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Biomedical subjects

B B Matsubara

Publications and source records attributed to B B Matsubara.

At least 19 recordsLinked to original sources
PubMed2006

Is 44-hour better than 24-hour ambulatory blood pressure monitoring in hemodialysis?

The aim of this study is to evaluate if hemodialysis (HD) patients with similar blood pressure (BP) in the whole inter-HD period could have different target organ lesions and survival if the behavior of BP differs from the first to the second day of the inter-HD period. The present study compares 44-hour ambulatory BP monitoring (ABPM) patterns in 45 HD patients. Three BP patterns emerged: group A (n = 15) had similar BPs throughout (138 +/- 11/88 +/- 12 in the first 22 h vs. 140 +/- 11/87 +/- 12 mm Hg in the second 22-hour period); group B (n = 15) had a significant systolic BP rise from the first to the second period (132 +/- 15/80 +/- 12 vs. 147 +/- 12/86 +/- 13 mm Hg, p < 0.05); group C (n = 15) had significantly higher BPs (p < 0.05) than the other 2 groups throughout the whole inter-HD period, with no significant change between the 2 halves (172 +/- 14/108 +/- 12 vs. 173 +/- 18/109 +/- 14 mm Hg). Ventricular mass and survival during the 30-month follow-up period were statistically significantly better in group A, intermediate in group B and worse in group C. The data suggest that a 44-hour ABPM is more accurate than a 24-hour one in evaluating organ lesion and prognosis in HD patients.

Adult↗
PubMed2004

Myocardial contractility of the isovolumetrically beating isolated rat heart.

Several indexes of myocardial contractility have been proposed to assess ventricular function in the isovolumetrically beating isolated heart. However, the conclusions reached on the basis of these indexes may be influenced by ventricular geometry rather than contractility itself. The objective of the present study was to assess the performance of widely used contractility indexes in the isovolumetrically beating isolated heart in two experimental models of hypertrophy, the spontaneously hypertensive rat (SHR) and infrarenal aortocava fistula. Compared to normotensive controls (N = 8), SHRs with concentric hypertrophy (N = 10) presented increased maximum rate of ventricular pressure rise (3875 +/- 526 vs 2555 +/- 359 mmHg/s, P < 0.05) and peak of isovolumetric pressure (187 +/- 11 vs 152 +/- 11 mmHg, P < 0.05), and decreased developed stress (123 +/- 20 vs 152 +/- 26 g/cm(2), P < 0.05) and slope of stress-strain relationship (4.9 +/- 0.42 vs 6.6 +/- 0.77 g/cm(2)/%). Compared with controls (N = 11), rats with volume overload-induced eccentric hypertrophy (N = 16) presented increased developed stress (157 +/- 38 vs 124 +/- 22 g/cm(2), P < 0.05) and slope of stress-strain relationship (9 +/- 2 vs 7 +/- 1 g/cm(2)/%, P < 0.05), and decreased maximum rate of ventricular pressure rise(2746 +/- 382 vs 3319 +/- 352 mmHg, P < 0.05) and peak of isovolumetric pressure (115 +/- 14 vs 165 +/- 13 mmHg/s, P < 0.05). The results suggested that indexes of myocardial contractility used in experimental studies may present opposite results in the same heart and may be influenced by ventricular geometry. We concluded that several indexes should be taken into account for proper evaluation of contractile state, in the isovolumetrically beating isolated heart.

Animals↗
PubMed2004

Food restriction induces in vivo ventricular dysfunction in spontaneously hypertensive rats without impairment of in vitro myocardial contractility.

Cardiac structures, function, and myocardial contractility are affected by food restriction (FR). There are few experiments associating undernutrition with hypertension. The aim of the present study was to analyze the effects of FR on the cardiac response to hypertension in a genetic model of hypertension, the spontaneously hypertensive rat (SHR). Five-month-old SHR were fed a control or a calorie-restricted diet for 90 days. Global left ventricle (LV) systolic function was evaluated in vivo by transthoracic echocardiogram and myocardial contractility and diastolic function were assessed in vitro in an isovolumetrically beating isolated heart (Langendorff preparation). FR reduced LV systolic function (control (mean +/- SD): 58.9 +/- 8.2; FR: 50.8 +/- 4.8%, N = 14, P < 0.05). Myocardial contractility was preserved when assessed by the +dP/dt (control: 3493 +/- 379; FR: 3555 +/- 211 mmHg/s, P > 0.05), and developed pressure (in vitro) at diastolic pressure of zero (control: 152 +/- 16; FR: 149 +/- 15 mmHg, N = 9, P > 0.05) and 25 mmHg (control: 155 +/- 9; FR: 150 +/- 10 mmHg, N = 9, P > 0.05). FR also induced eccentric ventricular remodeling, and reduced myocardial elasticity (control: 10.9 +/- 1.6; FR: 9.2 +/- 0.9%, N = 9, P < 0.05) and LV compliance (control: 82.6 +/- 16.5; FR: 68.2 +/- 9.1%, N = 9, P < 0.05). We conclude that FR causes systolic ventricular dysfunction without in vitro change in myocardial contractility and diastolic dysfunction probably due to a reduction in myocardial elasticity.

Animals↗
PubMed2004

Association between hypervolemia and ventricular hypertrophy in hemodialysis patients.

BACKGROUND: Left ventricular hypertrophy (LVH) is a well-known predictor of cardiovascular mortality in patients who have end-stage renal disease and are maintained on hemodialysis (HD), and LVH is not always correlated with the severity of hypertension in these patients. The purpose of this study was to investigate the role of other factors contributing to LVH. METHODS: A total of 50 patients with HD were classified in three groups according to whether their LV mass index (LVMI) was higher than (n = 15), equal to (n = 20), or lower than (n = 15) that predicted by a formula based on their ambulatory blood pressure monitoring (ABPM). RESULTS: Subjects with higher LVMI than predicted had significantly greater inter-HD weight gain (3.4 +/- 0.8 v 2.7 +/- 0.8 and 2.6 +/- 05 kg, respectively, in the other two groups, P < .05), and subjects with lower LVMI than predicted had a tendency toward a more pronounced nocturnal dipping pattern of BP (P = .07 v the other two groups), although daytime and night-time average BP levels did not differ between groups. All other clinical and laboratory parameters were similar among the three groups except higher cardiac output and various indices of LVH, which were more pronounced in the group with higher LVMI by ABPM. This group had also the lowest survival rate over the 2 to 3 years of follow-up, with five deaths versus two in each of the other two groups. CONCLUSIONS: The data suggest that correct management of inter-HD weight gain by nutritional counseling and shorter inter-HD intervals may prevent LVH and improve survival independently of BP control.

Adult↗
PubMed2001

Experimental myocardial hypertrophy induced by a minimally invasive ascending aorta coarctation.

Ascending aorta coarctation was produced by a minimally invasive technique in rabbits. Animal mortality was 5%. Morphometric and hemodynamic parameters were evaluated. A parabiotically isolated heart model was used to assess the hemodynamic parameters. Left ventricular weight/body weight ratio and muscle area showed clear evidence of hypertrophy when compared to control. The hemodynamic changes in the isolated heart model suggested decreased diastolic and systolic function in the coarcted group. The present model produced hypertrophy with low mortality rates as a result of its less invasive nature.

Animals↗
PubMed2000

Early rather than delayed administration of lisinopril protects the heart after myocardial infarction in rats.

BACKGROUND: ACE inhibitors have shown beneficial results in several studies after myocardial infarction (MI). However, these studies have shown conflicting results about the ideal starting time of the ACE inhibitors administration after MI and the importance of infarct size. OBJECTIVES: This study was designed to assess the long-term effects of lisinopril on mortality, cardiac function, and ventricular fibrosis after MI, in rats. METHODS: Lisinopril (20 mg/kg/day) was given on day 1 or 21 days after coronary occlusion in small or large infarctions. RESULTS: The mortality rate was reduced by 39 % in early treatment and 30 % in delayed treatment in comparison to the untreated rats. Early treatment reduced cardiac dysfunction in small MIs; however, delayed treatment did not. No statistical difference was observed among the groups for large MIs. No statistical difference was observed among the groups with large or small MIs on myocardial hydroxyproline concentration. CONCLUSIONS: Both early and delayed treatments with lisinopril increased survival. Treatment exerts no marked effects on fibrosis; early treatment has exerted beneficial influences on cardiac function whereas delayed treatment had no consistent effects. The protective effect of lisinopril is detectable only in small (< 40 % of LV) MIs.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed2000

Combination therapy with angiotensin converting enzyme inhibition and AT1 receptor inhibitor on ventricular remodeling after myocardial infarction in rats.

BACKGROUND: There are limited data regarding the effects of angiotensin II receptor blockade after myocardial infarction (MI). In addition, whether combined angiotensin converting enzyme (ACE) inhibitor and angiotensin II type I (AT(1)) receptor antagonist may be superior to either drug alone on ventricular remodeling remains unclear. The goal of this study was to determine if the cardiac effects of the combined administration of an ACE inhibitor and AT(1) receptor antagonist are greater than those produced by either of these agents administered individually after MI. METHODS AND RESULTS: After MI, rats were divided into 4 groups: 1) untreated animals, 2) lisinopril treatment (20 mg/kg/day), 3) losartan treatment (20 mg/kg/day), and 4) lisinopril plus losartan treatment. After 3 months, the cardiac parameters studied were: mortality, fibrosis (hydroxyproline), hypertrophy (ventricular weight/body weight ratio [VW/BW]), left ventricular enlargement (volume at end-diastolic pressure equaled zero/body weight ratio [V0/BW]), and ventricular function (isovolumetric developed pressure, dp/dt, -dp/dt). A lowest mortality rate in the animals treated with the combination of both ACE inhibitor and AT(1) receptor antagonist was observed. Although lisinopril and losartan significantly decreased VW/BW ratio, when administered concomitantly, VW/BW ratio was lower than when either agent was administered individually. There were no differences in right ventricle hydroxyproline concentration. Only combination therapy decreased V0/BW ratio. The treatment with lisinopril plus losartan resulted in increases in the development of pressure versus untreated group; without alteration in dp/dt and -dp/dt. CONCLUSIONS: The combination of the AT(1) receptor blockade and ACE inhibitor is more effective than individual treatment on ventricular remodeling and survival after MI in rats.

Angiotensin Receptor Antagonists↗
PubMed2000

Alterations in myocardial collagen content affect rat papillary muscle function.

We investigated the influence of myocardial collagen volume fraction (CVF, %) and hydroxyproline concentration (microg/mg) on rat papillary muscle function. Collagen excess was obtained in 10 rats with unilateral renal ischemia for 5 wk followed by 3-wk treatment with ramipril (20 mg. kg(-1). day(-1)) (RHTR rats; CVF = 3.83 +/- 0. 80, hydroxyproline = 3.79 +/- 0.50). Collagen degradation was induced by double infusion of oxidized glutathione (GSSG rats; CVF = 2.45 +/- 0.52, hydroxyproline = 2.85 +/- 0.18). Nine untreated rats were used as controls (CFV = 3.04 +/- 0.58, hydroxyproline = 3.21 +/- 0.30). Active stiffness (AS; g. cm(-2). %L(max)(-1)) and myocyte cross-sectional area (MA; micrometer(2)) were increased in the GSSG rats compared with controls [AS 5.86 vs. 3.96 (P < 0.05); MA 363 +/- 59 vs. 305 +/- 28 (P < 0.05)]. In GSSG and RHTR groups the passive tension-length curves were shifted downwards, indicating decreased passive stiffness, and upwards, indicating increased passive stiffness, respectively. Decreased collagen content induced by GSSG is related to myocyte hypertrophy, decreased passive stiffness, and increased AS, and increased collagen concentration causes myocardial diastolic dysfunction with no effect on systolic function.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed2000

End-systolic pressure-diameter relation of the left ventricle during transient and sustained elevations of blood pressure.

OBJECTIVE: To assess the effect of transient and sustained variations in cardiac load on the values of the end-systolic pressure-diameter relation (ESPDR) of the left ventricle. METHODS: We studied 13 dogs under general anesthesia and autonomic blockade. Variations of cardiac loads were done by elevation of blood pressure by mechanical constriction of the aorta. Two protocols were used in each animal: gradual peaking and decreasing pressure variation, the "transient arterial hypertension protocol" (TAH), and a quick and 10 min sustained elevation, the "sustained arterial hypertension protocol"(SAH). Then, we compared the ESDR in these two situations. RESULTS: Acute elevation of arterial pressure, being it "transitory" or "sustained", did not alter the heart frequency and increased similarly the preload and after load. However, they acted differently in end systolic pressure-diameter relation. It was greater in the SAH than TAH protocol, 21.0+/-7.3 mm Hg/mm vs. 9.2+/-1. 2 mm Hg/mm (p<0.05). CONCLUSION: The left ventricular ESPDR values determined during sustained pressure elevations were higher than those found during transient pressure elevations. The time-dependent activation of myocardial contractility associated with the Frank-Starling mechanism is the major factor in inotropic stimulation during sustained elevations of blood pressure, determining an increase in the ESPDR values.

Analysis of Variance↗
PubMed2000

Effects of losartan on ventricular remodeling in experimental infarction in rats.

OBJECTIVE: To evaluate the effects of losartan on ventricular remodeling and on survival after myocardial infarction in rats. METHODS: After surgical occlusion of left coronary artery, 84 surviving male Wistar rats were divided into two groups: LO treated with losartan (20mg/kg/day, n=33 ) and NT (n=51 ), without medication. After 3 months, we analyzed mortality; ventricular to body mass ratio (VM /BM ); myocardial hydroxyproline concentration (HOP); isovolumetric pressure, +dp/dt , -dp/dt , and diastolic volume/left ventricle mass ratio (VO/LV ). RESULTS: Mortality was: LO = 22 % , and NT = 47 % (p<0.05). Ventricular mass,(VM/BM , mg/g ) was 4.14 +/- 0.76 and 3.54+/-0.48, in the NT and LO groups, respectively (p<0.05). HOP (median) was 4.92 upsilong/mg in the LO and 5.54 upsilong/g in the NT group (p>0.05). The V0/LV values (median) were 0.24 mL/g in group LO and 0.31 mL/g in group NT (p<0.05) compared to NT group. There were no differences between the groups for +dp/dt and -dp/dt parameters. CONCLUSION: 1. The use of losartan myocardial infarction causes an attenuation of ventricular remodeling, bringing about an increased survival, an attenuation of ventricular hypertrophy and dilation, and an improvement of the isovolumetric pressure; 2. the treatment does not modify the myocardial collagen concentration.

Animals↗
PubMed1999

The effect of non-antihypertensive doses of angiotensin converting enzyme inhibitor on myocardial necrosis and hypertrophy in young rats with renovascular hypertension.

In renovascular hypertensive rats, low doses of angiotensin converting enzyme (ACE) inhibitors have been found to prevent myocardial hypertrophy independent of blood pressure level. This finding would suggest humoral rather than mechanical control of myocyte growth. The aim of this study was to examine the effect of nonantihypertensive doses of ACE inhibitor on myocardial hypertrophy and necrosis in hypertensive rats. Renovascular hypertension (RHT) was induced in four-week-old Wistar rats. Twenty-eight animals were treated for four weeks with three doses of ramipril (0.01, 0.1 or 1. 0 mg/kg/day, which are unable to lower blood pressure. Fourteen animals were not treated (RHT group). A sham operated, age/sex-matched group was used as control (n = 10). Myocardial histology was analysed in 3 microm thick sections of the ventricle stained with either haematoxylin-eosin, reticulin silver stain or Masson's trichrome. There was a significant correlation between systolic blood pressure and left ventricular to body weight ratio in both sets of animals: untreated plus controls and ramipril-treated rats. ACE inhibition prevented myocyte and perivascular necrosis and fibrosis in a dose-dependent manner. We conclude that myocardial hypertrophy in rats with renovascular hypertension is directly related to arterial pressure, and that this relationship is not affected by nonantihypertensive doses of ACE inhibitor. Myocardial necrosis/fibrosis and coronary artery damage induced by angiotensin II are prevented by ACE inhibitor in a dose-dependent manner, despite the presence of arterial hypertension.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1999

Effects of lisinopril on experimental ischemia in rats. Influence of infarct size.

OBJECTIVE - Angiotensin-converting enzyme inhibitors (ACEIs) have gained importance in preventing or attenuating the process of ventricular remodeling after myocardial infarction. The significance of infarct size in regard to the response to ACEIs, however, is controversial. This study aimed to analyze the effects of lisinopril on mortality rate, cardiac function, degree of cardiac hypertrophy and fibrosis in rats with different infarct sizes. METHODS - Lisinopril (20 mg/kg/day) dissolved in drinking water was administered to rats immediately after coronary artery occlusion. After being sacrificed, the infarcted animals were divided into two groups: one group of animals with small infarcts (< 40% of the left ventricle) and another group of animals with large infarcts (> 40% of the left ventricle). RESULTS - The mortality rate was 31.7% in treated rats and 47% in the untreated rats. There was no statistical difference between the groups with small and large infarcts in regard to myocardial concentration of hydroxyproline. In small infarcts, the treatment attenuated the heart dysfunction characterized by lower levels of blood pressure and lower values of the first derivative of pressure and of the negative derivative of pressure. The degree of hypertrophy was also attenuated in small infarcts. In regard to large infarcts, no differences between the groups were observed. CONCLUSION - Treatment with the ACEIs had no effect on mortality rate and on the amount of fibrosis. The protective effect of lisinopril on heart function and on the degree of hypertrophy could only be detected in small infarcts

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1998

Left ventricular adaptation to chronic pressure overload induced by inhibition of nitric oxide synthase in rats.

Recent studies have indicated that chronic inhibition of nitric oxide synthase induces arterial hypertension without myocardial hypertrophy. We investigated the mechanisms of left ventricular (LV) adaptation to this condition. Also, we analyzed the effect of the angiotensin-converting enzyme inhibitor (ACEI), lisinopril, in this experimental model of ventricular pressure overload. Fifty-eight Wistar rats received eight weeks of treatment with either NW-nitro-L-arginine-methyl ester (L-NAME group, n = 19), lisinopril (LISINOPRIL group, n = 19) or the combination of both drugs (LNAMELIS group, n = 20). All results were compared to age and sex matched untreated rats (CONTROL group, n = 18). Tail-cuff blood pressure rose significantly in L-NAME treated rats (195 +/- 29 mm Hg) compared to the CONTROL (141 +/- 12 mm Hg), LISINOPRIL (97 +/- 13 mm Hg), and LNAMELIS (113 +/- 16 mm Hg) groups. There was no myocardial hypertrophy in the chronically hypertensive rats. The ventricular unstressed volume was significantly reduced in the L-NAME group (0.119 +/- 0.027 mL) compared to the CONTROL (0.158 +/- 0.026 mL) indicating a disproportional reduction in ventricular volume related to the myocardial mass. The chamber size modification resulted in a systolic stress which was comparable to the CONTROL even though the isovolumetric systolic pressure was higher. The systolic functional data indicated preserved myocardial contractility in L-NAME. LV compliance was increased in the LISINOPRIL group and myocardial passive stiffness was lower in all treated rats compared to CONTROL. We conclude that LV. adaptation to chronic pressure overload without hypertrophy involves changes in chamber geometry and myocardial diastolic mechanical properties. Also, ACEI fully prevents L-NAME induced hypertension, reduces myocyte cross-sectional area, and myocardial passive stiffness. The combination of L-NAME plus lisinopril decreases the load independent index of myocardial contractility.

Adaptation, Physiological↗
PubMed1997

[Arterial dysfunction as a possible mechanism of cardiac injury in type II diabetic patients. A Doppler-echocardiographic study].

PURPOSE: To evaluate the left ventricular structure and function and the arterial stiffness in type II diabetic patients. METHODS: Thirteen diabetic patients, men and women (age 55 +/- 8 years) were included in the study. None of the patients had any other clinical disorders. Doppler-echocardiography and non-invasive monitoring of arterial blood pressure were performed. All the results were compared to an age and sex matched control group (n = 12). RESULTS: There were no differences between the groups for diastolic blood pressure, dimensions of cardiac chambers and ventricular systolic and diastolic function indexes. Diabetic patients had increased left ventricular mass index (101 +/- 10 vs 80 +/- 14 g/m2; p < 0.001) and increased arterial stiffness (0.86 +/- 0.26 vs 0.69 +/- 0.19 mmHg/mL; p < 0.05), when compared to control group. CONCLUSION: Diabetes mellitus is associated to increased systemic arterial stiffness and this may contribute to the adverse effects of diabetes on left ventricular morphology.

Blood Pressure↗
PubMed1997

Myocyte necrosis is the basis for fibrosis in renovascular hypertensive rats.

The pathogenesis of fibrosis and the functional features of pressure overload myocardial hypertrophy are still controversial. The objectives of the present study were to evaluate the function and morphology of the hypertrophied myocardium in renovascular hypertensive (RHT) rats. Male Wistar rats were sacrificed at week 4 (RHT4) and 8 (RHT8) after unilateral renal ischemia (Goldblatt II hypertension model). Normotensive rats were used as controls. Myocardial function was analyzed in isolated papillary muscle preparations, morphological features were defined by light microscopy, and myocardial hydroxyproline concentration (HOP) was determined by spectrophotometry. Renal artery clipping resulted in elevated systolic arterial pressure (RHT4: 178 +/- 19 mmHg and RHT8: 194 +/- 24 mmHg, P < 0.05 vs control: 123 +/- 7 mmHg). Myocardial hypertrophy was observed in both renovascular hypertensive groups. The myocardial HOP concentration was increased in the RHT8 group (control: 2.93 +/- 0.38 micrograms/mg; RHT4: 3.02 +/- 0.40 micrograms/mg; RHT8: 3.44 +/- 0.45 micrograms/mg of dry tissue, P < 0.05 vs control and RHT4 groups). The morphological study demonstrated myocyte necrosis, vascular damage and cellular inflammatory response throughout the experimental period. The increased cellularity was more intense in the adventitia of the arterioles. As a consequence of myocyte necrosis, there was an early, local, conjunctive stroma collapse with disarray and thickening of the argyrophilic interstitial fibers, followed by scarring. The functional data showed an increased passive myocardial stiffness in the RHT4 group. We conclude that renovascular hypertension induces myocyte and arteriole necrosis. Reparative fibrosis occurred as a consequence of the inflammatory response to necrosis. The mechanical behavior of the isolated papillary muscle was normal, except for an early increased myocardial passive stiffness.

Animals↗
PubMed1997

[Effect of lisinopril on cardiac parameters and mortality after myocardial infarction in rats].

PURPOSE: To analyse the effect of early (< 24h) administration of lisinopril on ventricular remodeling and mortality after myocardial infarction (MI) in rats. METHODS: Wistar rats weighing 200-250 g were submitted to ligation of the left coronary artery (LCA) and divided into three groups: SHAM (S, n = 9); infarcted and lisinopril (20mg/kg/day) treated rats (L, n = 38); infarcted and non-treated animals (NT, n = 24). Three months later, the cardiac function was studied in isolated heart preparation according to the Langendorff technique. Starling curves were constructed using fluid injection in the left ventricular balloon, which permitted to alter the diastolic pressure range from 0 to 30mmHg by means of pressure increments of 5mmHg. Body weight (BW), right ventricular weight (RVW), and RVW/BW were also determined. RESULTS: Three months after the surgery, the comparative mortality rate among groups was: S = 0; L = 34.4% and NT = 54.4% (p > 0.05, for L vs NT). In infarctions < 40% of the left ventricle (LV), the RVW/BW relation was S = L < NT (p < 0.05); the left ventricular systolic pressure was S > L > NT (p < 0.05). In infarctions > 40% of LV, the RVW/BW relation was S < L = NT (p < 0.05). For the Starling curves, the results were S > L > NT (p < 0.05). CONCLUSION: In our model lisinopril did not interfere with post-infarction mortality of rats, although decreasing the mortality risk in 49%, in the treated group. The drug also altered the remodeling process, preventing hypertrophy and systolic disfunction after MI, mainly in infarctions < 40% of LV.

Analysis of Variance↗
PubMed1997

Myocardial fibrosis rather than hypertrophy induces diastolic dysfunction in renovascular hypertensive rats.

The aim of the present study was to evaluate the effect of interstitial fibrosis alone or associated with hypertrophy on diastolic myocardial function in renovascular hypertensive rats. Myocardial function was evaluated in isolated papillary muscle from renovascular hypertensive Wistar rats (RHT, n = 14), renovascular hypertensive rats treated with the angiotensin converting enzyme inhibitor (ACEI) ramipril, 20 mg.kg-1.day-1 (RHT RAM, n =14), and age-matched unoperated and untreated Wistar rats (CONT, n = 12). The ACEI treatment for 3 weeks allowed the regression of myocyte mass and the maintenance of interstitial fibrosis. Myocardial passive stiffness was analyzed by the resting tension-length relationship. The myocardial fibrosis was evaluated by measuring myocardial hydroxyproline (Hyp) concentration and by histological studies of the myocardium stained with hematoxylin and eosin or picrosirus red. Left ventricular weight was significantly higher in RHT (0.97 +/- 0.12 g) compared with CONT (0.66 +/- 0.06 g) and RHT RAM (0.69 +/- 0.14 g). The Hyp levels were 2.9 +/- 0.4, 3.4 +/- 0.3, and 3.8 +/- 0.4 micrograms/mg of dry tissue for the CONT, RHT, and RHT RAM, respectively. Perivascular and interstitial fibrosis were observed in RHT and RHT RAM groups. There were lymphononuclear inflammatory exudate and edema around arteries, involving adjacent myocytes in the RHT group. There was an increased passive stiffness in RHT and RHT RAM groups compared with the CONT group. In conclusion, our results indicate that the impaired diastolic function in the renovascular hypertensive rats is related to interstitial fibrosis rather than to myocardial hypertrophy.

Angiotensin-Converting Enzyme Inhibitors↗