism in cat brain. 730 55


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