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The role of high sodium intake in the development of left ventricular hypertrophy (LVH), a well-known risk factor for cardiovascular disease, was examined. High sodium intake is one of several nonhemodynamic factors that could contribute to LVH. The study involved the assessment of the effects of various sodium intake regimes on spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto rats (WKY). The results showed high sodium intake increased cardiac mass in WKY rats, and further increased cardiac mass in SHR rats. These results indicate a role for high sodium intake in the pathogenesis of cardiac hypertrophy.

The effects of prolonged treatment (3 weeks) with nitrendipine (10 mg·kg−1 twice daily) on systemic and regional haemodynamics and cardiac mass were studied in SHR and WKY rats. Nitrendipine markedly decreased mean arterial pressure (26.0±0.4 vs 19.9±0.6 kPa, P<0.01) and total peripheral resistance (0.090±0.004 vs 0.066±0.004 U·kg−1, P<0.01) in SHR without significantly affecting cardiac output and heart rate, whereas in the WKY rats no significant systemic haemodynamic changes were noted. Increased splanchnic blood flow and a reduced splanchnic vascular resistance were found in the WKY rats; however, in the SHR rats, blood flows (ml·min−1·g tissue−1) increased and organ vascular resistances (kPa·ml−1·min−1·100 g tissue−1) decreased significantly (P<0.001) in the heart (5.25±0.28 vs 7.27±0.31 and 0.04±0.00 vs 0.02±0.00; P<0.01), and kidneys (6.53±0.4 vs 7.98±0.2 and 0.03±0.00 vs 0.02±0.00; P<0.01) respectively. Nevertheless, in both rat strains, absolute cardiac mass and left ventricular weight were reduced; but in the SHR rats, the relative weight of the heart and left ventricle to body weight was also reduced significantly (3.79±0.06 vs 3.31±0.09; P<0.01 and 2.85±0.06 vs 2.70±0.06; P<0.01, respectively). Thus, these studies show that nitrendipine, a slow-entry channel calcium blocker, regressed cardiac mass in rats through mechanisms that may be dissociated from their haemodynamic changes. [ABSTRACT FROM PUBLISHER]

Prolonged treatment of spontaneously hypertensive (SHR) rats with either methyldopa or clonidine significantly and similarly reduced mean arterial pressure. Heart rate increased with methyldopa but decreased with clonidine; other haemodynamic effects were similar. SHR treated with methyldopa, but not clonidine, had significantly reduced cardiac masses and heart weight to body weight ratios than did rats receiving the vehicle. Normotensive Wistar Kyoto (WKY) rats treated with methyldopa also had lower cardiac masses than their controls, but exhibited no significant changes in systemic haemodynamics. Treatment with the vasodilator hydralazine increased cardiac output and decreased total peripheral resistance in both SHR and WKY, but the decrease in mean arterial pressure was significant only in SHR. Heart rate was decreased and heart weight to body weight in WKY was elevated. Cardiac mass did not change. Minimal changes in regional haemodynamics were noted, with hydralazine eliciting a decrease in most organ vascular resistances. The data indicate the regression of hypertrophy following antihypertensive therapy was not solely dependent upon haemodynamic factors; nor was it necessarily the effect of suppression of the adrenergic system, since the results obtained with methyldopa and clonodine were similar. [ABSTRACT FROM PUBLISHER]

Studies were conducted in vitro to determine the permeability characteristics of the rabbit and dog pericardium. The hydraulic conductance (Lp), which was significantly higher than other tissue, was 1.6 ± 0.19 × 10−4 and 1.78 ± 0.18 × 10−4 g · cm−2 · min−1 · cm H2O−1* (mean ± SEM), respectively, for the rabbit and dog pericardium. For various solutes, the permeability coefficient (P) of the pericardium for the rabbit was: 1.40 ± 0.10 × 10−4 cm · s−1 for water, 0.50 ± 0.03 × 10−4 cm · s−1 for glucose, and 0.73 ± 0.005 × 10−4 cm · s−1 for albumin. The reflection coefficient, α, for various solutes was: glucose 8.89 ± 0.86 × 10−4, sucrose 15.7 ± 1.5 × 10−4, dextran (molecular weight 40 000) 0.39 ± 0.03, albumin 0.42 ± 0.05, and for haemoglobin 0.58 ± 0.06. These results, which indicate that the pericardium offers little resistance to the bulk transfer of liquids and to the passage of large molecules, are discussed as possible safety factors during pericardial effusion. [ABSTRACT FROM PUBLISHER]

Changes in left ventricular internal diameter resulting from increasing intrapericardial pressure induced by increasing the pericardial fluid volume were studied in closed chest, anaesthetized dogs. Left ventricular internal diameters were measured by placing an ultrasonic dimension catheter in the left ventricle at the time of the experiments. With increasing pericardial pressure, significant increases occurred in heart rate and mean left atrial pressure. Left ventricular end-diastolic and end-systolic diameter progressively decreased as the pericardial pressure was elevated. After beta adrenergic blockade with propranolol (1 mg/kg), the decline in end-systolic diameter during pericardial tamponade was significantly reduced. These observations indicate the importance of the systolic reserve and the role of beta adrenergic receptors in the adaptation of the left ventricle to increases in pericardial tamponade. [ABSTRACT FROM PUBLISHER]