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PubMed2004

[Structural and functional cardiac changes and sex hormone levels in men with sexual dysfunctions].

44 men with chronic prostatitis were examined for structural-functional heart alterations with reference to severity of erectile dysfunction (ED). Sex hormones were also estimated. Control group consisted of 20 healthy men. Doppler echocardiography, 24-h monitoring of arterial pressure (AP) and ECG, finger and ultrasound investigation of the prostatic gland and microscopy of its secretion were made. Blood plasm testosteron, prolactin and dehydroepiandrosterone-sulphate were estimated by enzyme immunoassay. Erectile function was assessed by the questionnaire "International index of erectile function". Thus, sexual hormone changes associated with sexual dysfunction in men promote left ventricular diastolic dysfunction. The type of intracardiac hemodynamics in this case is, as a rule, restrictive.

Adult↗
PubMed1990

Effects of short-term training on cardiac function during prolonged exercise.

To determine the relationship between the training-induced increases in plasma volume (PV) and alterations in cardiac performance during prolonged submaximal cycle exercise, seven male subjects were studied prior to and following a short-term (3 d) training period (2 h.d-1 at 65% VO2max). Mean (range) VO2max was 3.42 l.min-1 (2.96-3.87). Training resulted in a 20% increase (P less than 0.05) in plasma volume (PV) and a 12% increase (P less than 0.05) in total blood volume (TBV). In contrast, training had no effect (P greater than 0.05) in altering exercise VO2, VCO2, VE BTPS, or RER. Cardiac output (Q) was higher (P less than 0.05) posttraining at all exercise sampling times (30, 60, 90, and 120 min). The elevations in Q were accompanied by an average decrease (P less than 0.05) in stroke volume (SV) of 22 ml. Arteriovenous O2 (a-v O2) difference was depressed (P less than 0.05) during exercise following the training. Although elevations (P less than 0.05) in core temperature (degrees C) occurred during the exercise, the training-induced PV increases did not affect thermoregulatory behavior. These results indicate that an early adaptive response to exercise training is an elevation in Q, an increase in SV, and a reduction in HR. These effects persist during prolonged exercise in spite of the progressive increase in body heat content. It is proposed that the increase in Q serves primarily to increase muscle blood flow and maintain arterial O2 delivery, while the altered cardiodynamic behavior serves to increase cardiac reserve, providing a greater tolerance to prolonged heavy exercise.

Adult↗
PubMed1982

Renal transplantation and cardiac function in pediatric patients.

Nine pediatric patients underwent echocardiographic evaluation prior to and after renal transplantation. Prior to transplantation parameters of cardiac contractility such as mean velocity of circumferential fiber shortening, ejection time, ejection fraction and shortening fraction were within the normal ranges for the age group. Post transplantation there was a significant decrease in heart rate and cardiac index. In addition a dramatic increase in hemoglobin levels was observed. The improvement in circulating hemoglobin levels rather than the removal of uremia appears to be the dominant beneficial result in improving cardiovasuclar hemodynamics.

Adolescent↗
PubMed2005

[Significance of serum calcium and phosphorus control for the cardiac function in patients with long term hemodialysis].

We evaluated how serum calcium and phosphorus will effect a cardiomegaly of hemodialysis patients. The cardiac valve of hemodialysis patients have a high incidence of calcification. Forty four percent of mitral valve and seventy five percent of aortic valve occurred the calcification, and the progress of calcification involve with increasing LVMI. The consequence of this results was that we consider prevent calcification is important to inhibiting factor of cardiomegaly, but serum calcium and phosphorus wasn't effect a cardiomegaly. On the other hand, we detected a significant negative correlation between serum calcium and LVMI (P = 0.0008) and a significant positive correlation between serum phosphorus and LVMI (P = 0.0105) . Consequently we thought that to control the serum phosphorus is important factor to inhibit the cardiomegaly.

Aged↗
PubMed1987

Morphine sulfate depression of cardiac function is attenuated by opiate receptor antagonism with naloxone.

In previous work, morphine sulfate was shown to decrease heart rate (HR) and cardiac output (CO) in a dose-related fashion. It was hypothesized that this effect was mediated by opiate receptors located in the myocardium. The present study evaluated the effect of opiate receptor antagonism with naloxone using a modified Langendorff rat heart perfusion apparatus. Sixty-five rat hearts were excised and perfused with Krebs-Henseleit buffer (KHB) solution, to which morphine sulfate and naloxone (NAL) were added in different concentrations. In the initial studies, NAL (10(-5) M) was added to the perfusate prior to the incremental additions of morphine. This resulted in no antagonism of the previously described opiate agonist effects. Norepinephrine (NE; 10(-9) M) was then added to the perfusate prior to the NAL or morphine. The NE did not affect the dose-related decrease in HR and CO when morphine was added but did permit the attenuation of the morphine effect by the addition of increasing concentrations of NAL up to 10(-5) M. These results suggest that the agonist effect can be attenuated by opiate receptor antagonism with NAL; the data also suggest a possible interrelationship between opiate and catecholamine receptor activity in the myocardium.

Animals↗
PubMed1985

Effect of chronic prazosin treatment on the cardiac function and electrolytes in failing heart due to chronic mitral insufficiency.

The effect of three months of prazosin treatment on the hemodynamics, cardiac extracellular space; plasma, tissue and intra-cellular Na+, K+, and Ca++ were investigated in dogs with left ventricular failure due to chronic mitral insufficiency. Mitral insufficiency of 6 months duration significantly decreased the LV systolic pressure, LV dp/dt, LV (dp/dt)/IIP, LVWI, CI, and increased the LVEDP, mean right atrial pressure, heart rate and systemic vascular resistance. Associated with these hemodynamic changes were an increase in the extra-cellular space, tissue and intracellular K+; and a decrease in the tissue and intracellular Ca++. Prazosin treatment produced an improvement in the hemodynamics which was associated with a decreased in the extracellular space, and intracellular K+, and an increase in the intracellular Ca++. Plasma Na+ and Ca++ increased with 6 months of M.I. Prazosin treatment brought back the plasma Na+ and K+ to control level. However, plasma Ca+ decreased significantly with prazosin treatment. The changes in right ventricular hemodynamics and electrolytes were not consistent with the right ventricular failure. These results indicate that decrease in the myocardial contractility in chronic heart failure due to mitral insufficiency might be due to a decrease in the intracellular Ca++. Prazosin treatment was able to reverse the hemodynamic and electrolyte changes induced by failing heart due to mitral insufficiency.

Animals↗
PubMed1999

Abnormal cardiac function in the streptozotocin-induced non-insulin-dependent diabetic rat: noninvasive assessment with doppler echocardiography and contribution of the nitric oxide pathway.

OBJECTIVES: We sought to evaluate in vivo and in vitro left ventricular (LV) geometry and function in streptozotocin-induced diabetic rats and the possible role of the nitric oxide (NO) pathway. BACKGROUND: Diabetes results in cardiac dysfunction; however, the specific abnormalities are unknown. Because decreased NO contributes to abnormal vascular function in diabetics, we hypothesized that NO pathway abnormalities may contribute to diabetic cardiomyopathy. METHODS: Control rats and those with non-insulin-dependent diabetes mellitus (NIDDM) underwent echocardiography, hemodynamic assessment, isolated heart perfusion and measurement of exhaled NO and LV endothelial constitutive nitric oxide synthase (ecNOS). RESULTS: Diabetic rats had increased LV mass (3.3 +/- 0.6 vs. 2.6 +/- 0.3 g/g body weight [BW], p < 0.001) and cavity dimensions (diastolic 2.0 +/- 0.1 vs. 1.8 +/- 0.2 cm/cm tibial length [TL], p < 0.05). Diabetic rats had prolonged isovolumic relaxation time (IVRT) (40 +/- 8 vs. 26 +/- 6 ms, p < 0.0001), increased atrial contribution to diastolic filling (0.47 +/- 0.09 vs. 0.30 +/- 0.08 m/s, p < 0.0001), and elevated in vivo LV end-diastolic pressure (7 +/- 6 vs. 2 +/- 1 mm Hg, p = 0.04). Diabetic rats had increased chamber stiffness. Shortening was similar in both groups, despite reduced meridional wall stress in diabetics, suggesting impaired systolic contractility. Exhaled NO was lower in diabetic rats (1.8 +/- 0.2 vs. 3.3 +/- 0.3 parts per billion, p < 0.01) and correlated with Doppler LV filling. The ecNOS was similar between the groups. CONCLUSIONS: Diabetic cardiomyopathy is characterized by LV systolic and diastolic dysfunction, the latter correlating with decreased exhaled NO. The NO pathway is intact, suggesting impaired availability of NO as contributor to cardiomyopathy.

Animals↗
PubMed2005

Effect of beta-blockers on cardiac function and calcium handling protein in postinfarction heart failure rats.

OBJECTIVES: The normal expression of Ca2+-handling protein is critical for efficient myocardial function. The present study was designed to test the hypothesis that beta-blocker treatment may attenuate left ventricular (LV) remodeling and cardiac contractile dysfunction in the failing heart, which may be associated with alterations of Ca2+-handling protein METHODS: We investigated the change of LV remodeling and function in a rat model of heart failure due to myocardial infarction (MI) with or without carvedilol (30 mg/kg/d) or metoprolol (60 mg/kg/d) treatment for 6 weeks (n = 9 in the MI plus carvedilol group, and n = 8 in every other group). The expression of messenger RNA and proteins of sarcoplasmic reticulum Ca2+-adenosine triphosphatase (SERCA) and phospholamban in cardiomyocytes of all rats were also measured RESULTS: There was significant LV remodeling and cardiac contractile dysfunction in MI rats. The messenger RNA and protein expression of SERCA were down-regulated (p < 0.01), but the expression of phospholamban messenger RNA and protein were up-regulated (p < 0.01) in MI rats compared to sham-operated rats. After the treatment with beta-blockers, LV remodeling and function were clearly improved. Carvedilol was better in attenuating the weight of the LV and the relative weight of the right ventricle than metoprolol (p < 0.05). beta-Blockers restored the low expression of SERCA (p < 0.05) but showed no effect on phospholamban expression (p > 0.05). Moreover, carvedilol induced a more significant improvement of SERCA expression than metoprolol (p < 0.05) CONCLUSIONS: Beta-blockers are effective in preventing LV remodeling and cardiac contractile dysfunction in the failing heart. The molecular mechanism may be related to normalization of SERCA expression.

Adrenergic beta-Antagonists↗