The rate of force generation by the myocardium is not influenced by afterload

The influence of afterload on the rate of force generation by the myocardium was investigated using two types of preparations: the in situ dog heart (dP/dt) and isolated papillary muscle of rats (dT/dt). Thirteen anesthetized, mechanically ventilated and thoracotomized dogs were submitted to pharmacological autonomic blockade (3.0 mg/kg oxprenolol plus 0.5 mg/kg atropine). A reservoir connected to the left atrium permitted the control of left ventricular end-diastolic pressure (LVEDP). A mechanical constriction of the descending thoracic aorta allowed to increase the systolic pressure in two steps of 20 mmHg (conditions H1 and H2) above control values (condition C). After arterial pressure elevations (systolic pressure C: 119 ± 8.1; H1: 142 ± 7.9; H2 166 ± 7.7 mmHg; P<0.01), there were no significant differences in heart rate (C: 125 ± 13.9; H1: 125 ± 13.5; H2: 123 ± 14.1 bpm; P>0.05) or LVEDP (C: 6.2 ± 2.48; H1: 6.3 ± 2.43; H2: 6.1 ± 2.51 mmHg; P>0.05). The values of dP/dt did not change after each elevation of arterial pressure (C: 3,068 ± 1,057; H1: 3,112 ± 996; H2: 3,086 ± 980 mmHg/s; P>0.05). In isolated rat papillary muscle, an afterload corresponding to 50% and 75% of the maximal developed tension did not alter the values of the maximum rate of tension development (100%: 78 ± 13; 75%: 80 ± 13; 50%: 79 ± 11 g mm-2 s-1, P>0.05). The results show that the rise in afterload per se does not cause changes in dP/dt or dT/dt

Influência da elevaçáo transitória e da elevaçáo sustentada da pressáo arterial sobre a primeira derivada temporal da pressáo ventricular.

PURPOSE--To analyze the influence of transient and sustained elevations of arterial pressure (AP) on the rate of rise of the left ventricular pressure (dp/dt). METHODS--Thirteen anesthetized, thoracotomized and mechanically ventilated dogs, submitted to pharmacological autonomic block (oxprenolol-3 mg/kg plus atropine-0.5 mg/kg). The AP elevation was obtained by mechanical constriction of the descending thoracic aorta. Two protocols were applied to all animals: Transient Arterial Hypertension (TAH) and Sustained Arterial Hypertension (SAH) and the following variables were evaluated: heart rate (HR), systolic (LVSP) and end diastolic (LVEDP) left ventricular pressure and dp/dt. In TAH the variables were analyzed in the basal condition (To) and at the maximal value of AP attained during the transient pressure elevation (TM). In the protocol SAH the variables were evaluated in the conditions: Control (Ho), hypertension 1 (H1) and hypertension 2 (H2). RESULTS--Considering all conditions, there were no significant differences among the values of HR. In the protocol TAH, the LVSP varied from 133 +/- 22 mmHg to 180 +/- 27 mmHg, whereas in SAH the values of LVSP were as follow: HO = 129 +/- 25 mmHg; H1 = 152 = 23 mmHg; H2 = 182 +/- 24 mmHg. LVEDP changed in both protocols: To = 7 +/- 2 mmHg; TM = 13 +/- 2 mmHg (p < 0.05); Ho = 7 +/- 2 mmHg; H1 = 10 +/- 2 mmHg; H2 = 14 +/- 3 mmHg (p < 0.05). During TAH there was no difference between the values of dp/dt (To = 3.303 +/- 598 mmHg/s; TM = 3.350 +/- 653 mmHg/s; p > 0.05), however, there were increases of the dp/dt during SAH (Ho = 3.233 +/- 576 mmHg/s; H1 = 3.831 +/- 667 mmHg/s; H1 = 4.594 +/- 833 mmHg/2; p < 0.05). CONCLUSION--The values of dp/dt are not influenced by transient elevation of AP. Sustained increase of AP activates cardiac adjustments, which results in elevation of dp/dt, by stimulation of contractile state. Probably, the inotropic intervention mechanism is the length dependent activation due to the Frank-Starling mechanism.

Influencia da elevacao sustentada da pressao arterial sobre a dP/dt do ventriculo esquerdo mantendo-se constante a pressao diastolica do ventriculo esquerdo

Purpose - To evaluate the influence of sustained elevations of arterial pressure on dP/dt values, which the left ventricular end diastolic pressure was kept constant. Methods - Thirteen anesthetized dogs, mechanically ventilated and submitted to thoracotomy and pharmacological autonomic block (atropine - 0.5 mg/kg IV + oxprenolol - 3 mg/kg IV) were studied. The arterial pressure elevation was obtained by mechanical constriction of the descending thoracic aorta. Analyses were made in control (C) situation and after two successives increments of arterial pressure, sustained for 10min, called hypertension 1 (H1) and hypertension 2 (H2), respectively. The end diastolic left ventricular pressure was kept constant by utilization of a perfusion system connected to the left atria. Results - Heart rate did not change (C: 125 ± 13.9bpm; H1: 125 ± 13.5bpm; H2: 123 ± 14.1bpm; p > 0.05); the LVSP increased (C: 119 ± 8.1mmHg; H1: 142 ± 7.9mmHg; H2: 166 ± 7.7mmHg; p < 0.01); the AoDP increased (C: 89 ± 11.6mmHg; H1: 99 ± 9.5mmHg; H2: 120 ± 11.8mmHg; p < 0.01); the LVEDP (C: 6.2 ± 2.48mmHg; H1: 6.3 ± 2.43mmHg; H2: 6.1 ± 2.51mmHg; p > 0.05) and the dP/dt (C: 3068 ± 1057.1mmHg/s; 3112 ± 995.7mmHg/s; H2: 3086 ± 979.5mmHg/s; p > 0.05) did not change. Conclusion - dP/dt values are not influenced by a sustained elevation of arterial pressure, when the end diastolic left ventricular pressure is kept constant.