Anatomical variations of acromions in brazilian adult’s scapulas

Introduction: According to morphology, acromion can be classified into three types: I (flat), II (curved),and III (hooked) and its characteristics are related to age and rotator cuff pathology. Here we haveanalyzed acromion ́s morphology in scapulas of Brazilian human skeleton and tried to establish possiblemorphofunctional correlations to literature data.Materials and Methods:Fifty-seven scapulas from HumanAnatomy laboratories of Universidade Federal de Minas Gerais were selected and divided in groups accordingto acromion ́s tip morphology and angle.Results:We observed that distribution of acromial morphologywas 5,2% type I (flat), 57,9% type II (curved), 36,9% type III (hooked).Conclusion:Our data is importantto compare Brazilian scapula bones to those from various other regions or races and could contribute todemographic studies of shoulder disease probability in Brazilian population.

Influence of the sarcoplasmic reticulum on the inotropic responses of the rat myocardium resulting from changes in rate and rhythm

1. The role of the sarcoplasmic reticulum (SR) in the inotropic responses produced by changes in stimulation rate and rhythm and resting tension was investigated in the rat myocardium. 2. Rat papillary muscles contracting isometrically (basic stimulation rate = 30/min) were superfused in vitro with normal Krebs solution and after addition of ryanodine (1 microM). Post-rest potentiation was obtained after pauses of 5, 10, 15, 30, 60 and 120 s, and the stimulation rate was changed from 6 to 90 bpm. Post-extrasystolic potentiation was induced by interpolating an extra stimulus after an interval of 413 +/- 15 ms. NiCl2 (2 mM) was used to confirm that contractions obtained after SR blockade with ryanodine were activated only by sarcolemmal calcium influx. 3. In the presence of ryanodine, the post-rest potentiation phenomenon disappears and the force-frequency relationship changes from the typical force decrease produced by rate increase to force increase. Under the effect of ryanodine, resting tension increased with the increase in stimulation rate. This behavior was enhanced by reducing extracellular KCl from 5.4 mM to 1 mM. This maneuver decreases Na(+)-K(+)-ATPase and increases intracellular Na+ activity, which reduces Ca2+ extrusion through the Na(+)-Ca2+ exchange mechanism. 4. SR participation in the post-extrasystolic potentiation phenomenon is also suggested because ryanodine treatment reversed the extrasystolic force depression into potentiation. In the presence of ryanodine, blockade of Ca2+ influx with NiCl2 (2 mM) abolished isometric contractions indicating that after SR blockade contractions are mainly dependent on sarcolemmal Ca2+ influx. 5. The results suggest that the SR is involved in the genesis of post-rest potentiation and contributes to the typical force-frequency relationship of the rat myocardium and to the post-extrasystolic potentiation phenomenon. Moreover, SR activity seems to be important for the maintenance of low resting tension in the cardiac muscle, which may represent a safety factor against contractures during inotropic changes produced in rate and rhythm.

Mechanisms underlying the genesis of post-rest contractions in cardiac muscle

Post-rest potentiation reflects basic cellular mechanisms that control cardiac muscle contraction. Transmembrane calcium influx, the Na+/Ca*+ exchange and the function of intracellular stores that liberate activator calcium upon activation are some of the mechanisms involved. Three aspects of the post-rest potentiated phenomenon were investigated, using isometrically contracting rat papillary muscles and toad ventricle strips: dependence on 1) inotropic state of steady-state contractions, 2) pause duration and Na+/Ca*+ exchange activity, and 3) the extent of transmembrane calcium influx. The results suggest that the potentiated state of post-rest contractions increases linearly with the inotropic state of preceding steady-state control contractions. As the pause duration increases from 5 to 240 s, the post-rest potentiation also increases, attaining a steady level after 30-s pauses. During the pause, the Na+/Ca*+ exchange mechanism operates at an activity level that can alter the amount of activator calcium used for post-rest contractions. Interventions that increase intracellular Na+, such as the increase of the stimulation rate from 0.5 to 1 Hz or the increase of extracxellular NaCl concentration to 160 mM, reduce the Na+/Ca*+ activity, increasing intracellular Ca*+ and post-rest potentiation. The decrease of transmembrane Ca*+ and post-rest potentiation. The decrease of transmembrane Ca*+ influx during activation increases the relative participation of the sarcoplasmic reticulum in the development of post-r5est potentiation. Reduction of extracellular Ca*+ concentration from 1.25 mM to 0.25 mM or the use of 1 uM verapamil and 2 mM manganese increases the relative potentiation of post-rest contractions. This is particulary observed in toad ventricle strips since post-rest potentiation, which does not develop under control conditions, is observed after verapamil or manganese treatment. The results suggest that the excitation contraction coupling process operating for post-rest contraction activation, unlike that operating for steady-state contraction activation, depends more on the calcium stored at intracellular sites than on transmembrane calcium influx

Heterometric regulation and calcium sensitivity of the infarcted rat heart

The surviving hypertrophied muscle remaining after myocardial infarction in rats is less sensitive to extracellular Ca2+ than the normal myocardium. Since the inotropic effect of Ca2+ is modulated by sarcomere lenght, the present study was undertaken to determine if Ca2+ desensitization of infarcted left ventricles (LV) can be modulated by increasing the diastolic pressure (DP). Rats submitted to left coronary artery ligation (N+11) or sham-operation (N=9) were killed 8-10 days later and their hearts perfused by the Langendorff technique. A balloon was introduced into the LV cavity to measure the isovolumic systolic pressure (ISP) produced by DP changes (0 to 25 mmHg) at three Ca2+ concentrations (0.8, 1.25 and 2.5 mM). In control hearts submitted to a DP of mmHg, the ISP increased from 36ñ3 to 63ñ4 and to 74ñ4 mmHg as external Ca2+ was changed from 0.8 to 1.25 and to 2.5 mM, respectively. in contrast,in infarcted hearts submitted to the same DP and Ca2+ concentrations, the ISP increased from 19ñ2 to 26ñ2 and to 27ñ3 mmHg. The depressed response to Ca2+ was not modified by increasing DP up to 25 mmHg, the greatest DP tested. At this DP, ISP increased from 75ñ4 to 103ñ5 and 114ñ5 mmHg control hearts and from 45ñ2 to 54ñ3 and to 55ñ4 mmHg in infarted hearts. Ventricular function curve normalization in relation to a DP of 5 mmHg, indicated that the relative increases of ISP as a function of DP, produced by infarcted hearts, were higher than controls for DP higher than 10 mmHg. These results indicate that indicate that desensitization to extracellular Ca2+ of infarcted hearts cannot be reduced by increasing preload levels. However, the depressed mechanical response may be partially compensated for by an improvement of the length-dependent contractile response of the hypertrophied muscle surviving infarction

Post-rest contractions of amphibian cardiac muscle

Post-rest potentiated contractions have been reported to be more dependent on Ca2+ stored in intracellular sites than on transmembrana Ca2+ influx. The phenomenon was examined using toad ventricular strips contracting isometrically and superfused with Ringer solution. Toad ventricular strips did not present post-rest potentiation, a fact that may be explained be the reduced volume of the sarcoplasmic reticulum in the amphibian myocardium. Potentiated post-res contractins were obtained after calcium influx blockade with 10 µM verapamil or 2mM Mn2+ and the slow reduction of extracellular Ca2+ concentration obtained by slowly exchanging the bath fluid was accompanied by a progressive decrease of both steady-state and post-rest contractions. These data suggestion of the dependende of post-rest potentiation on activator calcium liberated from intracellular stores

Time course of changes in heart rate and sympathetic tone after coronary artery ligation in rats

The purpose of this study was to investigate the changes of heart rate (HR) and sympathetic tone occuring after myocardial infarction. Male rats (200-250 g) were submitted to ligation of the anterior branches of the left coronary artery to produce infarction (INF, N = 26) or to sham surgery (SO, N = 24). Groups of animals (N = 6-8) were studied 1, 3, 7 and 15 days later. A group not submitted to surgical procedures was used as control (C, N = 6). Bood pressure and HR were measured in conscious unrestrained animals after cannulation of the femoral artery. Basal HR and mean arterial pressure (MAP) of C groups were 336 ñ 8 beats/min (bpm) and 110 ñ 3 mmHg, respectively. Similar values were observed in SO subgroups. One day after INF, HR increased to 417 ñ 9 bpm and MAP decreased to 97 ñ 2 mmHg. While MAP was unchanged for the reminder of the study, HR progressively decreased and normal HR values (360 ñ 18 bpm) were observed two weeks after INF. The synpathetic tone, which was evaluated from the reduction of HR after propranolol (2 mg/Kg, iv), was increased during the tachycardic phase after INF. HR normalization paralleled the progressive reduction of sympathetic tone. The changes in HR after coronary artery ligation in rats seem to reflect the g=degree of sympathetic efferent activity during infarct healing

Activation of the langendorff perfused rat heart under depolarizing conditions

Myocardial activation under depolarized conditions was studied in spontaneoustly beating Langendorff perfused hearts from albino rats. Depolarization was obtained incrasing external potassium concentration in steps (5.4, 7.4, 10, 10.5, 11, 11.5 mM) in the perfusisng solution. Left ventricular isovolumic systolic pressure and coronary flow did not change as external potassium increased, but the atrial and ventricular beat rates decreased, the latter showing a larger decline. In the electrocardiogram, the P-R interval increased as a function of external potassium and the amplitude of the ORS complex diminished as its duration invreased. The mamjority of perfused hearts stopped punping when external potassium was raised to 11.5 mM

Effect of urea on the mechanical and electrical activity of the perfused rat heart

The mechanical and electrical activities of Langendorff perfused isolated hearts from albino female rats were studied before and after the addition of 17 mM urea to the medium. The effect of urea on the osmolarity of the perfusing solution was evaluated by also carrying out the measurement in 17 mM saccharose. The rate of the spontaneously beating hearts did not change after urea or saccharose treatment. However, urea promoted a decrease in the left ventricle isovolumic systolic pressure and a reduction of the total QRS amplitude. Saccharose did not alter mechanical or electrical characteristics. Although the concentration of urea which reduced systolic isovolumic pressure development and altered the ECG is well below that required to modify protein conformation in vitro, our results suggest that its action could be at the sarcolemmal level

Right ventricular contractility depression in chronically infarcted rats

We studied the in vitro mechanical performance of right ventricular strips obtained from male albino rats submitted to left coronary ligation for 30 days. The infarcted rats developed significant right ventricle hypertrophy together with a reduction of the isometric tension when compared to controls. The reduction was maintained even under positive inotropic intervention, i.e. the cumulative dose-response curves to calcium and adrenaline were displaced downward in parallel in the hypertrophied muscles. We conclude that after 30 days of left ventricle infarction the hypertrophied right ventricular myocardium presents a significant reduction of contractility

Depression of myocardial force development after urea treatment

Left ventricle papillary muscles from /wistar male rats were studied before, during and after urea treatment, Urea was used at a concentration (17 mM) equivalent to a plasma level of 100 mg/dl. To verify whether these effects were produced by an increase in osmolarity, the study was repeated using 17 mM saccharose. The results showed that isometric force development decreased after washing out urea from the bath but inotropic responses to isoproterenol (IPA) and increased extracellular calcium attained values similar to those obtained before urea treatment. Thus, the percentual increments due to IPA and calcium were enhanced after urea treatment. The increased osmolarity due to saccharose did not produce any change in contraction or in the responses to intropic interventions. It suggested that urea modifies the excitation-contraction coupling mechanism in heart muscle, reducing the force developed at the steady state control level without reducing the responses to the inotropic interventions

The effect of verapamil on potentiated rest contractions in the rat ventricular myocardium

The effects of verapamil (0.3 to 30 micronM) on potentiated rest contractions (PRC) were studied in isometric contractions of left ventricular papillary muscles of the rat. The post-rest potentiation was studied after rest periods of 5, 10, 15, 30, 60 and 120 s. Verapamil reduced the steady-state force and PRC in a dose-dependent manner, However, PRC were less depressed and the magnitude of this depression decreased as the rest period increased. The time constant of the recovery of steady state force after rest potentiation was shortened. These results indicate that the first PRC are less dependent on calcium entering the cell through the slow channels and apparently more dependent on an intracellular calcium store