Publications
145 results found
Fluck DS, Etherington PJE, Sheridan DJ, et al., 1998, Solute exchange in the rabbit myocardium: Ischaemia, reflow, and myocardial necrosis, BASIC RESEARCH IN CARDIOLOGY, Vol: 93, Pages: 354-360, ISSN: 0300-8428
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- Citations: 1
Stavrou BM, Sheridan DJ, Flores NA, 1998, Cardiac electrophysiological and haemodynamic effects of diadenosine polyphosphates in the isolated perfused guinea-pig heart, JOURNAL OF PHYSIOLOGY-LONDON, Vol: 509P, Pages: 150P-151P, ISSN: 0022-3751
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- Citations: 7
Huang WX, Turner MA, Kingsbury MP, et al., 1998, Evidence of an increase in vasodilator efficacy in isolated thoracic aorta from guinea-pigs after chronic ascending aortic banding, BRITISH JOURNAL OF PHARMACOLOGY, Vol: 123, Pages: U178-U178, ISSN: 0007-1188
Radvan J, Choudhury L, Sheridan DJ, et al., 1997, Comparison of coronary vasodilator reserve in elite rowing athletes versus hypertrophic cardiomyopathy, AMERICAN JOURNAL OF CARDIOLOGY, Vol: 80, Pages: 1621-&, ISSN: 0002-9149
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- Citations: 32
Siminiak T, Dye JF, Egdell RM, et al., 1997, The release of soluble adhesion molecules ICAM-1 and E-selectin after acute myocardial infarction and following coronary angioplasty, INTERNATIONAL JOURNAL OF CARDIOLOGY, Vol: 61, Pages: 113-118, ISSN: 0167-5273
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- Citations: 26
Sheridan DJ, 1997, Resources for cardiogenic shock, LANCET, Vol: 349, Pages: 951-951, ISSN: 0140-6736
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- Citations: 1
Siminiak T, Smielecki J, Dye JF, et al., 1997, Plasma levels in soluble adhesion molecules VCAM-1 and L-selectin during acute myocardial infarction, JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY, Vol: 29, Pages: 97044-97044, ISSN: 0735-1097
Siminiak T, Smielecki J, Dye JF, et al., 1997, Increased release of the soluble endothelial adhesion molecule ICAM-1 but not ELAM-1 during episodes of angina pectoris, JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY, Vol: 29, Pages: 7805-7805, ISSN: 0735-1097
Fluck DS, Etherington PJE, OHare D, et al., 1996, Myocardial tissue perfusion determined by particulate and diffusible tracers during ischaemia: What is measured?, CARDIOVASCULAR RESEARCH, Vol: 32, Pages: 869-878, ISSN: 0008-6363
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- Citations: 11
Flores NA, Botchway A, Cohen H, et al., 1996, Electrophysiological changes in isolated guineapig ventricular myocytes following exposure to products of the platelet release reaction, JOURNAL OF PHYSIOLOGY-LONDON, Vol: 497P, Pages: P55-P55, ISSN: 0022-3751
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- Citations: 2
Fluck DS, Etherington PJE, OHare D, et al., 1996, Solute exchange in the ischaemic myocardium: The voltammetric hydrogen clearance technique and radioactive microspheres., HEART, Vol: 75, Pages: 47-47, ISSN: 1355-6037
Carey PA, Sheridan DJ, de Cordoue A, et al., 1996, Effect of indapamide on left ventricular hypertrophy in hypertension: a meta-analysis., Am J Cardiol, Vol: 77, Pages: 17b-19b, ISSN: 0002-9149
Left ventricular hypertrophy is a major risk factor for cardiovascular morbidity and mortality. Angiotensin-converting enzyme inhibitors, calcium antagonists, and beta-blockers prevent, and cause regression of, left ventricular hypertrophy after short-term therapy. The ability of diuretics to do the same is unclear. We have performed a meta-analysis of studies documenting the effect on left ventricular mass of 6 months' treatment with 2.5 mg indapamide daily. Six studies comprising 197 patients, aged 20-75 years, were included. There was an overall mean reduction in left ventricular mass index of 13.3%, which was principally due to a reduction in left ventricular wall thickness rather than internal diameter.
Sheridan DJ, 1996, The pathophysiology of left ventricular hypertrophy and its importance as a coronary risk faster, Symposium on Hypertension - Other Risk Factors Considered, Publisher: ROYAL SOC MEDICINE PRESS, Pages: 6-9
Siminiak T, O'Gorman DJ, Shahi M, et al., 1995, Plasma mediated neutrophil stimulation during coronary angioplasty: autocrine effect of platelet activating factor., Br Heart J, Vol: 74, Pages: 625-630, ISSN: 0007-0769
BACKGROUND: Polymorphonuclear neutrophils are involved in the development of myocardial injury during ischaemia and reperfusion. Coronary angioplasty has been shown to result in neutrophil activation. This may be a result of contact with ligands expressed by endothelial cells or response to soluble stimuli released from ischaemic tissue into the plasma or both. OBJECTIVE: To investigate plasma mediated neutrophil activation during angioplasty. METHODS AND RESULTS: Plasma samples were collected from the coronary sinus, femoral artery, and femoral vein of 14 patients undergoing angioplasty, before and after the first balloon inflation and at the end of the procedure. Plasma samples were incubated with washed neutrophils isolated from healthy donors. Expression of the adhesion molecules CD18 integrin and L-selectin (Leu-8) was measured by flow cytometry, and superoxide anion production was measured by chemiluminescence. Plasma samples from the coronary sinus and femoral artery but not from the peripheral vein induced increased expression of neutrophil CD18 after balloon deflation. Modification of the expression of L-selectin was not noted. Production of superoxide anion by neutrophils was stimulated by plasma samples from the coronary sinus, but not by those from the femoral artery or vein. This plasma mediated neutrophil stimulation was prevented when the neutrophils were pretreated with platelet activating factor receptor antagonists BN52021 or BN50739. The platelet activating factor concentration detected in the coronary sinus was not higher than in control plasma. CONCLUSION: Brief ischaemia during coronary angioplasty leads to the release of soluble stimuli capable of inducing neutrophil integrin expression and free oxygen radical production. Platelet activating factor may act as an autocrine neutrophil stimulus under these conditions.
McAinsh AM, Turner MA, OHare D, et al., 1995, Cardiac hypertrophy impairs recovery from ischaemia because there is a reduced reactive hyperaemic response (vol 30, pg 113, 1995), CARDIOVASCULAR RESEARCH, Vol: 30, Pages: 1044-1044, ISSN: 0008-6363
Goulielmos NV, Enayat ZE, Sheridan DJ, et al., 1995, Nitric oxide and prostacyclin modulate the alterations in cardiac action potential duration mediated by platelets during ischaemia., Cardiovasc Res, Vol: 30, Pages: 788-798, ISSN: 0008-6363
OBJECTIVE: To investigate the effects of alterations of nitric oxide (NO) and prostacyclin (PGI2) availability on platelet-mediated electrophysiological effects during myocardial ischaemia. METHODS: Transmembrane action potentials and electrograms were recorded from isolated, Langendorff-perfused guinea-pig hearts during normal perfusion, global myocardial ischaemia and reperfusion during infusion of washed human platelets. Experiments were performed in the presence of 100 microM NG-nitro-L-arginine methyl ester (L-NAME), 30 microM L-arginine, 10 microM haemoglobin, 100 microM sodium nitroprusside and 2.3 nM iloprost, or using hearts obtained from DL-lysine monoacetylsalicylate (Aspisol, 50 mg.kg-1 i.p.)-treated animals. RESULTS: Perfusion with L-NAME and haemoglobin increased perfusion pressure by 33% (P = 0.0017) and 23% (P = 0.0026) while sodium nitroprusside and iloprost reduced it (17%, P = 0.0004, and 24%, P = 0.0006). In the absence of platelets, these compounds had no effect on arrhythmogenesis, but in the presence of platelets L-NAME reduced the onset time of ventricular tachycardia during ischaemia from 19.4 (s.e.m. 2.0) min to 12.9 (2.1) min, P = 0.04 and accentuated the ischaemia-induced reduction of action potential duration at 95% repolarization (APD95): 95(6) vs. 115(5) ms, P < 0.05 at 25 min. Sodium nitroprusside in the presence of platelets attenuated the ischaemia-induced reduction in APD95, while iloprost in the presence of platelets was antiarrhythmic (ventricular fibrillation 25 vs. 75%, P = 0.04) and attenuated the reduction in APD95 during ischaemia 115(4) vs. 94(4) ms, P < 0.05 at 20 min. Infusion of platelets into hearts obtained from DL-lysine-monoacetylsalicylate-treated guinea-pigs accentuated the ischaemia-induced reduction in APD95 (94(4) vs. 119(7) ms, P < 0.05 at 20 min) and this was reversed by sodium nitroprusside (117(7) ms, P < 0.05 at 20 min). L-NAME and haemoglobin had no effect on the aggregatory responses of the pl
Siminiak T, Egdell RM, O'Gorman DJ, et al., 1995, Plasma-mediated neutrophil activation during acute myocardial infarction: role of platelet-activating factor., Clin Sci (Lond), Vol: 89, Pages: 171-176, ISSN: 0143-5221
1. Polymorphonuclear neutrophils are involved in the development of myocardial injury during ischaemia through the release of free oxygen radicals and by adhesion of activated polymorphonuclear neutrophils to endothelium, resulting in plugging of coronary capillaries. Polymorphonuclear neutrophil activation may be a result of contact with ligands expressed by endothelial cells and/or a response to soluble stimuli released from ischaemic tissue to the plasma. 2. To investigate this we studied plasma-mediated polymorphonuclear neutrophil activation in vitro using plasma samples collected from 14 patients with acute myocardial infarction at time of admission and 6 h and 1, 2, 5 and 7 days later. Plasma samples were incubated with washed polymorphonuclear neutrophils isolated from healthy donors. Expression of adhesion molecules CD18/CD11b integrin and L-selectin (Leu-8) were measured by flow cytometry and superoxide anion production in polymorphonuclear neutrophils was measured by chemiluminescence. 3. Plasma samples obtained 6 h and 1 day after admission were capable of inducing CD18/CD11b antigen expression, superoxide anion production and L-selectin shedding in the washed polymorphonuclear neutrophils, and this effect was significant when compared with plasma taken at 5 and 7 days after admission. 4. The plasma-mediated polymorphonuclear neutrophil stimulation was prevented when the PMN were pretreated with platelet-activating factor receptor antagonists BN52021 or BN50739. The platelet-activating factor concentrations detected in the plasma samples were not higher than those detected in plasma from healthy subjects.(ABSTRACT TRUNCATED AT 250 WORDS)
MCAINSH AM, TURNER MA, OHARE D, et al., 1995, CARDIAC-HYPERTROPHY IMPAIRS RECOVERY FROM ISCHEMIA BECAUSE THERE IS A REDUCED REACTIVE HYPEREMIC RESPONSE, CARDIOVASCULAR RESEARCH, Vol: 30, Pages: 113-121, ISSN: 0008-6363
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- Citations: 25
Siminiak T, Flores NA, Sheridan DJ, 1995, Neutrophil interactions with endothelium and platelets: possible role in the development of cardiovascular injury., Eur Heart J, Vol: 16, Pages: 160-170, ISSN: 0195-668X
Polymorphonuclear neutrophils (PMN) cause myocardial injury during ischaemia and reperfusion by their direct effects on the myocardium; PMN release highly cytotoxic free oxygen radicals and proteolytic enzymes and PMN aggregates are involved in capillary plugging and the no-reflow phenomenon. In addition, PMN-derived factors including free oxygen radicals, lipoxygenase products, cytokines and proteolytic enzymes have been shown to modify the function of endothelium and platelets. However, both endothelium and platelets are capable of modulating PMN activation. Endothelial cells modulate PMN function by the expression of adhesion molecules and by release of soluble factors including nitric oxide, prostacyclin, endothelins, platelet activating factor and interleukin-8. Platelets affect PMN activation by release of thromboxane A2, platelet derived growth factor, serotonin, lipoxygenase products, proteases and adenosine. Thus, in addition to their direct injurious effect on ischaemic myocardium, neutrophils are involved in the functional balance between endothelium and platelets and exert an indirect effect on the myocardium.
Flores NA, Goulielmos NV, Seghatchian MJ, et al., 1994, Myocardial ischaemia induces platelet activation with adverse electrophysiological and arrhythmogenic effects., Cardiovasc Res, Vol: 28, Pages: 1662-1671, ISSN: 0008-6363
OBJECTIVE: The aim was to investigate how platelet activation during myocardial ischaemia can induce electrophysiological and arrhythmogenic effects, and examine the involvement of different platelet membrane receptors in producing these effects. METHODS: Transmembrane action potentials and electrograms were recorded from isolated, Langendorff perfused guinea pig hearts during normal perfusion, global myocardial ischaemia, and reperfusion during infusion of human platelets. Platelet reactivity was altered by treating platelets with forskolin, aspirin, the platelet activating factor (PAF) receptor antagonist BN 52021, the thromboxane A2 (TP) receptor antagonist GR 32191B, and the alpha 2 adrenoceptor antagonist yohimbine. Myocardial catecholamine depletion was induced by treatment with 6-hydroxydopamine. RESULTS: Platelet infusion had no electrophysiological effects during normal perfusion, but during ischaemia it enhanced the reduction in action potential duration at 95% repolarisation [APD95, 110(SEM 3) ms v 121(5) ms, p < 0.05, at 15 min] and increased the incidence of ventricular arrhythmias (from 56% to 94%, p = 0.04) compared to hearts receiving buffer but no platelets. The reductions in APD95 and the arrhythmogenic effects were attenuated when forskolin treated, aspirin treated or GR 32191B treated platelets were infused (VF: 50% v 94%, p = 0.03; 50% v 94%, p = 0.02; 22% v 94%, p < 0.001, respectively). Similar results were obtained when normal platelets were infused into catecholamine depleted hearts (VF: 60% v 94%, p = 0.0549). These differences were associated with inhibited aggregatory responses to thrombin (for forskolin treated platelets) and the thromboxane mimetic U44069 (for GR 32191B treated platelets). Yohimbine was antiarrhythmic in the presence and absence of platelets, suggesting direct myocardial effects, but BN 52021 had no antiarrhythmic effects. CONCLUSIONS: Myocardial ischaemia causes platelet activation resulting in electrophysiologic
GEROULAKOS G, OGORMAN DJ, KALODIKI E, et al., 1994, THE CAROTID INTIMA-MEDIA THICKNESS ASA MARKER OF THE PRESENCE OF SEVERE SYMPTOMATIC CORONARY-ARTERY DISEASE, EUROPEAN HEART JOURNAL, Vol: 15, Pages: 781-785, ISSN: 0195-668X
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- Citations: 180
Chakrabarty S, Fluck DS, Flores NA, et al., 1994, Effects of streptokinase on infarct size in rabbits in the presence and absence of coronary artery recanalization., Eur Heart J, Vol: 15, Pages: 699-704, ISSN: 0195-668X
Despite variable efficacy in achieving recanalization, different thrombolytic agents demonstrate similar abilities to reduce mortality following myocardial infarction. We investigated whether factors other than the ability to achieve coronary artery recanalization are important in mediating the beneficial effects associated with thrombolytic therapy during acute myocardial infarction using anaesthetized rabbits. Coronary artery occlusion was produced using either a single ligature (which was released to initiate reperfusion) or by placing two ligatures 5 mm apart to allow the formation of an intraluminal thrombus. In this case, ligature removal followed by thrombolysis was required for recanalization to occur. Experiments were performed in the presence and absence of streptokinase. Streptokinase was most effective in reducing myocardial necrosis when associated with thrombolytic recanalization (total left ventricular infarct size was reduced from 37 +/- 7% to 13 +/- 1%, P < 0.01). However, streptokinase also reduced infarct size in the absence of reperfusion (45 +/- 4% vs 35 +/- 2%, P < 0.05), although further work is needed to clarify the mechanisms.
Flores NA, Sheridan DJ, 1994, The pathophysiological role of platelets during myocardial ischaemia., Cardiovasc Res, Vol: 28, Pages: 295-302, ISSN: 0008-6363
CHOUDHURY L, RADVAN J, SHERIDAN DJ, et al., 1994, CORONARY FLOW RESERVE MEASUREMENT ALLOWS DIFFERENTIATION OF HYPERTROPHIC CARDIOMYOPATHY FROM THE ATHLETES HEART, JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY, Pages: A160-A160, ISSN: 0735-1097
Winterton SJ, Turner MA, O'Gorman DJ, et al., 1994, Hypertrophy causes delayed conduction in human and guinea pig myocardium: accentuation during ischaemic perfusion., Cardiovasc Res, Vol: 28, Pages: 47-54, ISSN: 0008-6363
OBJECTIVE: The aim was to investigate why cardiac hypertrophy causes increased vulnerability to arrhythmias during myocardial ischaemia. METHODS: The electrophysiological basis for this increased vulnerability was studied in isolated perfused guinea pig hearts obtained 50 and 150 d after aortic constriction, and in sham operated controls. Cellular electrophysiology, conduction, and refractory periods were examined during control perfusion and during low flow (coronary flow reduced to 10% of control) and zero flow ischaemia. ECGs in patients with left ventricular hypertrophy and in controls matched for age and heart rate were also studied. RESULTS: Aortic constriction increased heart weight:body weight ratio by 33% at 50 d and by 69% at 150 d. Action potentials were unchanged in hypertrophied hearts. Significant conduction delay occurred in 150 d hypertrophied hearts [conduction time index 23(SEM 4) ms v 18(3) ms, p < 0.001; QRS width 40(1) ms v 35(1) ms, p < 0.01], but not in 50 d hypertrophied hearts. Conduction delay was also present in humans with left ventricular hypertrophy [QRS width 96(13) ms v 87(8) ms, p < 0.01]. Although the QTc interval was increased in humans, at 422(23) ms v 411(17) ms in controls, p < 0.05, this could be explained by the increased QRS duration. During ischaemia, ventricular arrhythmias tended to occur earlier in hypertrophied hearts. Hypertrophy was also associated with a greater increase in conduction delay. Ischaemia reduced action potential duration and refractory periods; the reduction in action potential duration was attenuated by hypertrophy (p < 0.01), although the reverse was apparent during low flow ischaemia at 50 d. CONCLUSIONS: Delayed conduction is an important feature of severe cardiac hypertrophy in guinea pigs and man. Hypertrophy is associated with accentuated conduction delay and altered repolarisation during ischaemia.
Egdell RM, Siminiak T, Sheridan DJ, 1994, Modulation of neutrophil activity by nitric oxide during acute myocardial ischaemia and reperfusion., Basic Res Cardiol, Vol: 89, Pages: 499-509, ISSN: 0300-8428
Nitric oxide (NO) exerts an inhibitory effect on polymorphonuclear neutrophil (PMN) function, via a cyclic GMP-mediated mechanism, while PMNs are known to play an important role in myocardial ischaemia-reperfusion injury (MI-R). Since the major source of NO, vascular endothelium, becomes functionally impaired during MI-R, it is attractive to hypothesize that it is this loss of endothelial nitric oxide production that allows PMN adherence and activation. The studies reviewed here add substance to this hypothesis. Authentic NO, administered during MI-R both reduces myocardial necrosis and PMN accumulation, while basal NO release, as estimated by coronary artery ring responses to L-NAME, an NO synthase inhibitor, declines during reperfusion with a time-course mirrored by PMN adherence in the same preparation. Reduction in infarct size and decreased PMN accumulation can also be demonstrated with L-arginine and NO donors. Since endothelial dysfunction leads to PMN adherence and PMNs have been shown to contribute to endothelial dysfunction, it seems probable that a positive feedback loop is generated during MI-R, leading to the amplification of PMN activity and subsequent myocardial damage.
Thomas P, O'Gorman DJ, Sheridan DJ, 1993, Acute and chronic effects of flosequinan on resting and exercise haemodynamics in congestive heart failure., Br J Clin Pharmacol, Vol: 36, Pages: 539-546, ISSN: 0306-5251
1 The acute and chronic (8 weeks) haemodynamic responses to oral flosequinan have been investigated in 12 male patients of mean age 58.9 years with congestive heart failure of N.Y.H.A. classes II and III. 2 Flosequinan 125 mg orally significantly reduced right atrial pressure, pulmonary artery pressure and pulmonary wedge pressure prior to and following 8 weeks chronic treatment (125 mg daily). A significant decrease in systemic pressure and an increase in heart rate were also observed with acute flosequinan prior to chronic treatment. A reduction in systemic vascular resistance and an increase in cardiac index reached significance in response to flosequinan 125 mg orally following 8 weeks of therapy. 3 In the erect position, flosequinan reduced pulmonary wedge pressure and tended to reduce systemic vascular resistance, without decreasing mean arterial pressure. 4 Following chronic treatment, there was a trend towards a reduction in pulmonary wedge pressure and an increase in cardiac index, otherwise resting and exercise haemodynamics were unchanged. 5 The response to flosequinan was similar at week 1 and after 8 weeks of treatment for all of the haemodynamic parameters. 6 Flosequinan increased bicycle exercise times and attenuated exercise-induced increases in pulmonary arterial and systemic pressures. There was a trend towards an increase in treadmill exercise time. 7 Sublingual glyceryl trinitrate (0.5 mg) and oral flosequinan (125 mg) had similar effects on right atrial pressure, pulmonary arterial and pulmonary wedge pressures at 5 min and 2 h respectively post-dosing. A small additive effect on pulmonary arterial and wedge pressures was observed.
RADVAN J, CAMICI PG, MARWICK T, et al., 1993, PHYSIOLOGICAL HYPERTROPHY DOES NOT AFFECT CORONARY FLOW RESERVE IN MAN, CIRCULATION, Vol: 88, Pages: 214-214, ISSN: 0009-7322
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- Citations: 7
Davies RH, Sheridan DJ, 1993, The treatment of heart failure--what next?, Br J Clin Pharmacol, Vol: 35, Pages: 557-563, ISSN: 0306-5251
1. Despite demonstrable benefits in terms of symptomatic relief and improvement in prognosis, even the best treatments of heart failure currently available fall short of being ideal. We review the basis for newer approaches to the treatment of heart failure and discuss some of the agents which capitalize on current understanding of the underlying patho-physiology. 2. Several drugs, old and new, are presently being investigated by major clinical trials. We also consider some of the difficulties related to the design and conduct of such trials and suggest how drugs might be better assessed in the future.
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