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Results for “Heart development”

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At least 433 records · Page 24Linked to original sources
PubMed2000

Effects of combined angiotensin II and endothelin receptor blockade with developing heart failure: effects on left ventricular performance.

BACKGROUND: The goal of this study was to determine the comparative effects of angiotensin II type 1 (AT(1)) receptor inhibition alone, endothelin-1 (ET) receptor blockade alone, and combined receptor blockade on left ventricular (LV) function, contractility, and neurohormonal system activity in a model of congestive heart failure (CHF). METHODS AND RESULTS: Pigs were randomly assigned to each of 5 groups: (1) rapid atrial pacing (240 bpm) for 3 weeks (n=9), (2) concomitant AT(1) receptor blockade (valsartan, 3 mg/kg per day) and rapid pacing (n=8), (3) concomitant ET receptor blockade (bosentan, 50 mg/kg BID) and rapid pacing (n=8), (4) concomitant combined AT(1) and ET receptor inhibition and rapid pacing (n=8), and (5) sham-operated control (n=9). LV stroke volume was reduced from the control value after rapid pacing, was unchanged with either AT(1) or ET receptor blockade alone, but was improved with combination treatment. LV peak wall stress was reduced in both groups with ET receptor blockade compared with the rapid pacing group. Plasma norepinephrine levels were increased by >3-fold after rapid pacing, remained increased in the monotherapy groups, but were reduced after combination treatment. LV myocyte velocity of shortening was reduced after rapid pacing-induced CHF, remained reduced after AT(1) receptor blockade, increased after ET receptor blockade (compared with rapid pacing-induced CHF values), and returned to within control values after combined blockade. CONCLUSIONS: Combined AT(1) and the ET receptor blockade in this model of CHF improved LV pump function, and contributory factors included the effects of LV loading conditions, neurohormonal system activity, and myocardial contractile performance. Thus, combined receptor blockade may provide a useful combinatorial therapeutic approach in CHF.

Angiotensin II↗
PubMed1999

Angiotensin-converting enzyme and matrix metalloproteinase inhibition with developing heart failure: comparative effects on left ventricular function and geometry.

The progression of congestive heart failure (CHF) is left ventricular (LV) myocardial remodeling. The matrix metalloproteinases (MMPs) contribute to tissue remodeling and therefore MMP inhibition may serve as a useful therapeutic target in CHF. Angiotensin converting enzyme (ACE) inhibition favorably affects LV myocardial remodeling in CHF. This study examined the effects of specific MMP inhibition, ACE inhibition, and combined treatment on LV systolic and diastolic function in a model of CHF. Pigs were randomly assigned to five groups: 1) rapid atrial pacing (240 beats/min) for 3 weeks (n = 8); 2) ACE inhibition (fosinopril, 2.5 mg/kg b.i.d. orally) and rapid pacing (n = 8); 3) MMP inhibition (PD166793 2 mg/kg/day p.o.) and rapid pacing (n = 8); 4) combined ACE and MMP inhibition (2.5 mg/kg b.i.d. and 2 mg/kg/day, respectively) and rapid pacing (n = 8); and 5) controls (n = 9). LV peak wall stress increased by 2-fold with rapid pacing and was reduced in all treatment groups. LV fractional shortening fell by nearly 2-fold with rapid pacing and increased in all treatment groups. The circumferential fiber shortening-systolic stress relation was reduced with rapid pacing and increased in the ACE inhibition and combination groups. LV myocardial stiffness constant was unchanged in the rapid pacing group, increased nearly 2-fold in the MMP inhibition group, and was normalized in the ACE inhibition and combination treatment groups. Increased MMP activation contributes to the LV dilation and increased wall stress with pacing CHF and a contributory downstream mechanism of ACE inhibition is an effect on MMP activity.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed2002

HAART patients can face greater risk of developing heart disease--studies.

Investigators from the HIV Outpatient Study group, which is located at 10 sites in the United States, found that after a few years of taking protease inhibitors, HIV patients were beginning to show a significantly increased rate of myocardial infarctions. The researchers presented their findings at the 2001 IDSA Conference, held Oct. 25-28, 2001.

Antiretroviral Therapy, Highly Active↗
PubMed1987

Cardiac hypertrophy in the developing heart.

To gain information on physiologic postnatal cardiac growth in humans and to characterize the left ventricle (LV) when subjected to various types of overload during that period, angiocardiographic volume parameters in infants, children, and adolescents were analyzed. In normal subjects, the relationships between end-diastolic volume (EDV), end-systolic volume (ESV), and stroke volume (SV) of the LV and right ventricle (RV), as well as the muscle volume (MV) of the LV and body surface area (BSA) were best fit by power functions with exponents of between 1.2 and 1.3. The EDV and ESV of the LV were smaller than those of the RV. Ejection Fraction (EF), muscle volume index (MVI = MV/EDV), and cardiac index (CI) were constant. In pressure loaded LVs, the MVI was elevated, and increased with increasing pressure load. The ESV tended to be smaller and EF tended to be higher than normal. There was no correlation between EF and EDV. In volume loaded LVs, MV was increased; the MVI, as well as the EF, was normal. The EDV and ESV were elevated without correlation between EF and EDV. In complete transposition of the great arteries. MVI diminished, increasing within months as a response to pressure underloading and overloading. In all groups, there was a negative correlation between EF and ESV, as well as between EF and the shape parameter elongation in systole. During postnatal growth, the normal heart grows overproportionally with respect to BSA, with the LV ejecting the same SV as the RV at a higher EDV and ESV. EF, MVI, and CI are age-independent parameters for assessment of cardiac function.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1989

Troponin I switching in the developing heart.

Monoclonal antibodies identify two distinct isoforms of troponin I in rat cardiac muscle, one predominant in the embryonic and fetal heart and one predominant in the adult heart. The two isoforms can be resolved by sodium dodecyl sulfate-polyacrylamide gel electrophoresis, with apparent molecular weights of 27,000 and 31,500, respectively. The adult isoform is specifically recognized by a monoclonal antibody that is unreactive with the embryonic variant, while two other monoclonal antibodies recognize both isoforms. A monoclonal antibody to cardiac troponin T was used to isolate by affinity chromatography the troponin complex from adult and neonatal rat heart. Affinity purified troponin from neonatal heart was found to contain both the embryonic and adult isoforms of troponin I. Comparative immunoblotting analysis with different muscle tissues shows that embryonic troponin I is identical with respect to electrophoretic mobility and pattern of immunoreactivity to the major troponin I isoform found in adult slow skeletal muscle. Troponin I switching may be implicated in developmental changes involving Ca2+ and pH sensitivity of the contractile system and response to beta-adrenergic stimulation.

Aging↗