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W Motz

Publications and source records attributed to W Motz.

102 records · Page 6Linked to original sources
PubMed1985

Regression of cardiac hypertrophy after therapy in animal hypertension.

Studies on spontaneously hypertensive rats (SHR), which represent a model of genetically determined arterial hypertension, revealed that cardiac hypertrophy can be controlled by blood pressure normalization by use of various antihypertensive drugs such as hydralazine, captopril, metoprolol, guanethidine, and alpha-methyldopa. Adrenergic influences seem to play a part except for left ventricular (LV) systolic unloading on cardiac hypertrophy, because LV hypertrophy was quantitatively less expressed after a combined therapy with both metoprolol and hydralazine than after a single hydralazine treatment, although blood pressure was not different between the groups. To study whether nifedipine can cause an already existing cardiac hypertrophy to regress, 20-week-old SHR were treated with nifedipine for a period of 20 weeks. After nifedipine treatment, LV muscle mass/body weight ratio was significantly less than before therapy (2.13 +/- 0.18 vs. 2.37 +/- 0.30 mg/g; p less than 0.05). Mass to volume ratio, i.e., quotient of LV muscle mass and LV end-diastolic volume, dropped from 3.40 +/- 0.66 to 3.07 +/- 0.30 mg/microliters (p less than 0.05) after therapy. Accordingly, an antihypertensive treatment with the calcium channel blocker nifedipine can cause an already existing LV hypertrophy in SHR to regress. Because blood pressure reduction resulting from therapy with beta-receptor-blockers, vasodilators, sympatholytic drugs, angiotensin converting enzyme inhibitors, and calcium channel blockers has qualitatively similar effects with respect to causing regression of hypertrophy, reversal of cardiac hypertrophy seems to be mainly related to the reduced LV systolic load. Specific pharmacodynamic effects may only modulate the extent of LV mass reduction along with blood pressure normalization.

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PubMed1985

Regression of heart muscle hypertrophy after nifedipine therapy: changes in cardiac gene expression.

Changes in cardiac gene expression were studied during development and regression of cardiac hypertrophy in spontaneously hypertensive rats (SHR) in an attempt to determine some of the biochemical factors responsible for alterations in cardiac mass. Chronic nifedipine treatment of SHR (30 mg/kg per day for 20 weeks) led to a marked reduction in arterial blood pressure and to a subsequent regression of cardiac hypertrophy. Cardiac mRNA concentration decreased, whereas cardiac protein concentration remained unchanged. Changes in cardiac gene expression, as reflected by the decrease in cardiac mRNA concentration, were thus identified as a major factor responsible for the regression of cardiac hypertrophy after nifedipine therapy of SHR.

Animals↗
PubMed1985

The influence of sympathetic nervous activity on regression of cardiac hypertrophy.

Pharmacotherapeutical means of reversing cardiac hypertrophy (prazosin, clonidine and nifedipine) were analysed in concentrically, as well as eccentrically, hypertrophied left ventricles. Regression of cardiac hypertrophy, i.e. a therapeutic intervention on a critical precursor of hypertensive congestive heart failure, can be obtained by various antihypertensive agents. Prazosin, calcium channel blockers, clonidine and angiotensin converting enzyme inhibitors as well as a combined treatment regimen using alpha-receptor blockers together with diuretics and vasodilators can all induce regression of hypertrophy associated with an improvement in left ventricular function. Moreover, an improved coronary reserve may reduce the ischaemic risk of the hypertrophied myocardium. However, not all antihypertensive drugs seem equally effective in bringing about coronary regression of left ventricular hypertrophy (LVH). No regression or little regression has been found with diuretic monotherapy despite a satisfactory reduction in blood pressure. On the other hand, a trend towards a regression has been observed in patients in whom treatment with clonidine significantly reduced catecholamines.

Animals↗
PubMed1983

The role of clonidine in hypertensive heart disease. Influence on myocardial contractility and left ventricular afterload.

The hemodynamic and contractile effects of clonidine were studied in hypertrophied hearts of spontaneously hypertensive rats (Okamoto-Aoki strain, SHR). The hemodynamic pattern was characterized by dose-dependent decreases in systolic blood pressure and systolic wall stress, ie, the afterload imposed upon the left ventricle, whereas left ventricular ejection fraction and stroke volume were unchanged. Even at extremely high doses (10(-5)M/L) there was found no depression of isometric tension development and maximum isotonic shortening velocity of the isolated LV papillary muscle. It is concluded that clonidine may be beneficial in hypertensive heart disease, if ventricular unloading associated with a reduction in myocardial energy demand is desired.

Animals↗
PubMedDate not supplied

Prevention of hypertensive hypertrophy by medical therapy: effects on systolic wall stress and systolic function.

Left ventricular (LV) hypertrophy and LV systolic pumping function of spontaneously hypertensive rats (SHR) treated for 40 weeks with hydralazine (n = 8), metoprolol (n = 8) and both metoprolol and hydralazine (n = 9) were compared with those of 25 age-matched untreated SHR. LV pressure (PLV), peak systolic wall stress (SWS), cardiac index (CI), LV ejection fraction (EF), LV muscle mass to body weight ratio (LV/BW) and the mass volume ratio (M/V) were determined. In the rats treated with hydralazine and metoprolol and hydralazine combined PLV was 28.7% (129 +/- 19 mm Hg) and 31.5% (124 +/- 17 mm Hg) lower compared to the untreated control group (181 +/- 18 mm Hg). In spite of the same amount of blood pressure reduction, LV hypertrophy was less expressed after treatment with metoprolol and hydralazine than after hydralazine only (LV/BW: 2.48 +/- 0.17 versus 2.67 +/- 0.24 mg/g, p less than 0.01; M/V: 2.43 +/- 0.59 versus 3.09 +/- 0.47 mg/microliter, p less than 0.05 respectively). In the group treated with metoprolol and hydralazine LV systolic ejection function parameters (CI, EF) did not differ from those untreated due to an unchanged LV afterload as demonstrated by identical systolic wall stress values (169 +/- 43.4 X 10(3) versus 171 +/- 26.0 X 10(3) dyn/cm2, ns). The identical systolic wall stress values indicate that cardiac hypertrophy had regressed in proportion to the reduced LV peak systolic pressure. Following hydralazine therapy systolic wall stress was even lower (140 +/- 26.5 X 10(3) dyn/cm2) in comparison to the untreated group (171 +/- 26.0 X 10(3) dyn/cm3, p less than 0.05). This reflects an inappropriate low muscle mass reduction in relation to blood pressure reduction. In conclusion (I) antihypertensive therapy with an arteriolar vasodilator in combination with a beta-receptor blocker is more effective in preventing cardiac hypertrophy than therapy with a vasodilator only. (II) Myocardial working capacity remained unaltered after prevention of cardiac hypertrophy as well as LV pumping function.

Animals↗
PubMedDate not supplied

Influence of nifedipine on ventricular function and myocardial hypertrophy in spontaneously hypertensive rats.

We compared left ventricular (LV) hemodynamics, LV muscle mass (LVMM), and LV geometry of 13 spontaneously hypertensive rats (SHRs) treated for 20 weeks with nifedipine (30 mg/kg/day) with those of 11 age-matched untreated SHRs. LVMM, LVMM related to end-diastolic volume (LVMM/EDV), LV pressure (PLV), systolic wall stress (Tsyst), ejection fraction (EF), cardiac index (CI), and isovolumetric contractility indices (dP/dtmax, IP, t-dP/dtmax, and VCE) were determined. Nifedipine treatment lowered PLV from 170 to 136 mm Hg and Tsyst from 222 to 194 10(3) dyn/cm2. LVMM and LVMM/EDV decreased moderately from 800 to 744 mg and from 2.56 to 2.29 mg/microliter, respectively. Left ventricular ejection was markedly increased (EF from 52 to 64%; CI from 154 to 178 ml/min X kg), whereas isovolumic contractility indices remained unchanged. Thus, nifedipine reduced but did not totally prevent myocardial hypertrophy and enhanced LV function. These effects seem to result from reduction in LV afterload and not from altered myocardial contractility.

Animals↗
PubMedDate not supplied

Mechanisms of histamine-induced coronary vasodilatation: H1-receptor-mediated release of endothelium-derived nitric oxide.

Although the content of histamine in myocardial tissue is high, its contribution to the regulation of coronary blood flow has not been clearly defined. The aim of the present study was to investigate whether or not nitric oxide (NO), an important modulator of coronary vascular tone, is involved in histamine-induced coronary vasomotion and to characterize which histaminergic receptor subtype mediates this process. Isolated, constant-flow-perfused guinea pig hearts were challenged with histamine, the H1-receptor agonist pyridylethylamine (PYR) and the H2-receptor agonist dimaprit (DIM). Apart from coronary perfusion pressure (CPP), left ventricular pressure (LVP) and the development of contractile force (dp/dt), the release of NO and cyclic GMP (cGMP) were continuously measured. Histamine and DIM induced concentration dependently a coronary vasodilatation with an almost 50% decrease in CPP paralleled by an enhancement of LVP and dp/dt by more than 80%. PYR selectively reduced CPP by 47% without affecting LVP and dp/dt. Histamine- and PYR-induced coronary vasodilatation were paralleled by a more-than-twofold increase in basal cGMP release from isolated hearts, whereas DIM exerted no effects on cGMP release. Oxyhemoglobin (4 microM), an effective scavenger of NO, shifted the concentration-response curve for histamine- and PYR-induced changes in CPP significantly to the right and in parallel inhibited the increase in cGMP release. Histamine and PYR rapidly (within 2 s) decreased CPP, while the onset of DIM-induced coronary vasodilatation followed changes in LVP with a lag period of 10 s. Histamine increased basal NO release concentration dependently by a maximum of 351 +/- 21 pmol/min.(ABSTRACT TRUNCATED AT 250 WORDS)

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PubMedDate not supplied

Nifedipine in the long-term management of hypertensive heart disease.

Left ventricular (LV) hemodynamics, LV muscle mass, and LV geometry of 28 spontaneously hypertensive rats (SHR) treated for 20, 40, and 60 weeks with nifedipine (30 mg/kg/day) were compared with those of 29 age-matched untreated SHR. LV Pressure (PLV), systolic wall stress (Tsyst), ejection fraction (EF), cardiac index (CI), the ratio of LV muscle mass to body weight (LV/BW) and the ratio of LV muscle mass to end-diastolic volume (M/V) were determined. Myocardial contractility was analyzed through studies of the isolated LV papillary muscle. After 60 weeks of nifedipine treatment, PLV was 32.2% and Tsyst 22.9% lower in the treated group compared to the untreated control group (PLV 116 vs 171 mm Hg; Tsyst 165 vs 214 10(3)dyn/cm2). The degree of LV hypertrophy as indicated by LV/BW (-14%) and M/V (-21%) was less after treatment. LV pumping performance was considerably improved (EF = from 54% to 61%; Cl = from 175 to 220 ml/kg), whereas myocardial contractility indices such as maximum isotonic shortening velocity and isometric tension development remained unchanged. Thus, nifedipine reduced cardiac hypertrophy and improved LV function. These effects seem to result from a reduction in LV afterload.

Animals↗
PubMedDate not supplied

Regression of structural cardiovascular changes by antihypertensive therapy.

Left ventricular (LV) hypertrophy is the structural adaptation of the heart in response to chronic LV pressure load. Studies in spontaneously hypertensive rats (SHR), which represent a model of genetically determined arterial hypertension, reveal that cardiac hypertrophy can be controlled by long-term blood pressure normalization with the use of various antihypertensive agents, such as arterial vasodilatators (hydralazine), converting enzyme inhibitors (captopril), beta-receptor blockers (metoprolol), antiadrenergic substances (alpha-methyldopa, guanethidine), and calcium antagonists (nifedipine, felodipine). Additional drug-specific effects modulate the mechanical effect of LV systolic unloading on cardiac hypertrophy: after a combined treatment with metoprolol and hydralazine, LV hypertrophy was quantitatively lower than after single hydralazine therapy, although blood pressure had been lowered to the same extent. LV collagen concentration remained unchanged when medical treatment prevented the development of myocardial hypertrophy. However, when therapy was begun after hypertrophy had been completely established, reversal of hypertrophy was associated with an increased LV collagen concentration. In concentric LV hypertrophy with normal systolic wall stress, LV function was not impaired. Consequently, antihypertensive therapy could not improve LV function in this condition. However, in the case of LV dilatation with increased systolic wall stress, LV systolic unloading by antihypertensive therapy could considerably improve LV pumping function. Preventive studies reveal that chronic blood pressure control can prevent cardiac dysfunction in SHR, as frequently is seen in the later phase of untreated arterial hypertension in humans.

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