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Biomedical subjects

P J Tucci

Publications and source records attributed to P J Tucci.

At least 19 recordsLinked to original sources
PubMed1995

[Influence of mannitol added to the nutrient solution on the mechanical performance and on the degree of myocardial edema of isolated hearts of rats].

PURPOSE: To analyse the influence of mannitol added to Krebs-Henseleit (KH) solution on the myocardium edema and myocardial function. METHODS: Isolated rat heart under isovolumetric contractions studied according to Langendorff's technique were perfused with KH solution at constant flow during 90 min. The coronary perfusion pressure, diastolic and systolic pressures were recorded at every 15 min. At the end of the experiment, myocardium water content was measured in hearts perfused with KH solution (group I, n = 9) and in hearts perfused with KH solution plus 8mM mannitol (group II, n = 8). These results were compared to non-perfused control heart (n = 9). RESULTS: Myocardial water content was statistically higher in group I (80.8 +/- 1.3%) compared to group II (78.1 +/- 0.7%) and control group (75.5 +/- 0.5%). Systolic arterial pressure was statistically higher in group I (86.2 +/- 11.5mmHg) compared to group II (72.7 +/- 21.1mmHg). There was no difference in the diastolic pressure between the two groups. Coronary perfusion pressure (Pp) increased progressively during the experiment in both groups. However, Pp was lower in group II than in group I. CONCLUSION: Mannitol added to KH solution significantly attenuates the myocardium edema in the isolated perfused rat heart.

Animals↗
PubMed1993

[Influence of cardiac perfusion on relations of pressure/volume of the left ventricle].

PURPOSE: To analyze the influence of the myocardial engorgement due to coronary perfusion on the left ventricular diastolic pressure/volume (P/V) relations. METHODS: The study was undertaken in the isovolumic blood-perfused dog heart preparation (n = 7). The P/V relations were determined promoting ventricular volumes variations by steps of 2ml, in two conditions: during coronary perfusion pressure of 100mmHg and after occlusion of the perfusion line. RESULTS: It was verified that the P/V relations obtained without myocardial perfusion shifted to the down right in respect to the perfused heart. A exponential fitting of the P/V relations allows to conclude that there was no difference among the slopes of the curves obtained with and without perfusion. CONCLUSION: Our results indicated that coronary perfusion restrain the capacity of the left ventricle to receive blood, but there is no influence on the passive elastic stiffness of the chamber. This effect was taught to be consequence of the myocardial erectile property.

Animals↗
PubMed1993

Left ventricular mass estimated by M-mode echocardiogram is not altered by changes in cardiac shape and dimensions due to acute arterial hypertension.

The effect of changes in left ventricular (LV) shape and dimensions due to acute arterial hypertension induced by mechanical obstruction of the aorta for 10 min on LV mass values estimated by M-mode echocardiogram was studied in 14 anesthetized dogs. Although the systolic pressure increased from 117.5 +/- 19.9 to 175.4 +/- 22.9 mmHg altered ventricular diameter from 2.77 +/- 0.49 cm to 3.17 +/- 0.67 cm (P < 0.05) and wall thickness from 0.83 +/- 0.09 to 0.75 +/- 0.09 cm (P < 0.05), LV mass estimated before (73.5 +/- 19.1 g) and after (78.3 +/- 26.4 g) hypertension was not significantly different. We demonstrate here for the first time that changes in LV dimensions induced by acute arterial hypertension do not modify LV mass values estimated by the M-mode electrocardiogram method.

Acute Disease↗
PubMed1993

Characteristics of arterial hypertension in response to bolus injection of phenylephrine in atropinized patients.

The changes of arterial pressure promoted by bolus injection of 50 micrograms phenylephrine (PHE) were studied in 20 atropinized patients (5 normal subjects, 13 patients with mitral valve disease, 1 patient with essential arterial hypertension and 1 patient with hypertrophic cardiomyopathy) submitted to routine catheterism. Patients with aortic valve disease, left ventricular outflow tract obstruction and intracardiac shunt were excluded from the study. All patients were in sinus rhythm, without heart failure. Arterial pressure started to increase at 14.8 +/- 5.4 s (range, 5.6 to 27 s; mean +/- SD) after PHE. There was an increase of 37.8 +/- 16.7 mmHg (range, 12.5 to 70 mmHg) in systolic pressure and of 26.6 +/- 11.1 mmHg (range, 7.5 to 42.5 mmHg) in diastolic pressure. Peak hypertension was attained at 36.6 +/- 16.4 s (range, 10.8 to 64.9 s) and hypertension continued for 176 +/- 92 s (range, 11 to 365 s). Heart rate was 114 +/- 21 bpm before PHE and 111 +/- 21 bpm (P < 0.05) after PHE. There were no adverse events associated with intravenous PHE injection in any patient, in accordance with the general view that bolus injection of PHE is a safe and practical maneuver to promote arterial hypertension.

Atropine↗
PubMed1992

Coronary vascular and myocardial lesions due to experimental constriction of the abdominal aorta.

The development and evolution of arterial and myocardial lesions were morphologically evaluated in Wistar rats submitted to constriction of the abdominal aorta. The control (sham-operated) and operated groups were evaluated 1, 2, 4 and 6 weeks after surgery. The aorta-constricted groups developed arterial hypertension followed by myocardial hypertrophy evidenced from the first week onwards by the increase in ventricular weight and in the diameters of left and right ventricular myofibers. The histopathologic study of the myocardium revealed in aorta-constricted groups, since the first week, widespread necrotizing changes of the intramural coronary branches surrounded by multifocal areas of myofiber degeneration and necrosis. The lesions were more extensive in the wall of the right ventricle and were gradually replaced by scar tissue. At the 6th week patchy focal fibrotic scars were found scattered in the myocardium of both ventricles. There were no systemic lesions in aorta-constricted or sham-operated groups. The close association between the arterial and myocardial lesions shows that muscle necrosis and scars are due to ischemia. They may influence the contractile performance of the myocardium in this model of pressure-induced hypertrophy of the heart.

Animals↗
PubMed1992

[Influence of transient and sustained increase of blood pressure on the 1st temporal derivative of the ventricular pressure].

PURPOSE: To analyze the influence of transient and sustained elevations of arterial pressure (AP) on the rate of rise of the left ventricular pressure (dp/dt). METHODS: Thirteen anesthetized, thoracotomized and mechanically ventilated dogs, submitted to pharmacological autonomic block (oxprenolol-3 mg/kg plus atropine-0.5 mg/kg). The AP elevation was obtained by mechanical constriction of the descending thoracic aorta. Two protocols were applied to all animals: Transient Arterial Hypertension (TAH) and Sustained Arterial Hypertension (SAH) and the following variables were evaluated: heart rate (HR), systolic (LVSP) and end diastolic (LVEDP) left ventricular pressure and dp/dt. In TAH the variables were analyzed in the basal condition (To) and at the maximal value of AP attained during the transient pressure elevation (TM). In the protocol SAH the variables were evaluated in the conditions: Control (Ho), hypertension 1 (H1) and hypertension 2 (H2). RESULTS: Considering all conditions, there were no significant differences among the values of HR. In the protocol TAH, the LVSP varied from 133 +/- 22 mmHg to 180 +/- 27 mmHg, whereas in SAH the values of LVSP were as follow: HO = 129 +/- 25 mmHg; H1 = 152 = 23 mmHg; H2 = 182 +/- 24 mmHg. LVEDP changed in both protocols: To = 7 +/- 2 mmHg; TM = 13 +/- 2 mmHg (p < 0.05); Ho = 7 +/- 2 mmHg; H1 = 10 +/- 2 mmHg; H2 = 14 +/- 3 mmHg (p < 0.05). During TAH there was no difference between the values of dp/dt (To = 3.303 +/- 598 mmHg/s; TM = 3.350 +/- 653 mmHg/s; p > 0.05), however, there were increases of the dp/dt during SAH (Ho = 3.233 +/- 576 mmHg/s; H1 = 3.831 +/- 667 mmHg/s; H1 = 4.594 +/- 833 mmHg/2; p < 0.05). CONCLUSION: The values of dp/dt are not influenced by transient elevation of AP. Sustained increase of AP activates cardiac adjustments, which results in elevation of dp/dt, by stimulation of contractile state. Probably, the inotropic intervention mechanism is the length dependent activation due to the Frank-Starling mechanism.

Animals↗
PubMed1991

Functional and ultrastructural evaluation of myocardial protection provided by intermittent coronary sinus perfusion in the isolated dog heart.

1. The protection offered by intermittent perfusion of cardioplegic solution through the coronary sinus was investigated in isovolumic blood-perfused dog heart preparations submitted to 60 min of ischemia and 45 min of reperfusion. 2. The preparations were divided into three treatment groups: a) coronary sinus, consisting of preparations (N = 10) perfused through the coronary sinus under 40 cm water pressure; b) aortic, consisting of preparations (N = 10) perfused through the aortic stump under 100 mmHg pressure; c) control, consisting of hearts (N = 9) that were not perfused with cardioplegic solution. 3. Properties of contractile capacity and relaxation were markedly impaired in the control group but were preserved to a comparable extent in the groups perfused with cardioplegic solution through the aorta and coronary sinus. Developed pressure decreased in the control group (before ischemia: 70 +/- 5.5 mmHg; after reperfusion: 35 +/- 12 mmHg; P less than 0.05) and didn't vary in the aortic group (from 69 +/- 4 mmHg to 65 +/- 13 mmHg; P greater than 0.05) and coronary sinus group (from 69 +/- 4.6 mmHg to 60 +/- 10 mmHg; P greater than 0.05). Myocardial relaxation was evaluated by the +/- dp/dt ratio. In the control group there was impairment of myocardial relaxation as indicated by an increase of this index after reperfusion (from 1.05 +/- 0.05 to 1.46 +/- 0.23; P less than 0.05), whereas in the aortic (from 1.10 +/- 0.13 to 1.15 +/- 0.20; P greater than 0.05) and the coronary sinus (from 1.03 +/- 0.14 to 1.08 +/- 0.16; P greater than 0.05) groups there was no variation. Ultrastructural changes in the myocardium were negligible in all three groups at the end of reperfusion. 4. We conclude that intermittent perfusion of a hypothermic cardioplegic solution through the coronary sinus is effective for the protection of the myocardium during total ischemia.

Animals↗
PubMed1991

Left ventricular maximal systolic elastance calculated by a combination of M-mode echocardiography and standard manometry.

1. A method for obtaining the end-systolic left ventricular (LV) pressure-diameter and stress-diameter relationships in man was critically analyzed. 2. Pressure-diameter and stress-diameter relationships were determined throughout the cardiac cycle by combining standard LV manometry with M-mode echocardiography. Nine adult patients with heart disease and without heart failure were studied during intracardiac catheterization under three different conditions of arterial pressure, i.e., basal (B) condition (mean +/- SD systolic pressure, 102 +/- 10 mmHg) and two stable states of arterial hypertension (HI, 121 +/- 12 mmHg; HII, 147 +/- 17 mmHg) induced by venous infusion of phenylephrine after parasympathetic autonomic blockade with 0.04 mg/kg atropine. 3. Significant reflex heart rate variation with arterial hypertension was observed (B, 115 +/- 20 bpm; HI, 103 +/- 14 bpm; HII, 101 +/- 13 bpm) in spite of the parasympathetic blockade with atropine. The linear end-systolic pressure-diameter and stress-diameter relationships ranged from 53.0 to 160.0 mmHg/cm and from 97.0 to 195.0 g/cm3, respectively. 4. The end-systolic LV pressure-diameter and stress-diameter relationship lines presented high and variable slopes. The slopes, which are indicators of myocardial contractility, are susceptible to modifications by small deviations in the measurement of the ventricular diameter or by delay in the pressure curve recording.

Adult↗
PubMed1990

[Left ventricular pressure-diameter and stress-diameter relations in humans. Standardization and critical analysis of the method].

PURPOSE: To provide a critical analysis of the fluid filled manometric system and M-mode echocardiography and, by their association, to standardize the determination of left ventricular (LV) pressure-diameter and stress-diameter relationships in humans. MATERIAL AND METHODS: The pressure curve and the LV M-mode image was obtained in 24 patients with cardiopathy. The dynamic characteristics of the fluid-filled system have been studied to define the amplitude, the resonance and the time gap of the pressure curve register. The delay of the pressure curve recording was determined in all cases by comparing pressure curve and echocardiographic aortic valve registers. The values of pressure, diameter, posterior wall thickness and LV meridional stress was calculated at every 0.02s. RESULTS: Preliminary analyses of the fluid-filled manometric system indicated that this system has variable dynamic characteristics. The pressure-diameter and stress-diameter loops obtained were similar to those of the literature. The values of end-systolic stress, percentage of fractional shortening, ejection fraction and circumferential fiber shortening rate of patients with dilated cardiomyopathy (n = 5) were significantly reduced when compared to the values of patients without left ventricular overload (n = 8) and patients with ventricular volume overload. It has been verified, also, that the retard of the pressure curve record introduced by the fluid-filled manometric system does not modify the values of these variables. CONCLUSION: The LV pressure-diameter and stress-diameter relationships obtained by the association of echocardiography and LV manometry showed functional characteristics of the ventricle that could not appear by the use of the echocardiography or by the LV manometry themselves.

Blood Pressure↗
PubMed1989

Morphometric evaluation of the time course of right ventricular hypertrophy after left coronary artery ligation in rats.

1. In order to describe the time course of compensatory right ventricular hypertrophy after infarction, rats submitted to left coronary obstruction and sham-operated controls were compared in terms of heart weight, chamber weight and right ventricular fiber diameter 1, 8 and 21 days after surgery. 2. One day after infarction, only the left ventricle weight increased (0.583 +/- 0.045 g vs 0.698 +/- 0.062 g, P less than 0.05), while right ventricular weight and fiber diameter suffered no change. 3. Eight days after infarction, heart weight (0.781 +/- 0.127 g vs 0.856 +/- 0.100 g, P greater than 0.05) as well as right ventricular fiber diameter (16.5 +/- 1.0 microns vs 17.5 +/- 2.1 microns, P greater than 0.05) and left ventricular weight did not differ between sham-operated animals and animals with left coronary obstruction. However, a significant increase in right ventricular weight was observed in infarcted animals (0.168 +/- 0.026 g vs 0.242 +/- 0.017 g, P less than 0.05). 4. Twenty-one days after infarction, right ventricular weight (0.198 +/- 0.034 g vs 0.316 +/- 0.118 g, P less than 0.05), heart weight (0.864 +/- 0.095 g vs 0.985 +/- 0.105 g, P less than 0.05) and right ventricular fiber diameter (15.0 +/- 1.8 microns vs 21.3 +/- 2.3 microns, P less than 0.05) were significantly increased in infarcted animals, whereas left ventricular weight (0.665 +/- 0.065 g vs 0.669 +/- 0.039 g, P greater than 0.05) was unchanged. 5. We conclude that hypertrophy occurs in the right ventricle of randomized infarcted rats 21 days after infarction, and that this phenomenon precedes the increase in fiber diameter.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

Does the oxygen tension of coronary sinus blood reflect myocardial oxygen tension?

Coronary sinus blood oxygen tension (CSpO2) and myocardial oxygen tension (MpO2) were measured simultaneously during cardiac ischemia and reperfusion. Oxygen tension was measured using a polarographic method. Myocardial ischemia caused a reduction (5 +/- 1.5%; P less than 0.05) in CSpO2 and a decrease (56.5 +/- 10.1%; P less than 0.001) in MpO2. Reperfusion induced a rapid but transient increase (35.9 +/- 4.3%; P less than 0.001) in CSpO2 above the basal state while MpO2 returned gradually to the basal state. These results indicate that CSpO2 is of little value for the detection of changes in myocardial oxygen metabolism during the initial phase (seconds) of cardiac reperfusion.

Animals↗
PubMed1988

Is coronary sinus blood oxygen tension behavior determined by myocardial oxygen tension variation during cardiac reperfusion?

The relationship between coronary sinus blood oxygen tension (CSPO2) and myocardial oxygen tension (MPO2) variations during cardiac ischemia and reperfusion was studied in anesthetized open-chest dogs. Oxygen tension was measured by a polarographic method. Ischemia resulted in a slightly decreased CSPO2 and a more pronounced reduction of MPO2. After reperfusion the CSPO2 rose rapidly and transiently before it returned gradually to the control level. By contrast, during the recovery period, the MPO2 increased slowly, with recovery occurring long after the peak of CSPO2. These data suggest that during the reperfusion phase, the CSPO2 variation is probably due to opening of the myocardial arteriovenous shunts instead of an increase of flow through the myocardial capillary bed.

Animals↗
PubMed1988

Changes in myocardial and coronary sinus blood oxygen tension induced by asphyxia and reoxygenation.

1. This study analyzes variations of oxygen tension induced by asphyxia in the myocardium (MpO2) and coronary sinus blood (CSpO2) of the anesthetized open-chest dog. Oxygen tension was measured polarographically and arterial blood pressure and coronary blood flow were recorded simultaneously. 2. Asphyxia increased arterial pressure and coronary blood flow but decreased both MpO2 and CSpO2. 3. During the reoxygenation phase, arterial pressure and coronary flow decreased gradually. Reoxygenation induced a rapid but transient increase in CSpO2 above control levels. In contrast, MpO2 returned gradually to the basal state. 4. The mechanism(s) involved in the differential effects of asphyxia followed by reoxygenation on MpO2 and CSpO2 remain to be elucidated.

Animals↗