Biomedical subjects
Publications and source records attributed to B B Matsubara.
Even though normally present in relatively small amounts, myocardial collagen strongly influences ventricular diastolic function. Removal of less than half of the normal amount results in a dilated ventricle with increased compliance. In contrast, an abnormal increase in collagen concentration results in a stiffer myocardium and ventricular diastolic dysfunction.
In both humans and experimental animals, mineralocorticoid (MC)-induced hypertension is associated with myocardial fibrosis. We have shown that this fibrous tissue response includes a reactive interstitial fibrosis not initiated by parenchymal cell loss, and a reparative fibrosis or scarring, occurring in response to cardiac myocyte necrosis. The reactive fibrosis is thought to be related to MC excess, while cell loss and microscopic scarring may be secondary to enhanced potassium excretion or a cytotoxic effect of aldosterone. This histologic study was undertaken to determine whether or not the potassium sparing diuretic amiloride would be effective in preventing the appearance of either form of fibrosis. Uninephrectomized male Sprague Dawley rats received either aldosterone (AL; 0.75 microgram/h), amiloride (AMC; 1 mg/kg/day), aldosterone+amiloride (ALAM), or vehicle (ALC) alone via subcutaneous osmotic minipumps for 8 weeks. All rats received 1% NaCl in their drinking water. Hearts were recovered, immersion-fixed, and tissue sections from both left and right ventricles stained with the collagen specific stain Sirius Red F3BA were morphometrically analyzed. The interstitial collagen volume fraction was elevated in AL and ALAM groups compared to ALC and AMC, but did not differ between AL and ALAM. Microscopic scarring, found in both ventricles, was evident in AL animals, but was not found in the ALAM, AMC, or ALC groups. These data suggest that chronic elevations in plasma aldosterone, relative to dietary sodium intake, do not have a direct cytotoxic effect on cardiac myocytes, but they are associated with a reactive interstitial fibrosis.(ABSTRACT TRUNCATED AT 250 WORDS)
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.
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.
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.
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.
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.
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