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Biomedical subjects

F Epelde

Publications and source records attributed to F Epelde.

16 recordsLinked to original sources
PubMed2003

Enalaprilat, losartan and LU 135252 in coronary blood flow regulation.

BACKGROUND: High plasma levels of angiotensin II are found in several pathologies such as hypertension, heart failure and myocardial infarction. The effect of high concentrations of angiotensin II on coronary circulation is not well defined. The aim of the present study was to assess coronary blood flow regulation during tachycardia in the presence of elevated coronary plasma levels of angiotensin II, and the changes induced by ACE inhibition and blockade of angiotensin II and endothelin-A receptors. DESIGN: Left anterior coronary artery was catheterized in 38 pigs to infuse the study drugs. Saline was infused for 15 min. Then, the first atrial pacing was performed. The pigs were distributed to: Group 1 (n = 7) angiotensin II; Group 2 (n = 7) enalaprilat + angiotensin II; Group 3 (n = 9) the bradykinin B2 antagonist HOE 140 + enalaprilat + angiotensin II; Group 4 (n = 7) losartan + angiotensin II; and Group 5 (n = 8) endothelin-A receptor antagonist LU 135252 + angiotensin II. After giving these infusions, a second pacing was repeated. RESULTS: The increase in coronary blood flow induced by pacing with angiotensin II was reduced from 181 +/- 21% to 116 +/- 37% (P = 0.006 vs. saline). Enalaprilat, losartan and LU 135252 restored the capacity of coronary blood flow to increase during pacing (151 +/- 39%, 162 +/- 35% and 161 +/- 16%, respectively; P = NS, vs. saline), while HOE 140 abolished the effect of enalaprilat. CONCLUSIONS: Moderately elevated coronary concentrations of angiotensin II reduced coronary blood flow during pacing. Enalaprilat, losartan and LU 135252 restored the hyperaemic coronary flow to similar values observed with saline. The beneficial effect of ACE inhibition is mediated through an increase in bradykinin.

Angiotensin II↗
PubMed2003

[Status of thrombolytic therapy for acute myocardial infarction in the emergency departments of Cataluna, Spain].

OBJECTIVES: The aim of the present study was to know the situation of thrombolysis in Catalonia. MATERIAL AND METHODS: A questionnaire was sent to all the hospitals in Catalonia regarding to the administration of thrombolytic treatment in their hospitals. RESULTS: 29 centres replied (18 primary, 10 secondary and 1 tertiary), serving a total catchment population of 4.2 million and with a total number of 2,853 AMIs in. The mean time from the onset of symptoms to arrival at hospital was 176.3 +/- 96 min and from arrival of the patient at the hospital to the initiation of thrombolysis was 78.7 +/- 73.8 min. Most commonly, it was the Emergency Department staff who took the decision on thrombolysis (17 centres). A total of 47 +/- 12% of the AMIs received thrombolytic treatment with 61.76 +/- 42.77% of these treatments being carried out in the Emergency Departments. The internal delay to initiating thrombolysis was of 33.7 +/- 11.9 min in the centres without an ITU versus 112 +/- 8 min in those centres with an ITU (p = 0.0067). In the centres with an ITU but in which it was the doctor in the Emergency Department who took the decision on thrombolysis (n = 7), the internal delay was shorter (84.3 +/- 80.59 min). CONCLUSIONS: There is a shorter delay in the administration of thrombolytic treatment in those emergency departments which do not have access to an ITU or Coronary Unit than in the Emergency Departments which do have this access. If the decision to carry out thrombolysis is taken by the emergency department doctors there is a substantial reduction in the time to its administration.

Emergency Service, Hospital↗
PubMed2000

[The use of acetylsalicylic acid in patients with ischemic cardiomyopathy cared for in Spanish emergency services (results of the EVICURE Study). Evaluacion del Manejo de la cardiopatia isquemica en los Servicios de Urgencias Hospitalarios of the Sociedad Espanola de Medicina de Urgencias y Emergencias (SEMES)].

BACKGROUND: Acetyl salicylic acid is a drug with demonstrated effectiveness in ischemic cardiomyopathy. The objective of our study was to know the use of this drug in the emergency services of Spain. PATIENTS AND METHOD: The EVICURE study analyzes the use of acetyl salicylic acid in 35 emergency services of Spanish hospitals. RESULTS: 2,168 patients were studied. Of the 473 patients with stable angina, 9.2% received acetyl salicylic acid before going to the hospital and 90,7% at the arrival to the hospital, of 1,067 with unstable angina 13% received acetyl salicylic acid before the arrival to the hospital and 56% at the arrival to the hospital. Of 600 patients affected of myocardial infarction only 17% received acetyl salicylic acid before the arrival to the hospital and 59.8% received this drug in the emergency room. CONCLUSIONS: The use of acetyl salicylic acid in patients affected of ischemic cardiopathy assisted in the emergency services of Spain is improperly low.

Aspirin↗
PubMed2000

[Effect of cyclooxygenase inhibition on the adaptation of coronary blood flow to tachycardia].

BACKGROUND: The role of different endothelium-derived vasoactive substances in the regulation of coronary circulation during tachycardia is not well defined. In order to elucidate the contribution of prostacyclin to the adaptation of coronary blood flow to tachycardia, the effect of meclofenamate, a cyclooxygenase inhibitor on the coronary blood flow response to rapid atrial pacing was analyzed in a porcine model. METHODS: A group of seventeen pigs were instrumented for coronary blood flow, aortic pressure and atrial pacing. Heart rate was increased by 20 beats every 5 minutes. Coronary blood flow and aortic pressure were measured, and coronary resistance calculated, basally and at each pacing interval, before and after saline serum (n = 6), meclofenamate 5 mg/kg, i.v. (n = 7) or meclofenamate 35 mg/kg, i.v. (n = 4). RESULTS: Neither saline nor meclofenamate modified the normal increase of coronary blood flow provoked by rapid atrial pacing (163 +/- 28% increase before versus 172 +/- 29% after saline; 159 +/- 21% increase before versus 161 +/- 22% after meclofenamate low doses and 201 +/- 39% before vs 172 +/- 36 after meclofenamate high doses). There were no differences in the response of coronary vascular resistance to tachycardia before and after meclofenamate (44% reduction vs 40% respectively). CONCLUSION: Cyclooxygenase blockade does not modify the response of coronary circulation to rapid atrial pacing, suggesting that prostacyclin does not play a limiting role in the regulation of coronary blood flow during tachycardia in this model.

Animals↗
PubMed2000

Nitric oxide inhibition intensifies the depressant effect of cocaine on the left ventricular function in anaesthetized pigs.

Myocardial ischaemia and left ventricular dysfunction have been described in cocaine users. Whether nitric oxide (NO) inhibition may potentiate the effects of cocaine on coronary circulation and ventricular function is still unknown. In order to test this hypothesis, 38 pentobarbital-anaesthetized pigs were instrumented for systolic blood pressure, coronary blood flow, left ventricular dp/dt, cardiac output, left ventricular end-diastolic and end-systolic lengths and shortening fraction. The pigs were randomized into three groups: control group: i.v. saline (n = 5); group 1: i.v. cocaine, 10 mg kg-1 over 20 min (n = 17); group 2: the same doses of cocaine 30 min after i.c. L-NAME 20 microg/kg min-1 infusion (n = 16). In order to know whether the observed effects were specific of NO inhibition, in five pigs i.c. L-arginine was simultaneously infused with L-NAME, in five pigs i.c. NTG, an endothelial-independent vasodilator, was simultaneously infused with L-NAME before cocaine was administered, and in nine additional pigs the proximal left anterior descending (LAD) flow was reduced to around 20% of the basal value by means of a mechanical occluder before cocaine was administered. Cocaine i.v did not change the coronary blood flow, while it induced a significant reduction in cardiac output, left ventricular dp/dt and shortening fraction (15 +/- 4-8 +/- 4%, P < 0.05). When cocaine was administered after L-NAME infused i.c. during 30 min, a significantly more severe reduction of the shortening fraction (12 +/- 3-4 +/- 2%, P < 0.0001) was induced; this effect was abolished by simultaneous perfusion of L-arginine i.c. NTG. The results when cocaine was administered after the 20% LAD flow reduction by mechanical occluder did not differ from those of cocaine alone. NO inhibition intensifies the cocaine-induced left ventricular dysfunction.

Anesthesia↗
PubMed2000

[Myocardial necrosis is not observed during acute cocaine abuse detectable by the serum levels of troponin T].

BACKGROUND: Recently we can use a new family of serological markers to objective myocardial damage with hig sensibility and specificity. One of these markers is T troponin (c-TNT). Some cocaine abusers have chest pain during drug consumption due to myocardial ischemia produced by the drug. OBJECTIVE: To study if in the chest pain appeared after cocaine consumption a c-TNT increased is objective, showing myocardial cellular damage. PATIENTS AND METHODS: We studied 65 patients; 35 cocaine abusers that were admitted into the emergency room for chest pain after cocaine consumption and 30 patients with no coronary chest pain. To all of them were determined c-TNT and CK. RESULTS: An increase in c-TNT or CK was not observed in both groups. CONCLUSION: We don't observe an increase in c-TNT in the group of cocaine abusers that evidence myocardial cellular damage.

Acute Disease↗
PubMed1999

[Usefulness of troponin T and troponin I in the diagnosis and prognostic stratification of patients with ischemic cardiopathy attending an emergency service].

BACKGROUND: Diagnostic of chest pain in the emergency services supposes a serious problem. This study wants objective if the new non enzymatic markers of myocardial necrosis (T troponin and I troponin) may be an aid for the diagnostic and prognostic stratification of patients with myocardial ischemia. PATIENTS AND METHODS: 82 successive patients who went to the emergency room for chest pain were studied. Electrocardiogram and blood samples were obtained at 0,4, and 12 house of admission. A clinic-evolutive study was performed at discharge, and they were classified in 3 categories: a) myocardial infarction, b) unstable angina (Braunwald classification) and no coronary pains. RESULTS: In the 27 patients with myocardial infarction the markers of troponin group were more sensitive than creatinine kinase to determine myocardial necrosis at 4 hours of admission. Of 41 patients with unstable angina, 34% were of Braunwald III-B class. Troponin group markers discriminate a group of high risk patients, 70% of the patients that need an emergency coronarography for bad clinical evolution were troponin group marker positive. CONCLUSIONS: The use in the emergency room of troponin necrosis markers (T and I troponin) allows to optimize the sanitary resources, detecting quickly the patients with acute myocardial infarction and discriminate a group of high risk of patients with angina.

Aged↗
PubMed1997

Cocaine administration enhances platelet reactivity to subendothelial components: studies in a pig model.

Myocardial infarction in cocaine abusers may be related to a direct platelet-activating effect. We analysed this possibility in an experimental model. Studies were carried out in eight normal, anaesthetized pigs with a weight of 30.7 +/- 3.7 kg. Blood samples were withdrawn before and 20 min after i.v. administration of cocaine (10 mg kg-1; at 1 mg kg-1 every 2 min). Modifications in platelet responses to arachidonic acid (AA; 1.4 mmol L-1), ADP (1-4 microM), synthetic thromboxane endoperoxide analogue (U46619; 1 microM), collagen (2.5-5 micrograms mL-1), adrenaline (10 microM) and ristocetin (0.8-1 mg mL-1) were tested by conventional aggregometry. Changes in the capacity of platelets to form aggregates on damaged subendothelium were assessed by means of an ex vivo perfusion system in which blood was circulated for 10 min at 800 s-1, a shear rate similar to that found in normal coronary arteries. The interaction of platelets with perfused denuded arterial segments was morphometrically quantified and expressed as a percentage of damaged vessel surface covered by platelets (%CS). Cocaine administration did not influence platelet aggregation patterns in pigs. However, there was a significant increase in the interaction of pig platelets with subendothelial structures after cocaine infusion (%CS = 40 +/- 17% vs. 27 +/- 16% baseline; mean +/- SD; P < 0.01). Cocaine administration in this animal model increases the reactivity of platelets exposed to subendothelium. These results support the concept that the administration of cocaine to pigs has a prothrombotic effect by facilitating the interaction of platelets with damaged arteries.

Animals↗
PubMed1996

The role of endogenous nitric oxide in the response of coronary blood flow to tachycardia.

BACKGROUND: The role of endogenous nitric oxide as mediator of flow-dependent dilation is well established. However, its role in the adaptation of coronary blood flow to tachycardia is less well defined. This study was designed to determine whether nitric oxide is a mediator in pacing-induced hyperaemia. METHODS: Twenty pigs were instrumented for coronary blood flow, aortic pressure and atrial pacing measurements. Their heart rate was increased by 20 beats every 5 min. Coronary blood flow was measured basally and at each pacing interval before and after each of the following interventions: intracoronary saline infusion (n = 6), N omega-nitro-L-arginine methyl ester infusion (L-NAME, 20 micrograms/kg per min intracoronarily, n = 9) and infusion of L-NAME plus L-arginine (0.3 mg/kg per min intracoronarily, n = 5). RESULTS: The coronary peak flow increased with atrial pacing. The maximum increase in coronary blood flow with pacing was significantly reduced after infusion of L-NAME (159 +/- 33 versus 143 +/- 30%), whereas no change was observed in the saline group (163 +/- 28 versus 172 +/- 29%). However, it increased significantly in the group receiving L-NAME plus L-arginine (147 +/- 29 versus 182 +/- 40%). CONCLUSIONS: In the pig, the increase in coronary blood flow and therefore the vasodilation of the microvasculature that accompanies tachycardia depend, partly, on the release of endogenous nitric oxide.

Animals↗