End-systolic Pressure-length Relations Research Articles

Ischemic preconditioning does not acutely improve load-insensitive parameters of contractility in in vivo stunned porcine myocardium

Objective: Ischemic preconditioning has been shown to have no beneficial effect on segment shortening in in vivo regionally stunned myocardium. The purpose of this study was to determine whether ischemic preconditioning improves the recovery of postischemic ventricular function when contractility is assessed by load-insensitive measurements including end-systolic pressure length relations, preload recruitable stroke work, and preload recruitable stroke work area in in vivo regionally stunned porcine myocardium. Methods: Open chest, pentobarbital-anesthetized pigs were used. Regional ventricular function was monitored by measurements of segment shortening, stroke work, end systolic pressure length relations, preload recruitable stroke work, and preload recruitable stroke work area. The control group was submitted to 15 minutes of left anterior descending coronary artery occlusion and 3 hours of reperfusion. The preconditioned group underwent 2 cycles of 5-minute left anterior descending coronary artery occlusion and 10-minute reperfusion before 15 minutes of occlusion. Results: There was no infarct in either group. The preconditioning protocol significantly depressed preischemic segment shortening but not regional stroke work. Ischemic preconditioning had no significant beneficial effect on regional stroke work, end-systolic pressure length relations, preload recruitable stroke work, or preload recruitable stroke work area. Conclusions: These results confirm that ischemic preconditioning does not ameliorate in vivo porcine myocardial stunning and indicate that ischemic preconditioning may have a limited cardioprotective role during cardiac operation. (J Thorac Cardiovasc Surg 1999;117:810-7)

Effects of endurance training on left ventricular performance: a study in anaesthetized rabbits.

Endurance training is known to increase ventricular performance during exercise and to decrease resting heart rate. The aim of this study was to evaluate a model for endurance training in rabbits and to study the effects of endurance training on local myocardial performance in the left ventricle during resting conditions. One group of rabbits underwent a 10-week exercise training programme. The rabbits trained 5 days a week on a treadmill. Training periods increased gradually from 15 min to 1 h with increments in speed from 0.5 to 1.2 km h-1. After the training programme the rabbits were anaesthetized and studied as acute open-chest preparations. A micro-tip pressure transducer was introduced via apex to the left ventricle and two pairs of ultrasonic crystals were implanted in the left anterior wall to measure segment lengths. One pair measured shortening in the circumferential direction whereas the other pair measured shortening in the longitudinal direction. Heart rate was lower in the trained group (n = 5), 172 +/- 9 beats min-1 (mean +/- SEM), compared with 235 +/- 19 beats min-1 in the control group (n = 8) (P < 0.02). Stroke volume, measured by radio-nuclidelabelled microspheres, was greater in the trained rabbits compared with controls (P < 0.03). Shortening in both segments was of similar magnitude for the trained and control groups. End-systolic pressure-length relations (ESPLR) obtained by occlusion of the descending aorta (balloon catheter) showed reduced slopes for longitudinal segments in the trained group compared with the control group (P < 0.05). We conclude that this endurance training programme in rabbits can be used to study myocardial effects of endurance training. Furthermore, the less steep slope of ESPLRs for the longitudinal segment in the trained animals might indicate a structural myocardial remodelling and increased contractile reserve that might be recruited during adrenergic stimulation in the trained group.

Regional nonischemic performance as assessed by end-systolic measures of shortening and thickening

Objectives. Nonischemic contractile segmental performance was characterized by the end-systolic pressure-length and pressure-thickness relations during regional ischemia induced by proximal left anterior descending and left circumflex coronary artery occlusions.Background. The increases in shortening and thickening of the nonischemic myocardium during acute ishemia have been attributed to alterations in the regional loading conditions. However, it is uncertain to what extent ischemia affects the contractile performance of the nonischemic zone.Methods. Twenty-seven beagle dogs were instrumented with sonomicrometers and micromanometer pressure gauges. End-systolic pressure-length and pressure-thickness relation data were obtained during vena cava balloon inflation. Control data were obtained in both left anterior descending and left circumflex regions. Then, in random order, either the left anterior descending or left circumflex coronary artery was occluded for 90 s, and hemodynamic and nonischemic end-systolic pressure-length and pressure-thickness data were obtained. After a 45-min recovery period, the other artery was occluded, and the same recordings were obtained.Results. The end-systolic pressure-length relation exhibited variable degrees of rightward and downward shifts and the end-systolic pressure-thickness relation variable degrees of leftward and downward shifts. Left circumflex coronary artery occlusion was associated with a greater downward displacement (decreased slope) of the nonischemic end-systolic pressure-length relation than left anterior descending coronary artery occlusion. The baseline slope was the best predictor of the change in slope of the end-systolic pressure-length and pressure-thickness relations. The left circumflex coronary artery supplied a larger proportion of left ventricular myocardial mass than the left anterior descending coronary artery.Conclusions. Acute ischemia profoundly affects the end-systolic performance of the nonischemic segment. Furthermore, the site, and probably size, of the ischemic zone may be important determinants of nonischemic contractile performance.

Negative inotropic effect of propranolol is attenuated in underperfused feline heart with an acute ischemic region.

beta-Adrenergic blockade alleviates myocardial ischemia, probably largely through heart rate (HR) reduction. We hypothesized that the negative inotropic effect of beta-blockade, which is believed to be potentially dangerous, is attenuated in underperfused hearts with an acute coronary artery occlusion. We studied the effect of intravenous propranolol (1 mg/kg i.v.) in feline hearts with acute circumflex coronary artery (LCX) occlusion by cross-oriented segments in normally perfused and mildly underperfused left ventricular (LV) anterior wall. A control group (n = 10) was compared with a stenosis group (n = 9) in which the mean coronary perfusion pressure was reduced (91 +/- 4 g vs. 136 +/- 5 mm Hg, p < 0.01). End-systolic pressure-length (ESP-ESL) relations during dynamic afterload increase and preload reduction were calculated to evaluate regional inotropy. HR and LV peak systolic blood pressure (LVSP) decreased in both groups after beta-blockade (p < 0.05). Subendocardial and mid-myocardial blood flow measured by radiolabeled microspheres decreased in the control group (p < 0.05) but was unchanged in the stenosis group. Systolic shortening of circumferential segments also decreased in the control group (p < 0.05) but was unchanged in the stenosis group. ESP-ESL relations of circumferential segments shifted markedly rightward in the control group, whereas a modest rightward shift was noted in the stenosis group. This study in feline heart with acute LCX occlusion showed an attenuated negative inotropic effect of beta-blockade in underperfused LV anterior wall.

End-systolic pressure length relations of stunned right and left ventricles after inotropic stimulation

Regional end-systolic pressure-segment length relationships (ESPSLR) were used to compare the degree of right and left ventricular stunning induced by a 10-min occlusion of the left anterior descending coronary artery and the response to subsequent atrial pacing (50 beats/min above intrinsic heart rate) without and with dobutamine (2 micrograms.kg-1.min-1) in nine anesthetized open-chest pigs. From the ESPSLR, the slope (Ees) (at 100 mmHg for the left and 25 mmHg for the right ventricle) and the total area of the pressure-length relationship (PLA) were determined. From the latter, the distribution into external work (EW) and potential energy (PE) as well as the efficiency of energy transfer (EET = EW/PLA) were calculated. In both the stunned left and right ventricular myocardium Ees and EW were reduced according to the same linear regression equations (delta Ees = 0.7 Ees,baseline - 11.4, r2 = 0.86 and delta EW = 0.4 EWbaseline + 2.3, r2 = 0.67), where Ees,baseline and EWbaseline are Ees and EW at baseline, respectively. EET of the stunned left and right ventricular segments decreased as PLA remained unchanged, due to an increase in PE. EET decreased from 0.84 +/- 0.02 to 0.71 +/- 0.03 (P < 0.05) in the stunned right ventricular segment and from 0.71 +/- 0.02 to 0.44 +/- 0.03 (P < 0.05) in the stunned left ventricular segment. Atrial pacing did not affect EET with respect to stunning levels, whereas the additional infusion of dobutamine restored Ees, EW, and PE and consequently EET to baseline values. In conclusion, the right ventricle is susceptible to stunning. During atrial pacing the EET was lower than expected from the Ees, which could, in agreement with the time-varying elastance concept, be explained by an increase in afterload (a consequence of the decrease in stroke volume). Dobutamine not only increased Ees, EW, and EET but also restored the relationship between Ees and EET in both ventricular stunned segments.

Non‐uniformity of two‐dimensional myocardial deformation in response to chronotropic and inotropic stimulation in cats

The degree of uniformity of myocardial deformation for cross-oriented segments in the anterior wall of the left ventricle is influenced both by loading conditions and by infusion of isoprenaline. The aim of this study was to clarify the chronotropic influence (atrial pacing) compared to the combined inotropic and chronotropic effects of isoprenaline on uniformity of contraction. In eight open-chest pentobarbitone-anaesthetized cats segment performance was measured by orthogonal sonomicrometry. Heart rate (HR) increased from control state, 199 +/- 5 (mean +/- SEM) beats min-1, to 224 +/- 6 and 227 +/- 7 beats min-1 during atrial pacing and isoprenaline infusion, respectively (P < 0.0005). Circumferential segment shortening remained unchanged during pacing but increased with isoprenaline (P < 0.0005). Longitudinal segments showed reduced shortening during pacing (P < 0.05), whereas shortening during isoprenaline infusion did not differ from control shortening. The ratio between shortening of longitudinal and circumferential segments, long/circ ratio, changed from 0.52 +/- 0.13 in the control state to 0.36 +/- 0.10 during pacing and 0.39 +/- 0.11 with isoprenaline (P < 0.05). End-systolic pressure-length relations were unchanged by atrial pacing but showed leftward shifts during isoprenaline infusion. Myocardial tissue blood flow (microspheres) was unchanged during interventions. We conclude that both atrial pacing and isoprenaline infusion lead to a more non-uniform deformation in the anterior wall. However, non-uniformity during atrial pacing was primarily related to reduced longitudinal shortening whereas the non-uniformity during isoprenaline infusion was due to increased circumferential shortening.

Postjunctional alpha-adrenergic stimulation of inotropy in hypoperfused myocardium outside an acute infarct.

The functional significance of myocardial postjunctional alpha-adrenergic support of inotropy in the vicinity of an acute regional ischemic zone was addressed in pentobarbital-anesthetized, beta-adrenergic blocked cats with circumflex coronary artery occlusion. Regional myocardial performance was measured by ultrasonic crystals in the anterior wall perfused by the left anterior descending coronary artery (LAD) before and during postjunctional alpha-adrenergic antagonism (SK&F 104078 2 mg/kg). A group with unrestricted flow in the LAD (control group) was compared with a group perfused below the autoregulatory pressure range (stenosis group). End-systolic pressure-length relations during dynamic after-load elevation were calculated for assessment of regional contractility. Regional myocardial blood flow (RMBF) was measured by radioactive microspheres. SK&F 104078 did not alter regional myocardial shortening or the slope of end-systolic pressure-length relations in the control group. In the stenosis group, however, alpha-adrenergic antagonism produced significant deterioration of shortening as well as consistent reduction of the slope of the end-systolic pressure-length relations (p < 0.05). As a reflection of reduced demands for perfusion, impairment of midmyocardial and endocardial blood flow occurred in the stenosis group (p < 0.05). These findings imply a negative inotropic effect of SK&F 104078 in metabolically vasodilated myocardium in the vicinity of an acute ischemic region.

Compensatory regional contraction following coronary artery occlusion depends on subendocardial hyperaemia and hyperkinesis.

The effects of circumflex coronary artery occlusion on regional myocardial performance and blood flow in the left ventricular anterior wall was studied, using 16 thoracotomized pentobarbital-anaesthetized cats. Two pairs of ultrasonic crystals were placed in the midwall; one segment (longitudinal) parallel to the subendocardial fibres, the other (circumferential) being aligned to the fibres of the outer half-layer. A shunt line from the right subclavian artery to the main left coronary artery was unrestricted in eight cats (Group A) and clamped in another eight cats (Group B) until coronary perfusion pressure was clearly reduced with only a minor reduction in shunt flow, but without changes in global cardiac function. After circumflex coronary occlusion hyperkinesis was most pronounced in segments parallel to subendocardial fibres (longitudinal), also validated as a marked leftward shift in the end-systolic pressure-length relation of these segments. Such a shift may indicate decreased regional afterloading along the cardiac major axis. Hyperkinesis of longitudinal segments was attenuated in Group B where a fixed shunt stenosis hampered subendocardial and mid-myocardial hyperaemia. The lesser hyperkinesis of Group B was associated with decreased left ventricular systolic pressure and cardiac output. Thus, impaired compensatory contraction outside an acute ischaemic region was produced by a significant coronary stenosis which precluded the subendocardial hyperaemia and hyperkinesis of that region.

Non-uniform and non-linear end systolic pressure-length relations at low left ventricular pressures in anaesthetised cats

The aims were (1) to establish a basis for measurements of regional inotropy using the slope (E) of the linear part of the end systolic pressure-length relation; (2) to investigate the range of end systolic pressure where linearity is valid, and particularly its lower pressure limit, called turning point pressure; (3) to determine whether local myocardial inotropy measured by normalised slope, E(n), varies with segment orientation Pressure and two cross oriented segment lengths were measured in the left ventricle. One pair of crystals measured a longitudinal segment, aligned with anterior midwall fibre direction; another pair measured a transverse segment, aligned with endocardial and epicardial fibre direction. Temporary obstruction of the inferior caval vein and descending aorta were performed to produce a wide pressure range of end systolic pressure-length relations during basal as well as high inotropic states (isoprenaline). Seven open chest cats anaesthetised with sodium pentobarbitone and nitrous oxide were used. MEASUREMENTS AND MAIN RESULTS - Turning point pressure for longitudinal segments showed lower values than for transverse segments (p less than 0.05). With isoprenaline, turning point pressure increased for all transverse segments, at 103(SEM 8) v 153(19) mm Hg (p less than 0.05), whereas no change occurred for longitudinal segments, at 82(4) v 87(7) mm Hg. In the basal state, E(n) showed lower values in all longitudinal segments compared to transverse segments, except for one pair. E(n) of all segments increased during isoprenaline infusion, except in one segment where no change occurred. CONCLUSIONS - There is a lower limit for linearity of end systolic pressure-length relations; this is affected by segment orientation as well as by the inotropic state of the heart. E(n) as a measure of regional inotropy varies with segment orientation, but offers a local measure of changes in inotropic state.

End systolic pressure-length relations in halothane anaesthetised dogs: effects of regional ischaemia and inotropic agents

The aim was to investigate the effects of regional myocardial ischaemia, calcium, and verapamil on (a) the hysteresis and (b) slope and length axis intercept of the left ventricular end systolic pressure-length relationship. Segment length in myocardium supplied by the left anterior descending coronary artery was measured in anaesthetised dogs using sonomicrometry. Three levels of regional myocardial ischaemia were produced by stenosis and occlusion of the left anterior descending artery (ischaemia 1, ischaemia 2, and occlusion). A snare placed around the descending thoracic aorta was used to obtain temporary aortic occlusions. Seven open chested mongrel dogs were used, weight 17 kg (range 16-20). After abrupt release of temporary aortic occlusions, end systolic lengths were greater than before the occlusion in the normal myocardium. This hysteresis was abolished by regional myocardial ischaemia. However, hysteresis was insensitive to calcium and verapamil. The length axis intercept of the end systolic pressure-length relationship was increased during ischaemia 2, during coronary occlusion, and after administration of verapamil; its slope was increased after coronary occlusion. (1) Viscoelastic properties of the myocardium make a major contribution to hysteresis of the end systolic pressure-length relationship; and (2) the length axis intercept of this relationship is not constant and its slope does not appear to be a sensitive indicator of regional myocardial contractility during regional ischaemia.

Comparison of End-Systolic Pressure—Length Relations and Preload Recruitable Stroke Work as Indices of Myocardial Contractility in the Conscious and Anesthetized, Chronically Instrumented Dog

Development of an index of myocardial contractility that is both load independent and easily quantified in vivo has been a difficult task. Recently, three measures of contractile state have been advocated that appear to fulfill these requirements: the end-systolic pressure-length relationship (ESPLR), the ESPLR area, and regional preload recruitable stroke work (PRSW). Because the effects of halothane and isoflurane on these indices of contractility have yet to be studied, the purpose of this investigation was to compare the effects of these volatile anesthetics on contractile function as evaluated via these techniques in chronically instrumented dogs. Because autonomic nervous system tone substantially influences systemic hemodynamics in vivo, experiments were performed in the presence of pharmacologic blockade of the autonomic nervous system. Four groups comprised the 36 experiments that were performed with nine dogs. Following inhalational induction, the dogs were maintained on 1.5 MAC and 2 MAC of halothane or isoflurane. Pressure-length loops were generated after 1 h of equilibration using preload reduction via partial inferior vena caval occlusion or afterload augmentation by a phenylephrine infusion. The PRSW and ESPLR were then calculated, respectively. Slope and length intercept variables obtained from the ESPLR failed to significantly change from control with increasing levels of anesthetic depth despite substantial decreases in other indices of contractility. However, combination of slope and length intercept parameters into the ESPLR area model proved to be a sensitive and easily calculable measure of depressed myocardial function. Similarly, regional PRSW slope precisely reflected changes in contractile state when halothane (62 +/- 10 for control to 30 +/- 6 erg.cm-2.10(-3).mm-1 at 2 MAC) or isoflurane (83 +/- 14 for control to 55 +/- 8 erg.cm-2.10(-3).mm-1 at 2 MAC) were administered. The PRSW slope also demonstrated a significant difference in depressed contractility when equianesthetic concentrations of halothane and isoflurane were compared (63 +/- 7% of control with halothane versus 86 +/- 4% of control with isoflurane at 1.5 MAC; 50 +/- 5% of control with halothane versus 70 +/- 6% of control with isoflurane at 2 MAC). The ESPLR area also accurately demonstrated the differential depression in contractile function suggested by recent in vitro studies when equianesthetic doses of halothane and isoflurane were compared in vivo. Therefore, while ESPLR slope and length intercept variables fail as indices of myocardial contractility, ESPLR area and regional PRSW slope were shown to be useful indicators of contractile state in the conscious and anesthetized dog.

Neutrophil depletion does not prevent myocardial dysfunction after brief coronary occlusion

Recent evidence suggests that oxygen free radicals generated during ischemia or reperfusion may contribute to myocardial dysfunction after brief coronary occlusion (“myocardial stunning”). Because neutrophil leukocytes represent a potential source of oxygen radicals, the concept of whether depletion of neutrophils could attenuate myocardial stunning after 10 min of ischemia was examined. In 16 anesthetized dogs, the left anterior descending coronary artery was perfused by an extracorporeal circuit, either with (n = 8) or without (n = 8) neutrophil filters in the perfusion line. The group with filters had near total absence of neutrophils in blood perfusing the left anterior descending coronary artery territory (16 ± 8 versus 1,826 ± 399/μl in the control group). Systolic myocardial shortening and end-systolic pressure-segment length relations were recorded during rest conditions and during incremental intracoronary infusion of dobutamine (5 to 15 μg/min) before and after 10 min of coronary flow occlusion.Before coronary occlusion, systolic myocardial shortening at rest was similar in control (15.4 ± 1.7%) and neutropenic (12.4 ± 2.2%) groups. Dobutamine (15 μg/ min) resulted in increased shortening in both control (18.2 ± 1.4%, p < 0.01) and neutropenic (15.8 & 1.5%, p < 0.05) groups and in a leftward shift of the end-systolic pressure-length relation. During coronary occlusion, collateral coronary flow to the left anterior descending coronary artery territory was not significantly different in the control (0.10 ± 0.03 ml/min per g) and neutropenic (0.18 ± 0.06 ml/min per g) groups.After 20 min of reperfusion, myocardial shortening was equally reduced in both groups (control 5.6 ± 2.8%; neutropenic 4.5 ± 2.4%, p = NS versus control), and the end-systolic pressure-length relation was similarly shifted to the right, consistent with reduced myocardial contractility. Intracoronary dobutamine (15 μg/min) produced similar increases in systolic shortening in the two groups (control 10.8 ± 1.6%, p < 0.01 versus rest; neutropenic 9.6 ± 2.6%, p < 0.01 versus rest; p = NS versus control). However, myocardial shortening remained less than preocclusion levels and the end-systolic pressure-length relations remained shifted to the right, indicating persistent contractile dysfunction in both groups. These observations do not support a major role for neutrophil leukocytes in the pathogenesis of myocardial stunning after brief coronary occlusion.

Time-dependent increase in left ventricular contractility following acute volume loading in the dog.

Acute volume alterations were produced in eight anesthetized dogs to determine if the contractility of the left ventricle is partially volume-dependent. Pressures were measured in the left ventricle with a micromanometer and regional ventricular function was measured with sonomicrometers implanted in the midwall of the anterior, lateral, and posterior left ventricle. Regional end-systolic pressure-length relations (ESPLR) were determined with transient venae cavae occlusions. The ESPLR data were fitted to a quadratic equation, then end-systolic lengths were compared at matched end-systolic pressures at multiple time periods after the acute load alterations. Bilateral vagotomy, carotid sinus denervation, and stellate ganglion denervation were performed to prevent reflex alterations in contractility. The heart was paced at a constant rate. In seven animals, dextran was infused intravenously over 77 +/- 23 seconds (+/- SD) to increase left ventricular end-diastolic pressure from 5 +/- 2 to 13 +/- 3 mm Hg and peak pressures from 113 +/- 11 to 147 +/- 18 mm Hg. The end-diastolic lengths increased 14 +/- 6% in the anterior, 9 +/- 2% in the lateral, and 12 +/- 4% in the posterior segments. The ESPLR was measured immediately (77 +/- 23 seconds), early (3 +/- 1 minutes), and late (10 +/- 2 minutes) after initiation of the volume load. In all three regions, there was a significant time-dependent leftward shift in the ESPLR. From 1 to 10 minutes after the volume load, the regional end-systolic lengths decreased by a mean of 4-6% when compared at a matched end-systolic pressure of 96 +/- 10 mm Hg, and decreased by 7-9% when compared at a matched pressure of 139 +/- 20 mm Hg. The end-systolic lengths immediately after the volume load were not significantly different from the control value (compared at a matched end-systolic pressure) but were significantly shorter 10 minutes after the volume load. The leftward shift of the ESPLR represented a true increase in contractility and not merely a recovery from a transient myocardial depression. A similar leftward shift in the ESPLR occurred in four animals after release of a partial venae cavae occlusion, producing an acute volume load without acute hemodilution. Acute volume loads in four animals treated with propranolol also produced a leftward shift in the ESPLR, ruling out the possibility that a time-dependent increase in circulating catecholamines was responsible for the alterations in contractility. In five animals, the ESPLR shifted to the right after a transient (1-2 minutes) decrease in venous return.(ABSTRACT TRUNCATED AT 400 WORDS)

Response of the Heart to Acute Hypertension during Halothane, Enflurane, and Isoflurane Anesthesia

In the open chest dog model, the response of the left ventricle exposed to acute mechanical hypertension was evaluated while the animals were receiving various concentrations of halothane, enflurane, and isoflurane. Myocardial contractility was quantified by the end-systolic pressure-length relation (ESPL). When the mean aortic pressure was increased by 40% above the control value for a given concentration of inhalation agent, the end-diastolic volume increased and thereby maintained stroke work. However, as the end-tidal concentrations of the anesthetics increased, this compensatory mechanism became progressively more ineffective as a result of myocardial depression caused by the anesthetics. No evidence could be found of an improvement in myocardial contractility as the aortic pressure was increased. Mild depression of myocardial contractility could be demonstrated for 1.1 MAC halothane, 0.6 MAC enflurane, and 1.0 MAC isoflurane. Severe depression of contractility occurred at 2.3 MAC halothane, 1.2 MAC enflurane, and 1.5 MAC isoflurane.

Effect of repeated episodes of drug-induced ventricular dyskinesia on subsequent regional function in the dog: Comparison with myocardial stunning produced by repeated coronary occlusions

Stunned myocardium can be produced by repeated short episodes of ischemia. Histochemical and ultrastructural abnormalities such as sarcomere lengthening and myofiber thinning have been noted in myocardium soon after the onset of ischemia and have been attributed to the mechanical stretching that occurs during ventricular systole. To test whether mechanical forces alone could produce the residual dysfunction seen in stunned myocardium, regional dyskinesia was produced in open chest dogs by six repeated intracoronary infusions of either potassium chloride, 0.2 mEq/min for 2.5 minutes, or lidocaine, a 10 mg bolus followed by 1 to 3 mg/min for 5 minutes. These dogs were matched with dogs that had six repeated coronary occlusions of 2.5 and 5 minutes' duration, respectively. Regional function was analyzed using fractional systolic shortening and the load-independent end-systolic pressure-length relation. Both potassium chloride and lidocaine produced regional dyskinesia that was similar to the dyskinesia produced by coronary occlusion. Although regional ventricular function after repeated coronary occlusions remained significantly reduced, function returned completely to normal within 5 minutes after the last drug-induced dyskinesia. In conclusion, regional dysfunction produced by potassium chloride and lidocaine does not produce residual dysfunction despite mechanical forces during systole similar to those seen during coronary occlusion.

Quantitative analysis of regional wall motion in dogs in situ--characteristics of end-systolic pressure-length relation.

Regional wall motion was analyzed to deduce the muscle property unique to regional contractile states. End-systolic pressure length relations were evaluated under global changes in a contractile state, under selective intracoronary administration of inotropic agents to produce regional hypo- or hyper-kinesis, and before and after extension of size of the ischemia. Linearity of the end-systolic pressure-length relation was confirmed in each perturbation; however, the behavior of this relation with regard to changes in the slope and X-axis intercept differed among the three situations. When the contractile state was altered globally by intravenous administration of inotropic agents such as dobutamine and propranolol, the slope of the end-systolic pressure-length relation changed in a manner similar to that seen with the pressure-volume relation or stress-strain relation, with no significant changes in the X-axis intercept. Namely, the level of global cardiac function determined the slope of the end-systolic pressure length relation. When regional hypokinesis was produced pharmacologically by selective intracoronary infusion of lidocaine, the X-axis intercept moved rightward, depending on the degree of regional hypokinesis. Expansion in the size of the ischemic area also shifted the X-axis intercept rightward. The latter two phenomena suggested that the hypokinetic segments were stretched by the surrounding intact myocardium. Accordingly, end-systolic pressure-length relations provide useful information concerning the functional state of regional myocardium. The systolic properties of the regional myocardium rendered hypokinetic have to be quantified so as to include the total geometry of the heart.

End-systolic pressure-volume, pressure-length, and stress-strain relations in canine hearts.

End-systolic pressure-volume relationship (ESPVR) of the in situ heart in the dog was measured during changes in contractile state and was compared with end-systolic pressure-length (ESPLR) or stress-strain relationship (ESSSR). Circumferential segmental length and wall thickness at the equator and external long and short axis diameters of the left ventricle (LV) were determined sonomicrometrically, and LV volume was calculated by an ellipsoidal model. Circumferential wall stress at the equator was calculated by a very thin shell model. Contractile state was enhanced by an intravenous infusion of dobutamine and was suppressed by propranolol. ESPVR, ESPLR, and ESSSR were determined during a reduction of arterial pressure by occluding temporarily the inferior caval vein (IVC). ESPVR, ESPLR, and ESSSR during changes in end-systolic pressure from 108 +/- 3 to 71 +/- 2 mmHg were linear, irrespective of inotropic states (r greater than 0.92). Slopes of these relationships increased similarly in case of dobutamine and were reduced after propranolol, yet the extrapolated X-axis intercept of ESPVR, ESPLR, and ESSSR remained unchanged. Thus the slope of ESPVR is unique to the inotropic state, and both ESPLR and ESSSR are useful as a substitute for ESPVR when there is no regional wall motion abnormality.

End-systolic pressure-length relations during changes in regional contractile state

End-systolic pressure-length relationship (ESPLR) was examined in the heterogenously contracting heart in open-chest dogs. Regional length was measured sonomicrometrically in the areas of both the left circumflex coronary artery (LCX) and left anterior descending coronary artery (LAD). ESPLR was linear during a transient reduction in arterial pressure following occlusion of the inferior caval vein (IVC). In group 1 (12 dogs), saline as a control condition (Cont) and isoproterenol (Iso, 0.05 microgram/min) to enhance the regional contractile state were infused into the LCX. Percent shortening in the LCX area increased from 13 to 16% (P less than 0.01) in Iso. The slope (Ees) of ESPLR increased from 57 to 71 mmHg/mm (P less than 0.01) in Iso. The extrapolated X-axis intercept (Lo) of ESPLR was unchanged. In the LAD area, Ees and Lo remained constant. In group 2 (13 dogs), lidocaine (1 mg/min, Lid 1; 5 mg/min, Lid 5) was infused into the LCX to induce mild and severe hypokinesis, respectively. Percent shortening in the LCX area was reduced from 14 to 8% (P less than 0.01 vs. Cont) in Lid 1 and 5% (P less than 0.01 vs. Cont, P less than 0.05 vs. Lid 1) in Lid 5. Ees tended to decrease in Lid 1 but to increase in Lid 5 (statistically not significant).(ABSTRACT TRUNCATED AT 250 WORDS)