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Biomedical subjects

M G Trivella

Publications and source records attributed to M G Trivella.

At least 37 records · Page 2Linked to original sources
PubMed1990

Beta-receptor subtypes in the canine coronary circulation.

The principal difficulty in determining the subtype of coronary vascular beta-receptors in vivo is to avoid the local metabolic coronary vasodilation that occurs secondary to activation of myocardial beta-receptors. Therefore, a nonbeating cardiac preparation without chronotropic or inotropic effects is needed. In this study, the coronary circulation was perfused at constant pressure in closed-chest chloralose-anesthetized dogs. The increase in coronary blood flow due to intracoronary injections of the combined beta 1- and beta 2-agonist isoproterenol was determined during prolonged asystoles after the cessation of cardiac pacing in atrioventricular heart-blocked animals. Both beta 1-selective (practolol and L 650,744) and beta 2-selective (ICI 118,551) antagonists blocked isoproterenol-induced coronary vasodilation. In contrast, isoproterenol vasodilation in the femoral circulation was blocked by beta 2- but not by beta 1-selective antagonists. In conclusion, both beta 1- and beta 2-receptors in coronary resistance vessels are stimulated by isoproterenol to produce vasodilation during prolonged asystoles, when cardiac chronotropic and inotropic effects are absent.

Adrenergic beta-Antagonists↗
PubMed1989

Regional and global biventricular function during dipyridamole stress testing.

This study assesses the relation between regional ventricular performance (using 2-dimensional echocardiography) and global systolic and diastolic indexes of biventricular myocardial function (using hemodynamic monitoring) during dipyridamole stress testing. Simultaneous 2-dimensional echocardiographic and biventricular hemodynamic monitoring during dipyridamole infusion (0.56 mg/kg over 4 minutes) was performed in 19 patients. All patients had a normal resting function. Eleven of the 19 patients had a positive echocardiography test (new wall motion dyssynergy with dipyridamole) and they formed group 1. Eight patients had a negative echocardiography test (group 2). During baseline conditions, no significant differences were found in the 2 groups: rate pressure product (107 +/- 16 vs 108 +/- 13 mm Hg x beats/min x 1/100), positive left ventricular (LV) dP/dt (1,950 +/- 473 vs 2,262 +/- 430 mm Hg/s), negative LV dP/dt (-2,069 +/- 620 vs -2,205 +/- 245), LV end-diastolic pressure (8.2 +/- 4.4 vs 9.6 +/- 4.0 mm Hg), right ventricular positive dP/dt (368 +/- 133 vs 400 +/- 190 mm Hg/s) and negative dP/dt (-281 +/- 89 vs -383 +/- 147). At peak dipyridamole, the 2 groups were different for LV end-diastolic pressure (20 +/- 10 vs 8 +/- 5 mm Hg, p less than 0.01), LV positive dP/dt (2,100 +/- 688 vs 3,013 +/- 851 mm Hg/s, p less than 0.01) and negative dP/dt (-1,868 +/- 518 vs -2,564 +/- 272, p less than 0.01). At peak ischemia, LV positive dP/dt increased slightly, but not significantly, while negative dP/dt decreased significantly (p less than 0.01) in comparison with resting values.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1989

Coronary effects of adenosine in conscious man.

Adenosine has been reported to play an important role in several cardiac functions, including the regulation of total and regional myocardial perfusion. This hypothesis is based on extensive investigations in animal models, but very limited information is available on the cardiovascular actions of adenosine in conscious man and the effects of the intracoronary administration of adenosine are unknown. The purpose of this study was to measure total and regional coronary blood flow after bolus injections of 0.1, 0.5, 1.0, and 2.5 mg of adenosine into the left anterior descending coronary branch. A three-thermistor thermodilution catheter was advanced into the coronary sinus to measure simultaneously the great cardiac vein flow and the coronary sinus flow. Six patients with normal coronary angiograms and normal ventricular function completed the study. Intracoronary injections of adenosine were free from significant adverse effect and caused a dose-related increase of great cardiac vein flow. A linear relation was found between flow increment and the log of adenosine dose (y = 18.929x + 74.84, r2 = 0.951). The highest flow, measured after the maximal dose, was almost three times greater than control flow (155 +/- 2 vs 58 +/- 3 ml min-1, P less than 0.001). We also observed a flow response in the territory not directly exposed to adenosine, as indicated by a marked increase of coronary sinus blood flow that was linearly related to the adenosine dose (y = 29.113x = 112.635, r2 = 0.98). These preliminary observations suggest: (1) Intracoronary injections of adenosine in conscious man can be performed without significant adverse effects.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine↗
PubMed1988

Persistence of subendocardial perfusion after subtotal coronary embolisation.

The effects of acute subtotal embolisation of small coronary arteries on regional coronary flow and vasodilator reserve were investigated in seven open chest dogs. Unlabelled plastic microspheres (26(2) micron in diameter) were injected as boluses of 200,000-400,000 microspheres into the circumflex artery. Embolisation was repeated until reactive hyperaemia was totally abolished, which occurred after the injection of 62,000(4000) microspheres per gram. Intracoronary adenosine was then infused for 20 min at 1.2 mg.min-1. Regional myocardial blood flow was measured by radioactive microspheres under control conditions, after coronary embolisation, and during adenosine infusion. Coronary blood flow (0.98(0.07) ml.min-1.g-1) was reduced to 0.66(0.08) ml.min-1.g-1 after embolisation (p less than 0.005) when reactive hyperaemia was practically abolished. Embolisation reduced epicardial flow from 0.93(0.08) to 0.40(0.09) ml.min-1.g-1 (p less than 0.001), whereas endocardial flow was unchanged (1.03(0.11) vs 0.92(0.14) ml.min-1.g-1; NS); as a consequence, the endocardial to epicardial flow ratio increased from the control value of 1.11(0.06) to 2.31(0.35) (p less than 0.005). Adenosine infusion increased coronary blood flow from 0.66(0.08) to 1.66(0.41) ml.min-1.g-1 (p less than 0.05). Endocardial blood flow increased more than epicardial blood flow, leading to a further increase in the endocardial to epicardial flow ratio (3.79(0.13); p less than 0.05). Thus it is concluded that (a) embolisation of small arteries abolishes the reactive hyperaemic response to transient coronary occlusion; (b) microembolisation predominantly reduces subepicardial perfusion; and (c) adenosine administration may increase total and regional flow after subtotal occlusion of coronary small arteries.

Adenosine↗
PubMed1987

Small artery occlusion: a theoretical approach to the definition of coronary architecture and resistance by a branching tree model.

The aim of this study was to evaluate the theoretical possibility of assessing the architecture of the coronary small artery circulation in vivo by the analysis of the increments in the total resistance of the vascular system caused by the progressive occlusion of the terminal vessels as would be possible in animal experiments by microsphere embolization. Different distributions of the resistance values of all the vessels have been obtained in branching tree models by means of only two parameters: (a) the resistance ratio between daughter and parent vessels at each branching site (KO); and (b) the resistance ratio between the two daughter vessels at each branching site (KV). Simulation of branching tree occlusion has been performed under two main conditions of resistance distribution: (1) symmetric resistance distribution, characterized by equal KO values at each branching site of the same level and by KV = 1, that is, equal resistance values for the vessel of the same level; and (2) asymmetric resistance distribution in dichotomous branching trees, wherein all the vessels may have different values of resistance; the variability in these values has however been restricted on the basis of physiological considerations. The analysis of the function of the total resistance vs the number of occluded vessels, obtained by a simulated progressive occlusion of the terminal vessels in these two systems, gives the following results: (1) in a symmetric branching tree, discontinuities are present in the occlusion function which permit identification of both the architecture and the resistance value of each single vessel of any unknown vascular tree; and (2) in the asymmetric model, the function does not allow a direct definition of the branching architecture and the values of resistance of each vessel; however, also in this case, any branching tree can be analyzed by means of a nonlinear optimization procedure which produces an equivalent symmetric branching tree. We conclude that, theoretically, the analysis of the occlusion function represents a valuable indirect approach to the quantitative study of the coronary microcirculation as well as of other vascular districts under steady flow conditions.

Animals↗
PubMed1986

Dose-response scrutiny of coronary vasodilation after intracoronary verapamil in man. A quantitative cineangiographic study.

The effect of various doses of intracoronary verapamil on the diameter of angiographically normal left coronary artery segments was investigated in 22 patients with and without coronary atherosclerosis by quantitative angiography. Very low doses (50 micrograms) were given in 3 patients; doses of 250 micrograms, 350 micrograms and 500 micrograms were administered in 7, 6 and 13 patients, respectively. A single dose was administered in 15 patients, while two increasing doses of verapamil were tested in 7. The effect of verapamil was compared in each patient with that of nitroglycerin (NG; 0.6 mg), administered sublingually in all as the last step of the study. An additional group of 8 patients served as the control. These patients received 4 intracoronary injections of contrast medium without drugs and a fifth injection following 0.6 mg of sublingual NG. In the control group no significant changes in coronary artery diameter were observed following the four control injections of contrast medium, while a 18 +/- 9% increase in vascular diameter was observed following NG. When verapamil was injected a dose-dependent vasodilation was observed, which began to be significant with doses higher than 250 micrograms. Mean percent variations of coronary artery diameter relative to control were -0.2 +/- 3.6%, 4.6 +/- 5.5%, 11.4 +/- 7.5% and 19.9 +/- 10.7%, in response to verapamil doses of 50, 250, 350 and 500 micrograms, respectively. Subsequent nitroglycerin induced a 21.5 +/- 10.7% mean percent coronary artery dilation (NS vs verapamil 500 micrograms and vs NG in the control group). Thus, verapamil induced a dose-dependent coronary vasodilation which at a dose of 500 micrograms was comparable to that induced by NG. Both with verapamil and NG the smallest vessels exhibited the greatest vasodilation. It is concluded that at the doses used in this study, injection of verapamil into the left coronary artery is safe and markedly decreases tone in the large coronary arteries. This finding supports the use of verapamil in clinical conditions in which the role of coronary vasoconstriction is proven or thought to be relevant.

Adult↗
PubMed1986

Clinical application of monitoring techniques: hemodynamic monitoring.

In the diagnosis of myocardial ischemia continuous hemodynamic monitoring may contribute to detection of transient ischemia, to definition of location and to elimination of its pathogenesis, and to characterization of hemodynamic response to ischemia. It can be helpful in investigating the significance of negligible, non specific and/or short-lasting electrocardiographic changes accompanying typical anginal symptoms. Simultaneous right ventricular and left ventricular pressure monitoring gives information regarding biventricular interaction during episodes of transient ischemia: an early left ventricular dysfunction, with or without a late right ventricular impairment, a selective right dysfunction, and a simultaneous left ventricular and right ventricular impairment all represent the hemodynamic patterns associated with left, right and biventricular ischemia respectively. Monitoring of hemodynamic parameters related to myocardial oxygen consumption and the study of their changes preceding the onset of ischemia during both spontaneous and provoked episodes of ischemia, may help in identifying whether functional or organic factors or both are involved in the pathogenesis of transient ischemia in individual patients. Two principal hemodynamic patterns appear to be associated with transient ischemia: a) left ventricular and/or right ventricular impairment, usually beginning shortly before the onset of electrocardiographic changes, followed by a rapid recovery and often an overshooting, b) a sudden and sustained increase in systolic pressure and heart rate, simultaneous with the onset of ST-T changes. In both cases, the 'excitatory' pattern appears to be unrelated to pain.(ABSTRACT TRUNCATED AT 250 WORDS)

Coronary Disease↗
PubMed1985

Effect of dilazep on coronary and systemic circulations.

In order to assess the effects of dilazep on central hemodynamics and regional flows, 0.2 mg/kg of the drug were administered intravenously to 6 open-chest anesthetized dogs. Hemodynamic and flow measurements were performed under control conditions, and approximately 5, 10 and 25 min after treatment. Dilazep caused a marked and sustained reduction of coronary resistance and increased coronary blood flow. Flow increased uniformly in the subendocardial and subepicardial layers of the left ventricle so that no significant change occurred in the endo/epi flow ratio. Dilazep caused a significant reduction of total systemic resistance and aortic pressure, however flow to the liver, kidney and spleen was not reduced. We conclude that dilazep exerts a dilating action on the coronary and systemic arterial beds and increases uniformly regional myocardial blood flow. Dilazep does not alter the transmural distribution of coronary blood flow and does not impair kidney, liver and spleen perfusion.

Animals↗
PubMed1984

Effects of dilazep on coronary and systemic hemodynamics in humans.

The cardiovascular effects of dilazep, a new antianginal drug, were investigated in 18 patients, who underwent cardiac catheterization and coronary angiography for the evaluation of chest pain. Dilazep, 0.2 mg/kg, was injected intravenously over 1 to 2 minutes. The changes induced by dilazep in coronary tone were assessed by quantitative angiography in four patients, changes in systemic and coronary hemodynamics and blood gases in eight patients, and changes in systemic and pulmonary hemodynamics and blood gases in six. In 6 of the 18 patients the effects on hemoglobin-O2 oxygen binding were also investigated. Following dilazep administration, we observed a marked reduction of coronary resistance (six patients) (0.5 vs 1.0 mm Hg X min X ml-1, p less than 0.01) and of aortic-coronary sinus oxygen difference (seven patients) (4.6 vs 12.3 vol%, p less than 0.01), and a 23% increase in coronary diameter (four patients) (p less than 0.001). Total systemic resistance was also reduced by dilazep (six patients). Conversely, only minimal or insignificant changes were observed in heart rate (14 patients), aortic pressure (14 patients), total pulmonary resistance (six patients), myocardial oxygen consumption (six patients), double product (14 patients), blood gases (seven patients), and hemoglobin-oxygen affinity (six patients). We conclude that dilazep exerts a powerful dilating action on coronary vasculature without appreciable increase of myocardial oxygen consumption and cardiac work simultaneously with a reduction of peripheral resistance.

Adult↗
PubMed1981

Time-dependent response of coronary flow to prolonged adenosine infusion: doubling of peak reactive hyperaemic flow.

UNLABELLED: In 11 anaesthetised, Open chest dogs the time course and degree of the coronary vasodilating response to intracoronary adenosine infusion was assessed. Continuous adenosine infusion, at a rate of 2.5 to 13.5 mumol . min-1, produced rapid (15 to 30s) vasodilation of the same degree as that evoked by a 30 s period of ischaemia (reactive peak hyperaemia), a finding reported previously by others. However, continuing the infusion led to further coronary vasodilation, reaching a maximum 20 to 45 min from the beginning of the infusion and remaining constant for up to 2 h, independently of further increases in the dose. This late response produced, on average, vasodilatation twice as great as that observed during reactive hyperaemia and was not associated with any haemodynamic change or with the opening of arterio-venous shunts. THE RESULTS: 1) suggest the existence of a double, time-dependent response of coronary receptor(s) to adenosine; 2) demonstrate, in the presence of a prolonged vasodilating stimulus, a possible increase in coronary blood flow to a degree far beyond that of post-ischaemic reactive peak flow, which is generally considered to be the maximal value of coronary blood flow that can be achieved.

Adenosine↗
PubMed1981

[Selective vasodilatation of the subepicardial coronary vasculature induced by carbochromen (author's transl)].

The effect of carbochromen on total and regional coronary blood flow was investigated in 6 anesthetized open-chest dogs. Total and regional myocardial blood flow was measured by radioactive microspheres, using the reference sample method. Left circumflex coronary flow was monitored by an electromagnetic flowmeter. In 4 dogs (Group 1) carbochromen was injected intravenously; in 2 dogs (Group 2) it was infused directly in the circumflex coronary artery. No significant changes in heart rate, left atrial left ventricular and aortic pressures were observed following carbochromen administration in both Groups. Left circumflex coronary blood flow progressively increased and a level slightly higher than peak reactive hyperemia was reached in both Groups. Regional myocardial blood flow measurements in Group 1 showed that the inner third of the left ventricular wall (ENDO) increased 2.7 times relative to control, the middle layer increased 3.4 times relative to control and the external third 4.5 times relative to control. A similar pattern was observed after intracoronary administration of carbochromen (Group 2). The ENDO/EPI flow ratio dropped from 0.98 +/- 0.16 to 0.58 +/- 0.18 in Group 1 and from 1.03 and 1.20 to 0.71 and 0.53 respectively in the two experiments of Group 2. Replacement of carbochromen with adenosine infusion in Group 2 produced a further increase in flow, mainly in the subendocardium resulting in ENDO/EPI flow ratio close to unity. These data demonstrate that the powerful coronary vasodilatory effect of carbochromen is not uniform being vasodilation more prominent in the vasculature of the external third of the left ventricular wall as compared to the inner third. Consequently a major redistribution of coronary blood flow, favouring the external layers of the left ventricle, results from carbochromen administration. This effect distinguishes carbochromen from other vasodilating stimuli than elicit a uniform response in the coronary vasculature and do not affect the ENDO/EPI ratio, including transient ischemia, adenosine, and dipyridamole.

Animals↗
PubMed1980

Some clinical considerations regarding the relation of coronary vasospasm to coronary atherosclerosis: a hypothetical pathogenesis.

This study explores the relation between coronary arterial spasm and the development of coronary atherosclerosis. The clinical history and coronary angiographic and electrocardiographic data in 212 consecutive patients with ischemic heart disease were correlated. These patients were classified into four groups: Group 1, patients without angiographic evidence of atherosclerosis; Group 2, patients with single vessel disease; Group 3, patients with double vessel disease; and Group 4, patients with significant narrowing of major coronary arteries. Although spontaneous angina occurred in all four groups, it was more common (55 percent) in the patients in Group 1, who were predominantly female and young. Spontaneous angina was confirmed in Group 1 with several techniques, including thallium-201 scintigraphy, ergonovine administration and electrocardiography during attacks of pain. Prior myocardial infarction was present with similar frequency in all four groups. A patient is discussed whose spontaneously occurring coronary arterial spasm later progressed to fixed arteriosclerotic narrowing requiring coronary bypass surgery. These observations and a review of the literature lend support to the hypothesis that coronary arterial spasm can be a possible antecedent leading to the later development of fixed atherosclerotic coronary arterial obstruction.

Adult↗