Force Of Ventricular Contraction Research Articles

Adverse effects polystyrene microplastics exert on zebrafish heart – Molecular to individual level

In the present study the effects of sublethal concentrations of polystyrene microplastics (PS-MPs) on zebrafish were evaluated at multiple levels, related to fish activity and oxidative stress, metabolic changes and contraction parameters in the heart tissue. Zebrafish were fed for 21 days food enriched with PS-MPs (particle sizes 3–12 µm) and a battery of stress indices like DNA damage, lipid peroxidation, autophagy, ubiquitin levels, caspases activation, metabolite adjustments, frequency and force of ventricular contraction were measured in fish heart, parallel to fish swimming velocity. In particular, exposure to PS-MPs caused significant decrease in heart function and swimming competence, while enhanced levels of oxidative stress indices and metabolic adjustments were observed in the heart of challenged species. Among stress indices, DNA damage was more vulnerable to the effect of PS-MPs. Our results provide evidence on the multiplicity of the PS-MPs effects on cellular function, physiology and metabolic pathways and heart rate of adult fish and subsequent effects on fish activity and fish fitness thus enlightening MPs characterization as a potent environmental pollutant.

Aqueous-methanolic extract of sweet flag (Acorus calamus) possesses cardiac depressant and endothelial-derived hyperpolarizing factor-mediated coronary vasodilator effects

This investigation was aimed to probe the pharmacological base of medicinal use of Acorus calamus in ischemic heart diseases. Effect on heart parameters was studied in isolated rabbit heart while coronary vasodilator effect was studied in isolated bovine coronary arterial rings, suspended in tissue baths filled with Krebs solution, maintained at 37°C, aerated with carbogen and responses were measured on PowerLab data acquisition system. In Langendorrf's perfused rabbit heart, the crude extract of Acorus calamus (Ac.Cr) at 0.01-10 mg/mL partially suppressed force of ventricular contractions (FVC), heart rate (HR) and coronary flow (CF). The ethylacetate fraction completely suppressed FVC, partially suppressed HR and CF, while the nHexane fraction exhibited similar effect on FVC and HR but increased CF, similar to methacholine and arachidonic acid. In bovine coronary arterial preparations, Ac.Cr caused inhibition of U46619 (20 nM)-precontractions, which was blocked in presence of increasing concentration of K(+) (4.8-20 mM), tetraethylammonium (1 μM) and SKF525A (10 μM), similar to arachidonic acid and methacholine, indicating K(+) channels activation and possible involvement of endothelial-derived hyperpolarizing factor (EDHF). Activity-directed fractionation revealed that EDHF-mediated activity is concentrated in the nHexane fraction. When tested against high K(+), the ethylacetate fraction was found more potent than parent crude extract and nHexane fraction. These data indicate that Ac.Cr mediates coronary vasodilator effect primarily through EDHF, responsible for the increase in CF, while the cardiac depressant effects may be due to the presence of additional cardiac depressant constituent(s), thus provides possible mechanistic basis to its medicinal use in ischemic heart diseases.

Extraction and phytochemical investigation of Calotropis procera: Effect of plant extracts on the activity of diverse muscles

Context: Calotropis procera (Ait.) R.Br. (Asclepiadaceae) is a shrub or small tree that grows wild in Egypt. Calotropis acts as a purgative, anthelmintic, anticoagulant, palliative (in problems with respiration, blood pressure), antipyretic, and analgesic, and induces neuromuscular blocking activity. Little research has been done to study the electrophysiological effects of this plant’s extracts on cardiac, smooth, and skeletal muscle activities.Objective: The present study was conducted to determine the phytochemical composition and the effect of the total alcohol extract of the shoot of the plant, which contains almost all of C. procera’s cardiac glycosides, flavonoids, and saponins. Also, this study attempted to throw more light on the electrophysiological effects of the plant extracts on cardiac, smooth, and skeletal muscle activities and to clarify the mechanism(s) of their observed action(s).Materials and methods: The aerial parts of the plant were air dried and their ethanol extracts partitioned with successive solvents. Cardiac, smooth, and skeletal muscles were used in this study to investigate the physiological and pharmacological effects of the plant extracts from different solvents. The data were analyzed by paired t-test.Results: The phytochemical investigation of Calotropis procera revealed the presence of cardenolides, flavonoids, and saponins. The effects of ethanol, n-butanol, and ethyl acetate (EtOAc) extracts were each evaluated on isolated toad heart and their mechanisms of action determined. Perfusion with 2 μg/mL ethanol, 0.2 μg/mL butanol, and 0.2 μg/mL EtOAc extracts caused a significant decrease in heart rate (bradycardia), significant increase in the force of ventricular contraction, and increase in T-wave amplitude. In addition, the effects of different extracts of the studied plant on smooth muscle and skeletal muscle were investigated in this study. The different extracts and latex of C. procera induced a negative chronotropic effect and decreased the heart rate (HR) of isolated toad heart. The different extracts increased the power of contraction of the duodenum (trace a). Pretreatment with atropine sulfate as a muscarinic receptor blocker abolished the stimulatory effect of the different plant extracts and latex of C. procera (trace b).Discussion: The present data suggest that ethanol, butanol, and EtOAc extracts of Calotropis procera have negative chronotropism and positive inotropism. Verapamil could abolish the inotropic effect of ethanol as well as that of butanol and EtOAc extracts. Meanwhile, atropine did not abolish the observed negative chronotropic effect. The ethanol extract increased the power of contraction of rabbit duodenum, but atropine abolished this effect. It also decreased the skeletal muscle contraction; this effect could be through blocking of the nicotinic receptors. Butanol and EtOAc extract data for smooth and skeletal muscles are very close to those for the corresponding ethanol extract of the studied plant. The present data for C. procera indicate its direct action on the myocardium, its increase of smooth muscle motility, and its relaxation of skeletal muscle contraction. The chemical constituents could directly affect the cell membrane probably through receptors coupling to G proteins. They regulate the ion channel physiology as in the myocardium.Conclusion: The present data on the extracts of C. procera indicate a direct action on the myocardium, stimulatory effect on smooth muscle motility, and relaxant action on skeletal muscle contraction. Chemical constituents could directly affect the cell membrane probably through receptors coupling to G proteins. They regulate the ion channel physiology as in the myocardium.

Possible mechanism of selective inotropic activity of the n-butanolic fraction from Berberis aristata fruit

Berberis aristata is an edible plant employed in South Asian traditional medicine; in particular, its fruit is used as a tonic remedy for liver and heart. In isolated cardiac tissues, Berberis aristata fruit extract exhibits a positive inotropic action. Activity-directed fractionation using organic solvents revealed that the cardiotonic activity is concentrated in the n-butanolic fraction (BF). The cardiac action of BF was investigated in spontaneously beating right atria and in electrically driven right ventricular strips and left atria obtained from reserpinized guinea pigs. The results show that this fraction produces a dose-dependent positive inotropic action with little effect on heart rate. To study its possible mode of action, guinea pig atria were pretreated with propranolol, a β-adrenoceptor blocking agent. This treatment abolished the cardiotonic effect of isoprenaline, whereas the cardiotonic effect of BF remained unaltered, suggesting that this effect does not involve stimulation of β-adrenoceptors. On the other hand, application of carbachol reverses only part of the BF-induced increase in ventricular force of contraction, indicating that besides a cyclic AMP (cAMP)-dependent mechanism, a cAMP-independent mechanism underlies the inotropic action of BF. This is in line with the observation that the dynamics of isometric twitch contractions are not significantly altered by BF. Investigations in skinned myocardial preparations showed that BF modulates the calcium-dependent interaction of actin and myosin, apparently by reducing the cooperativity of the calcium-dependent binding of myosin to actin, i.e., there is enhanced calcium activation at low to physiological intracellular calcium, and reduced calcium activation at high intracellular calcium concentrations as present, for example, in ischemic calcium overload. These data indicate that the edible plant, Berberis aristata, contains active principle(s) that cause(s) a selective inotropic effect, involving—in the form of the modulatory effect on actin myosin cooperativity—a novel mechanism of action. Further phytochemical and pharmacological studies may lead to isolation and structural identification of an attractive, new cardiotonic agent from Berberis aristata fruit.

Hemodynamics and aneurysm development in vascular allografts

Purpose: Mechanical and immunologic factors may play a role in the development of native arterial and biologic graft aneurysms. We developed an experimental rat aortic allograft aneurysm model in which segments of infrarenal aorta were transplanted between hypertensive and normotensive rats to study these factors in this model.Methods: Aortic allografts and autografts were inserted into spontaneously hypertensive (SHR) and normotensive Wistar Kyoto (WKY) rats. Effects of immunologic and antihypertensive therapy were evaluated. Graft diameters were followed up with magnetic resonance imaging and at harvest. Direct-pressure measurements were taken and dp/dtmax (force of ventricular contractions) was calculated before harvest.Results: Autografts remained isodiametric and maintained their histologic architecture. Aneurysmal dilation of transplanted segments occurred in SHR host allografts but not in WKY host allografts. Histologic examination of all allograft specimens noted a rejection reaction characterized by inflammatory cell infiltration and medial smooth muscle cell loss. Antigenic enhancement accelerated aneurysm development in SHR hosts but had no significant effect on WKY hosts. Rates of allograft enlargement and final allograft diameters were similar in antihypertensive treated and untreated SHR hosts. The dp/dtmax in untreated SHR hosts was greatest and differed significantly from that in the WKY rats but only marginally from that in treated SHR hosts.Conclusions: Immunologic rejection but not abnormal hemodynamics is necessary for development of allograft aneurysm in this model.

Heart rate—QT interval relationship during postural change and exercise

The QT interval of the electrocardiogram, although often coordinated in an inverse relationship to heart rate, appears from the existing evidence to be regulated by mechanisms separate from those that govern heart rate. The purpose of this inquiry was to explore further the relationship of the two and to test other factors that may contribute to the regulation of QT. Heart rate and QT duration were measured in healthy human subjects during postural change and exercise. The data showed that, while coordinated in an inverse relationship under some circumstances, under others heart rate and QT were discordant, leading to the inference that there is no fixed linkage between the two. Previous work by the authors and other published studies have suggested that ventricular contractility may have more predictable association with QT shortening than do increases in heart rate. Observations of force of ventricular contraction (HI and IJ velocity) as reflected in ballisto-cardiographic tracings were made using each of 12 human subjects as the authors' own control. The data revealed a highly significant correlation between the velocity measures and QT duration (p less than 0.01) but not heart rate. These findings led to the conclusion that there is clearly not a fixed relationship between heart rate and QT interval and to the hypothesis that QT may more closely reflect the degree of cardiac contractility.

Insulin worsens ischemia-induced myocardial contracture in the isolated rat heart.

We used a modification of Langendorff's isolated perfused nonworking rat-heart model to study the effects of diabetes, insulin-treated diabetes, and hyperinsulinemia on left ventricular pressure, force of ventricular contraction, and myocardial contracture, before, during, and after 20 min of complete normothermic global ischemia. Untreated diabetic rat hearts behaved the same as normal hearts, but insulin-treated diabetic hearts had more ischemic and postischemic contracture (p less than .01), and less return of left ventricular function. Chronic insulin treatment potentiated ischemic contracture in diabetic and nondiabetic rat hearts. These results support the hypotheses that insulin can increase Ca++ actin-myosin ATPase activity, and increase the affinity of myofibrillar receptors for calcium, which may lead to increased ischemic contracture. Insulin as a risk factor in myocardial ischemia, cardiothoracic surgery and cardiac resuscitation, and other pathogenetic factors of "stone heart" development, deserve further investigation.

Innervation of bat heart: cholinergic and adrenergic nerves innervate all chambers

Adult Miniopterus schreibersii were anesthetized with chloroform, and in vitro preparations of cardiac chambers were prepared. Stimulation of intramural nerves in right ventricles paced at 6 Hz caused an inhibition (56.3 +/- 3.5% decrease on basal force) mediated by cholinergic nerves and an excitation (91.5 +/- 9.9% increase on basal force) mediated by adrenergic nerves. Mean pD2s (-log effective concentration, 50%) for ventricular beta-adrenoceptors and muscarinic cholinoceptors were 6.99 +/- 0.03 and 6.42 +/- 0.07, respectively. The inhibition of ventricular contractility, by nerve stimulation or exogenous acetylcholine, occurred even after blockade of beta-adrenoceptors. The results were comparable to those obtained on atria. In some experiments, the heart was perfused in situ and paced via electrodes on the ventricle: stimulation of the right vagus nerve decreased right ventricular contractility by up to 90%. The results show that, at least in this hibernating mammal, there is an adrenergic innervation of the ventricle. The presence of a cholinergic vagal innervation capable of inhibiting the basal force of ventricular contraction has not been shown in any other mammal.

Cardiovascular effects of thoracic afferent nerve stimulation in conscious dogs.

Afferent stimulation of a severed thoracic autonomic nerve in 18 conscious dogs produced in 13 instances hypertension and in 5 instances hypotension. Reflex hypertension was usually accompanied by augmented atrial and ventricular force of contraction. The hypertension could be maintained for over 5-min duration by constant stimulation. Inotropic changes accompanying this hypertension were accentuated following atropine administration and abolished by propranolol. Blood pressure changes following atropinization were initially augmented. On the other hand reflex hypotension was accompanied by bradycardia and decreased atrial contractility. These changes were essentially abolished by atropine. Afferent nerve stimulation with frequencies as low as 1 Hz initiated reflex changes. Maximal responses were obtained by stimulation frequencies of 10-15 Hz. It is concluded that significant and relatively sustained cardiovascular reflexes can be generated by stimulation of cardiac afferent nerves in conscious dogs.

Sites of action of Mojave toxin isolated from the venom of the Mojave rattlesnake.

1 Mojave toxin isolated from the venom of the Mojave rattlesnake (Crotalus scutulatus scutulatus) produced an irreversible blockade of the contractile response of the mouse hemidiaphragm to stimulation of the phrenic nerve in vitro, at concentrations of 0.16 to 20 mug/ml; the response to direct stimulation was not affected over a testing period of several hours.2 Mojave toxin (1 to 4 mug/g) was injected into the tail vein of mice and the intoxicated hemidiaphragm preparation was removed either for testing the contractile response or for intracellular recording.3 In fully intoxicated hemidiaphragms the contractile response to indirect stimulation was either small and transient or absent, whilst the response to direct stimulation was well maintained.4 Intracellular recording showed that resting membrane potentials of the muscle fibres were within the normal range. Endplates were difficult to locate but miniature endplate potentials (m.e.p.ps) were recorded at sites at which neurally evoked responses either could not be detected or did not exceed 2 mV which corresponds to transmitter release of a few quanta only.5 The mean frequency of m.e.p.ps at fully intoxicated endplates was not significantly different from controls but potassium depolarization produced only a small increase in m.e.p.p. frequency relative to the control response. A 50 Hz tetanus had no effect on m.e.p.p. frequency.6 When a sub-lethal dose (3 mug) of Mojave toxin was injected into one hindlimb of mice and the tissues examined at 72 h, there was histological evidence of myonecrosis.7 The isolated perfused heart of the rat was exposed to recycled Mojave toxin (50 and 100 mug/ml) but showed no change in rate or force of ventricular contraction.8 Post-mortem examination of intoxicated mice showed a frequent incidence of localized areas of interstitial and intra-alveolar haemorrhage in the lungs. Other organs including skin and muscle were not affected.9 Mojave toxin showed antigenic similarities to crotoxin, the lethal neurotoxin in the venom of the South American rattlesnake, as determined by the ability of antiserum raised against crotoxin to neutralize Mojave toxin.10 With systemic Mojave intoxication of rapid onset, the cause of death was respiratory paralysis. However, the toxin acts at multiple sites at differing rates of action. With a slower rate of intoxication, impaired respiration may act synergistically with cardiovascular changes to produce circulatory failure. The desirability of using an antivenin with a high titre against Mojave toxin is indicated.

Monitoring tissue oxygenation of the heart after myocardial revascularization

A polarographic technique capable of simultaneous monitoring of myocardial tissue oxygen tension (MPO 2) and intramyocardial electrograms by way of the same electrodes has been developed. Initially, the method was evaluated in dogs to verify the appropriateness of the directional changes of MPO 2 in function of selected determinants of myocardial oxygen supply (regional coronary blood flow, arterial blood oxygen tension) and demand (heart rate, force of ventricular contraction). A combined reduction of MPO 2 and elevation of the S-T segment in the corresponding electrograms was observed only when a 50 percent or greater reduction of blood flow to the sampled area was effected. Subsequently, in nine patients undergoing aortocoronary bypass surgery, MPO 2 was measured from 48 areas for 2 weeks postoperatively. In 11 normal and 31 revascularized areas, MPO 2 increased during the postoperative period. In four areas subsequently found to be supplied by occluded grafts, MPO 2 decreased from 12.7 ± 3.1 (mean ± standard error) to 10.1 ± 3.3 mm Hg ( P < 0.05). In two areas, MPO 2 decreased during the 3rd postoperative day from 16 to 3 and from 14 to 4.2 mm Hg, respectively. This reduction was attended by a significant rise in the S-T segment of the corresponding electrograms. This finding preceded by 24 hours standard electrocardiographic evidence of myocardial infarction. This technique appears to be sensitive and reliable, and thereby capable of enhancing the management of patients during the high risk early postoperative period after coronary bypass surgery.

Influence of Atrial Systole on First Derivative of the Apexcardiogram

A well-timed left atrial contraction increases left ventricular end-diastolic volume and thereby enhances the strength of ventricular contraction.1 This force of ventricular contraction is reflected in measurements of ventricular and arterial pressures and in the rate of rise of pressure (dp/dt) at these sites.2-5 Despite certain limitations in the usefulness of the ventricular dp/dt as an index of myocardial contractility,6 the rate of rise of the left ventricular apexcardiogram (da/dt) appears to be a useful tool for its external evaluation.

Relationship between cardiac contractility and energy supply to the heart

When nicotinic acid was given intraperitoneally to rats, there was a marked decrease in the ventricular force of contraction and in the inotropic response to 1-norepinephrine at 2 and 4 hours after administration of the drug; 6 hours after the injection of nicotinic acid, myocardial contractility had returned to normal. Severe impairment in cardiac contractility coincided with the period when heart triglycerides and myocardial glycogen were depleted by the nicotinic acid. Inclusion of oleic acid, triglyceride, or glucose in the medium perfusing the heart restored normal contractility and the inotropic response to 1-norepinephrine. Results of these experiments indicate a direct relationship between myocardial contractility and the availability of energy-supplying substrates.

The dynamics of the coronary venous pressure in the dog.

The dynamics of the pressure in the great cardiac vein and coronary sinus was studied in 30 anaesthetized, artificially ventilated dogs. The pressure in the coronary venous system was found to be pulsatile and two positive pressure waves were distinguished. The a-wave, coinciding with the right atrial systole, appeared in the distal parts of the coronary sinus only, whereas the v-wave, concurring with the ventricular systole, was observed at all levels of the coronary venous system investigated, being most distinct in its proximal portions. The a-wave was accentuated during rapid atrial infusion which raised the right atrial pressure level. On the other hand, the v-wave was very markedly exaggerated following sympathetic stimulation and, particularly administration of norepinephrine (1 and 5 γ/kg i.v.), this concurring with the increase of ventricular contractile force. The amplitude of pressure pulsations rose, on the average, from 6.2–10.6 mm Hg following sympathetic stimulation, and from 7.7 to as much as 31 mm Hg with a 5 γ/kg dose of norepinephrine. The amplitude of pressure pulsations within the coronary sinus was also increased by papaverine (2.5 mg/kg i.v.) which elicited a marked augmentation of coronary blood flow without causing any significant rise of ventricular contractile force. The amplitude of pressure pulsations rose, on the average, from 8,8–13,7 mm Hg. Increasing the heart rate, over a range of 70 to 300 beats per minute, brought about a reduction of pulsations paralleling the reduction of ventricular contractile force despite the concomitant augmentation of coronary blood flow. It is concluded that the pulsations of the coronary venous pressure are due to mechanical effects of ventricular contractions mainly, which acting as a muscle-pump promote the emptying of the coronary veins. The actual amplitude of pressure pulsations is determined by the force of ventricular contractions, and by the state of filling of the coronary veins correlated with the level of coronary blood flow.

INDUCED PRESSURE GRADIENTS ACROSS INFUNDIBULAR ZONE OF RIGHT VENTRICLE IN NORMAL DOGS.

In these experiments we have demonstrated that: 1. Right ventricular outflow-tract pressure gradients of significance can be induced in normal dogs by a sympathomimetic amine which increases the rate and force of ventricular contraction. 2. Such outflow-tract pressure gradients are magnified by the addition of other inotropic drugs, such as acetyl strophanthidin and calcium chloride. 3. These outflow-tract pressure gradients are not the result of an increase in the volume and rate of blood flow but are due to forceful contraction of the infundibulum.

A Hemodynamic Technic for the Detection of Hypertrophic Subaortic Stenosis

In the presence of valvular aortic stenosis or of discrete subvalvular stenosis, the narrowed orifice is constant and its size is not altered by changes in the force of ventricular contraction. In hypertrophic subaortic stenosis the orifice narrows during systolic contraction of the hypertrophied muscle in the left ventricular outflow tract and the orifice size therefore is a function of the force of left ventricular contraction. In 75 patients, proved to have the discrete, "fixed" type of aortic or subaortic stenosis the beats following the compensatory pause after a premature contraction were always characterized by higher left ventricular systolic pressures and larger systemic arterial pulse pressures than the normal beats, i.e., arterial pulse pressure varied directly with left ventricular systolic pressure and with the duration of diastole. In 12 patients proved to have hypertrophic subaortic stenosis, the beats following premature contractions always exhibited lower arterial pulse pressures than did the normal beats, i.e., arterial pulse pressure varied inversely with left ventricular systolic pressure and with the duration of diastole. The distinction between these two types of obstruction to left ventricular outflow may be established with confidence by this analysis of the effects of premature ventricular contractions on either the simultaneously recorded left ventricular and arterial pressure pulses, or on the arterial pressure pulses alone. The recognition of hypertrophic subaortic stenosis is essential in formulating a rational plan of treatment for all patients with obstruction to left ventricular outflow, and the hemodynamic technic described affords a simple but reliable diagnostic approach.

Genesis of the Force Ballistocardiogram of the Dog

Force ballistocardiograms from the dog were obtained before, during and after pulmonary and aortic artery ligation. Ballistocardiographic waves persisted during the experimental conditions. By inflating with air balloons placed in the left and right ventricles, blood flow was interrupted and, in addition, the ventricles were stretched so that the force of ventricular contraction was increased. Again ballistocardiograms were obtained with forces occurring throughout the entire systolic period. The amplitude of the complexes obtained was roughly proportional to the degree of stretch or the amount of air put into the balloons within the ventricular cavities. The ballistocardiograph waves during cessation of blood flow were found to correspond to those noted during the control period. It is concluded that myocardial forces per se can be of significant magnitude and under certain circumstances can produce movements even greater than those noted during the normal hemodynamic state. It is further postulated that the ballistocardiogram represents a complex wave form made up of both right and left ventricular forces, in addition to blood flow in both the pulmonary and aortic arteries and that no single segment contains a monogenetic force. Submitted on November 4, 1957

Regulation of the degree of emptying of the left ventricle by the force of ventricular contraction.

Results are presented which indicate that left ventricular end-systolic volume is determined by the force-length relationship of the ventricular muscle at the end of systole. In other words the muscle continues to shorten until it meets a certain force the magnitude of which depends on the length of the musclc fibers at that time; when it meets this force it shortens no further. Since the end-systolic volume is an important determinant of stroke volume the suggestion is made that future studies should be directed toward measuring the effect of various influences on the force-length relationship and the modulus of elasticity of the end of systole in addition to studying the effects on the end-diastolic volume.

Direct measurement of changes in cardiac contractile force; relationship of such measurements to stroke work, isometric pressure gradient and other parameters of cardiac function.

Direct measurements of changes in the force of ventricular contraction with the strain gauge arch represent a sample of changes in the force of contraction of the entire ventricular muscle under conditions of an intact circulation. The responses of any given area of the ventricular muscle to repeated injections of the same dose of a cardiac stimulant drug are consistently similar. Further, there is a linear relationship between changes in the force of contraction as measured with the strain gauge arch and changes in the duration of the isometric pressure gradient. A direct relationship also exists between changes in contractile force and changes in stroke work. The relative advantages and limitations of the strain gauge arch and of the heart lever system, equipped with a strain gauge coil, are discussed in detail. Evidence is presented to show that the strain gauge arch is most useful in experiments in which substantial changes in the size of the heart do not occur. The heart lever system should be employed in experiments in which the size of the heart does undergo substantial change since adjustment may be made for changes in the initial diastolic fiber length. The time relations existing between direct recordings of contractile force made with the strain gauge arch and recordings of intravascular pressures have been demonstrated. A substantial portion of the contractile force is developed during the isometric phase of systole. There is a direct relationship between the amount of left ventricular contractile force developed during the isometric phase of contraction and the aortic diastolic pressure. A similar direct relationship exists between the total amount of contractile force measured by an arch on the left ventricle and the aortic systolic pressure. Mechanical stretching of the segment of muscle between the two points of attachment of the strain gauge arch produced length-tension curves which showed that a marked increase in contractile force occurs with increases in length of up to 40–60%. Stretching beyond these limits results in a progressive decrease in contractile force. The depth to which the sutures used in the attachment of the arch to the heart penetrated the myocardium has a moderate, but limited, quantitative influence upon the magnitude of contractile force measured. An arch attached with sutures penetrating deeply into the muscle measures more contractile force than an arch attached to the heart by superficially placed sutures.