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PubMed1988

[Experimental mitral regurgitation in ischemia-induced papillary muscle dysfunction].

Mitral regurgitation (MR) reportedly develops by ischemia of the papillary muscles, which is called papillary muscle dysfunction. This report deals with the roles of papillary muscles and left ventricular walls on the pathogenesis of MR using graded injuries of these structures in 23 dogs. Implanted ultrasonic microcrystal and occluder with an electromagnetic flowmetry for the left circumflex coronary artery were the main experimental setting. Graded occlusion of the artery was done by the six-step approach regarding coronary blood flow (CBF) reduction (C1-C6). Left ventricular (LV) pressure, systolic thickening (%W: sonomicrometry) of the LV anterior (AW) and posterior walls (PW), and systolic longitudinal shortening (%S: sonomicrometry) of both the anterior and posterior papillary muscles (PPM) were measured. MR was assessed by left ventricular contrast two-dimensional echocardiography. In eight dogs, all the data were adequate for analysis. In category 3 (C3: 55-70% CBF of control), %S in PPM decreased, but %W did not change significantly, and only mild MR developed in three of the eight dogs. MR clearly developed in category 4 (C4: 40-54% CBF as compared with the control stage), where %S was replaced by holosystolic lengthening and %W reduced to 50% of the control state, and total occlusion (C6) accompanied by significant thinning of both the PW and AW. Thus, the asynergy of the LVPW was needed to induce the MR in seven of the eight dogs. It was concluded that the injury of the PPM alone is not sufficient to cause MR, and the associated ischemic changes of the LV free wall as well as LV dilatation are necessary to induce severe MR.

Animals↗
PubMed1996

The role of aging on the control of contractile force by Na(+)-Ca2+ exchange in rat papillary muscle.

BACKGROUND: Sarcolemmal Na(+)-Ca2+ exchange system is believed to be fundamental to the control of cardiac contractility. However, the relation between Na(+)-Ca2+ exchange and the control of contractile force has not been studied in senescent myocardium. METHODS: The role of Na(+)-Ca2+ exchange in the regulation of the cardiac muscle's contractile force was studied in adult and senescent papillary muscles by simultaneously measuring intracellular sodium activity (aNai), action potential, and contractile force while varying extracellular concentration of sodium and/or calcium. RESULTS: Reduction of [Na+]o decreased aNai from 8.0 +/- 1.8 to 4.1 +/- 0.8 in adult (-3.9 mM) and from 8.7 +/- 1.9 to 4.7 +/- 0.9 in senescent (-4.0 mM) papillary muscles, while developed tension (DT) increased by 80.2% in adult and by 135.6% in senescent papillary muscles (p < .01 vs adult). During low [Ca2+]o and high [Na+]o, aNai and DT modifications were similar both in adult and senescent papillary muscles. During high [Ca2+]o, aNai decreased to a similar extent in both adult and senescent papillary muscles, while DT increased by 37.8% in adult and by 67.8% in senescent (p < .05 vs adult). Simultaneous reduction of [Na+]o and [Ca2+]o decreased aNai from 8.1 +/- 1.2 to 6.8 +/- 1.1 mM in adult (-1.3 mM), and from 8.4 +/- 1.0 to 7.2 +/- 1.0 mM in senescent (-1.2 mM) papillary muscles while DT decreased by 22.1% in adult and by only 12.0% in senescent (p < .01 vs adult) papillary muscles. Simultaneous increase of [Na+]o and [Ca2+]o similarly increased aNai in both adult senescent papillary muscles, but decreased DT by 28.5% in adult and by 11.7% in senescent (p < .01 vs adult). After [Na+]o modifications, the equilibration time for the ratio of external and internal sodium ion activities was slowed in senescent papillary muscles (i.e., in low [Na+]o solution the equilibration time was 4.6 +/- 0.9 min in adult and 6.3 +/- 1.2 min in senescent papillary muscles, p < .001). CONCLUSIONS: Similar changes of aNai during transmembrane Na+ and Ca2+ gradients modifications associated to changes in contractile force seem to demonstrate that Na(+)-Ca2+ exchange is probably not modified by the aging process. However, the slow equilibration time for the ratio of Na+ activities might reflect an age-related reduction of the Na(+)-K+ pump activity.

Action Potentials↗
PubMed1986

A physiological approach to surgery for acute rupture of the papillary muscle.

There is controversy regarding the optimal management of patients in whom acute papillary muscle rupture develops. This study evaluates the effect of division of the anterolateral papillary muscle on left ventricular (LV) function and compares two methods of treatment--mitral valve replacement (MVR) and mitral valve repair. Thirteen pigs were placed on cardiopulmonary bypass, and interventions were performed in an isolated beating heart preparation. LV function was assessed with a compliant intraventricular balloon at baseline, after division of the anterolateral papillary muscle (Divided), after repair of the divided papillary muscle (Repair), and finally after MVR. Division of the anterolateral papillary muscle caused a significant deterioration in LV function. Function was maintained at this level after mitral valve repair but deteriorated with MVR. Developed pressure measured at baseline was 179 +/- 13 mm Hg; Divided, 148 +/- 11 mm Hg (p less than 0.05 versus baseline); Repair, 149 +/- 15 mm Hg; and MVR, 95 +/- 8 mm Hg (p less than 0.05 versus Divided) at a balloon volume of 20 ml. These results suggest that LV function is impaired by papillary muscle rupture. Repair of the ruptured papillary muscle is associated with better LV function than is MVR.

Acute Disease↗
PubMed1975

Influence of temperature on the positive inotropic effects mediated by alpha-and-beta-adrenoceptors in the isolated rabbit papillary muscle.

On the isolated rabbit papillary muscle experiments were carried out to determine whether the positive inotropic effects mediated by alpha- and by beta- adrenoceptors are brought about by different mechanisms or not.--For this reason the influence of temperature and the effect of the calcium antagonist D600 on the responses to phenylephrine and to isoprenaline were compared. 1. The maximal inotropic effects of phenylephrine, isoprenaline and calcium were not affected by raising the temperature of the organ bath from 37 degrees to 42 degrees C, wheras the basal developed tension of the muscle was significantly decreased. 2. The dose-response curve for phenylephrine was markedly shifted to the right by raising the temperature (pD2=0.89), while that for isoprenaline was also shifted to the right, but to a lesser extent (pD2=0.23). 3. In the presence of 1.5 times 10-8 M pindolol the shift of the dose-response curve for phenylephrine induced by elevation of temperature was more prominent (pD2=1,91), whereas phentolamine (3 times 10-6 M) inhibited the temperature-induced shift. 4. The positive inotropic effect of phenylephrine--mediated by alpha-adrenoceptors under blockade of beta-adrenoceptors by 1.5 times 10-8 M pindolol--was markedly depressed by D600 (10-7 and 3 times 10-7 M): the dose-response curve was shifted to the right ant the maximal response was depressed. On the other hand, the positive inotropic effect of isoprenaline--mediated by beta-adrenoceptors--was affected to a lesser extent by D600 and the maximal response was not changed. It indicates that the stimulation of alpha- adrenoceptors in the rabbit papillary muscle induces a positive inotropic response through a biochemical process different from that caused via beta- adrenoceptors, i. e., stimulation of alpha- adrenoceptors may increase the intracellular calcium level mainly by changing the transmembrane calcium flux.

Animals↗
PubMed1995

N-3 and N-6 fatty acids modulate the inotropic response to calcium in hypothyroid rat papillary muscle.

The calcium sensitivity of papillary muscles was enhanced at low [Ca2+] in euthyroid rats fed a diet enriched in n-3 fatty acids compared to rats fed diets high in n-6 and saturated (SAT) fatty acids. At the same time, the maximum developed tension was 44% lower in animals fed the n-3 diet compared to those fed the n-6 diet and 62% lower than the rats fed the SAT diet. In hypothyroid animals fed the n-3 diet, the inotropic response to added Ca2+ was only 60% of that in euthyroid controls and 50 and 65% of euthyroid controls in n-6 and SAT diet-fed animals, respectively. Although the response was again lower in n-3-fed animals, the differences among the diet treatments were not as great as those seen in euthyroid animals, and there were no apparent diet-dependent differences in sensitivity to Ca2+ in hypothyroid animals. The potency of the calcium-channel blocker nifedipine was diet-dependent in euthyroid animals, with the order of decreasing sensitivity being n-3 > n-6 > SAT. Papillary muscles were not as sensitive to nifedipine in hypothyroid animals, although n-3-fed animals again showed the greatest inhibition of tension development. On the other hand, nitrendipine-binding affinity was not different among euthyroid and hypothyroid animals fed the n-6 diet.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2000

Mitral repair in patients with a ruptured papillary muscle.

BACKGROUND: The objective of this study was to evaluate the feasibility of a modified papillary muscle repair procedure for a group of patients with ischemic mitral regurgitation when ischemia/infarction has resulted in the rupture of a papillary muscle. From January 1997 to January 1999, 843 patients underwent mitral valve surgery in our hospital. Mitral reconstruction was performed in 520 (61.7%) patients, and 6 (1.2%) of these patients were found to have a rupture of a papillary muscle at initial examination. METHODS AND RESULTS: A modified papillary muscle repair procedure to reimplant the tip of the ruptured papillary muscle "height- and/or length-adjusted" into a corresponding papillary muscle, with the use of a sandwiched pericardium pledget-reinforced polytetrafluoroethylene suture, was performed in 6 patients. Although the underlying cause in this group of patients was ischemic, concomitant coronary artery bypass grafting was performed in only 3 patients, with 1.3 grafts per patient. Of these 6 patients, 3 (50%) were men; the mean age was 60.2 +/- 12.8 years. All patients had in addition to the papillary muscle repair procedure an annuloplasty with a Carpentier-Edwards Physio-Ring. There was no early death in this group of patients. Postoperative Doppler echocardiography showed satisfactory mitral valve function in all patients and a significant postoperative ventricular remodeling: The left ventricular end-diastolic diameter decreased from 72.8 +/- 3.1 mm before surgery to 54.6 +/- 9.3 mm (P <.1) after surgery; left ventricular systolic diameter also decreased (48.5 +/- 4.9 mm vs 38. 4 +/- 9.8 mm; P <.1), and a substantial reduction of left atrial diameter (58.8 +/- 1.5 mm vs 49.7 +/- 4.1 mm; P <.1) was observed. Within the short mean follow-up period of 8.6 +/- 7.5 months (2 to 26 months), there were no late deaths, reoperations, or thromboembolic or bleeding complications. All patients were in New York Heart Association functional class I or II at the time of follow-up. CONCLUSIONS: Our results indicate that our modified papillary muscle reimplantation procedure is a valuable surgical tool with good survival results in patients with ischemic mitral regurgitation caused by papillary muscle rupture.

Adult↗
PubMed1980

Role of the papillary muscle in opening and closure of the mitral valve.

Dimensional changes of the left ventricular anterolateral papillary muscle of six open-chest dogs were measured continuously throughout the cardiac cycle in order to evaluate the role of the papillary muscle in opening and closing of the mitral valve. Dimensional changes were measured with ultrasonic dimension gauges. Maximal shortening and maximal elongation of the papillary muscle followed maximal shortening and elongation of a segment of the free wall of the left ventricle by 65 +/- 6 (SE) ms. Maximal elongation of the papillary muscle occurred 25 +/- 2 ms after the onset of ejection. Maximal shortening of the papillary muscle occurred 68 +/- 5 ms after the aortic incisura and 10 +/- 2 ms after the crossover of left ventricular and left atrial pressure. The papillary muscle shortened 14 +/- 4%. The percentage of papillary muscle shortening that occurred after the aortic incisura was 39 +/- 7%, and the percentage of shortening that occurred after the crossover of left ventricular and left atrial pressure was 3 +/- 1%. The observed shortening of the papillary muscle throughout left ventricular isovolumic relaxation suggests that the papillary muscle may have a role in opening the mitral valve. Conversely, elongation of the papillary muscle in the late portion of diastole appears necessary to permit proper closure of the mitral valve leaflets.

Animals↗
PubMed1985

Assessment of papillary muscle function in the intact heart.

A technique is described to localize the anterolateral papillary muscle and to assess its performance in vivo. Using this technique, we measured sequentially the pressure generated within the anterolateral papillary muscle and its changes in length during the cardiac cycle in eight open-chest anesthetized dogs. Pressure within the anterolateral papillary muscle was measured with a 1.6 mm diameter micromanometer probe. Its dimensional changes were measured with ultrasonic crystals. Pressure within the anterolateral papillary muscle exceeded left ventricular pressure throughout the entire cardiac cycle. A difference of 200 +/- 23 mm Hg was present between systolic pressure in the anterolateral papillary muscle and left ventricular systolic pressure (348 +/- 25 vs 149 +/- 6 mm Hg) (p less than .001). Shortening of the anterolateral papillary muscle began 25 +/- 2 msec after the upstroke of the aortic pressure, continued throughout isovolumic relaxation, and was maximal 68 +/- 5 msec after the apex of the aortic incisura. The extent and velocity of shortening of the anterolateral papillary muscle were maximal when pressure within the muscle was lowest. This temporal dissociation between pressure and dimensional changes of the anterolateral papillary muscle appeared to result from cyclic changes of loading imposed on the muscle.

Animals↗
PubMed1997

The vital role of papillary muscles in mitral and ventricular function: echocardiographic insights.

The two left ventricular (LV) papillary muscles are small structures but are vital to mitral valve competence. Partial or complete rupture, complicating acute myocardial infarction, causes severe or even catastrophic mitral regurgitation, potentially correctable by surgery. Papillary muscle dysfunction is a controversial topic in that the role of the papillary muscle itself, in causing mitral regurgitation post infarction, has been seriously questioned; it is less confusing if this syndrome is attributed not only to papillary muscle but also to adjacent LV wall ischemia or infarction. Papillary muscle calcification is easily and frequently detected on echocardiography, but its clinical significance remains uncertain. Papillary muscle hypertrophy accompanies LV hypertrophy of varied etiology and may have a significant role in producing dynamic late-systolic intra-LV obstruction in hypertrophic cardiomyopathy and other hyperdynamic hypertrophied LV chambers. All the above abnormalities can be adequately assessed by 2-D echocardiography and the Doppler modalities. In selected cases, transesophageal echocardiography can provide additional valuable data by improving visualization of papillary muscles and mitral apparatus.

Cardiomyopathies↗
PubMed1982

The influence of the rate of electrical stimulation on the effects of the Anemonia sulcata Toxin ATX II in guinea pig papillary muscle.

In guinea pig papillary muscle, the rate of electrical stimulation (0.1-2 Hz) strongly influenced the effects of the Anemonia sulcata toxin ATX II on action potential duration (APD) and contractile force. In the concentration range studied (10-8-10-7 M), ATX II always produced a larger prolongation in APD at low rates of stimulation. At 0.1 Hz there was a temporal dissociation between the onset of the APD-prolonging and the positive inotropic effect. However, under equilibrium conditions there was a positive relationship between the APD expressed as a fraction of the time during which the membrane was depolarized, and the contractile force irrespective of the change in experimental conditions being variation of stimulation frequency or the addition of ATX II. The results suggest that the positive inotropic effects of both ATX II and increased stimulation frequency could be induced by a similar mechanism, e.g. an increase in sodium of the heart muscle.

Action Potentials↗
PubMed1985

The influence of 'diastolic' length on the contractility of isolated cat papillary muscle.

Isometrically contracting cat papillary muscles were studied. Muscle length was changed during diastole and returned to control just before the next contraction such that developed force was always measured at the same length. When the diastolic length was increased from a control length, systolic force at the control length increased slowly over several minutes. When the muscle was then held at the increased length, there was an immediate increase in systolic force followed by a small secondary slow increase. Conversely, a decrease in diastolic length from a control length resulted in a slow decrease in systolic force at the control length. When the muscle was then held at the decreased length there was an immediate decrease in systolic force followed by a small secondary decrease. No change in the time course of contraction accompanied the slow force changes after a maintained change of length or a change of diastolic length alone. The magnitude of the slow change of force was proportional to the duration of time in each diastole for which the length was altered and independent of the onset time of a given duration of diastolic length change. The contractility changes were not linearly related to the amplitude of the diastolic length changes. The potentiating effect of a given stretch was greater than the depotentiating effect of a similar release. The development of inotropic changes as a result of diastolic length changes occurred whether or not the muscle was stimulated during the period of the length changes.

Animals↗
PubMedDate not supplied

Mechanical contribution of endocardium during finite extension and torsion experiments on papillary muscles.

Finite extension and torsion tests on cardiac papillary muscles are presently the best way to directly measure the response to shear along myocardial fibers. Quantifying this response is necessary for determining the complete three-dimensional constitutive behavior of myocardium as a transversely isotropic material. Analysis of such tests is complicated, however, since papillary muscles are materially inhomogeneous, consisting of a myocardial core surrounded by an endocardial sheath that is rich in collagen. In this article, we show that the papillary muscle response to extension and torsion additively decouples into the response of the bare myocardial core plus the response of an endocardial sheath filled with fluid (assuming the muscle is a radially inhomogeneous and incompressible continuum with cylindrical symmetry). This result allows the endocardial response to be subtracted from the intact papillary muscle response to obtain the response of the bare myocardial core. An initial estimate suggests that the endocardial sheath affects the axial moment significantly (50% of torque for all twists at low stretch) but affects the axial force only slightly (<10% at moderate twists).

Animals↗
PubMed1986

Effect of sotalol, aprindine and their combination on maximum upstroke velocity of action potential in guinea-pig papillary muscle.

Microelectrode experiments were performed on papillary muscle of 11 guinea-pigs at driven heart rates of 60 and 120 b.p.m. to study the effect of sotalol 10(-4) M, aprindine 10(-6) M and the combination of both on Vmax, action potential duration and effective refractory period. Only sotalol exerted tonic Vmax block. Aprindine, sotalol and their combination produced an increase in phasic, combined tonic and phasic, and in steady state Vmax block: the effect of the combination on these parameters being larger than the effect of the single agents alone. Action potential duration was lengthened by both drugs and their combination. A statistically significant increase in effective refractory period was observed for sotalol and the combination sotalol-aprindine but not for aprindine. It can be concluded that simultaneous application of sotalol and aprindine enhances phasic, combined tonic and phasic, and steady state Vmax block with an unchanged effect of sotalol on repolarization. The effect of combinations can be explained on the basis of competition for the same receptor in the Na+ channel.

Action Potentials↗
PubMed1965

INFLUENCE OF GLUCOSE ON THE TRANSMEMBRANE ACTION POTENTIAL OF ANOXIC PAPILLARY MUSCLE.

The response of the cat papillary muscle to anoxia has been found to alter depending on the glucose concentration in the medium. At a glucose concentration of 5 mM anoxia caused a marked reduction in force of contraction and action potential duration within 20 minutes. At a glucose concentration of 50 mM anoxia induced similar changes in the force of contraction but little or no change in action potential duration. Elevation of glucose concentration during an anoxic interval reversed the anoxia-induced changes in action potential but had little effect on force of contraction. This effect of glucose could be partially duplicated by xylose and 2-deoxyglucose and in addition, 2-deoxyglucose has been found to prevent the effect of subsequently added glucose. These sugars appear to be transported by a system responsible for glucose transport but are not metabolized to any extent. It would appear therefore that transport of glucose is in some way related to transport of potassium as increased potassium permeability is thought by many to be responsible for anoxia-induced changes in action potential duration.

Action Potentials↗
PubMed2001

Papillary muscle calcification after inferoposterior myocardial infarction.

Extensive papillary muscle calcification is quite a rare finding in echocardiographic examinations. A case of a 71 year old man with isolated calcification of the papillary muscles, detected by fluoroscopy and confirmed by echocardiography, is presented. Intracardiac calcifications in patients with prior right coronary artery occlusion and mitral regurgitation should suggest the possibility of posteromedial papillary muscle calcification and dysfunction.

Aged↗
PubMed1977

Influence of temperature and frequency on the positive inotropic action of phenylephrine in the isolated rabbit papillary muscle.

On the isolated papillary muscle of the rabbit the maximal developed tension induced by phenylephrine bia alpha-adrenoceptors was not affected by changing the temperature, while the basal developed tension of the muscle was significantly increased or decreased by lowering the temperature from 37 degrees C to 32 degrees C or by raising it to 42 degrees C, respectively. When the temperature was lowered from 37 degrees C to 32 degrees C in the muscle stimulated at a frequency of 0.5 Hz, the dose-response curve for phenylephrine via alpha-adrenoceptors was shifted to the left (delta pD2-0.47), while that for phenylephrine via beta-adrenoceptors was also shifted to the left to a similar extent (delta pD2=0.43). When the temperature was raised from 37 degrees C to 42 degrees C, the dose-response curve for phenylephrine via alpha-adrenoceptors was markedly shifted to the right (delta pD2=1.58), whereas that via beta-adrenoceptors was not affected at all by this elevation of the temperature (delta pD2=0.04). The change of the stimulation frequency affected chiefly the intrinsic activity of phenylephrine but not the affinity of the drug for alpha-adrenoceptors expressed as the pD2-value.

Animals↗
PubMed1988

Role of aiNa in positive force-frequency staircase in guinea pig papillary muscle.

In the ventricular papillary muscle of guinea pig heart, membrane potential, intracellular sodium activity (aiNa), and twitch force were measured simultaneously and continuously for many hours at stimulation rates of 0, 0.5, 1, 2, 3, 4, 5, and 6 Hz to investigate the relation of aiNa to twitch force and membrane potential both in the steady state and during the changes in these variables. After an increase in stimulation rate, both aiNa and twitch force increased progressively, reaching steady-state levels. The relation between twitch force and aiNa in the steady state was generally sigmoidal over the range of 0.5-5 Hz and steep in the 1- to 4-Hz range. After either increase or decrease in stimulation rate, the time course of change in aiNa was exponential and similar to that of change in twitch force. Moreover, the force-aiNa relation observed after increase in stimulation rate from 0.5 to 3 Hz resembled that observed after decrease in the rate from 3 to 0.5 Hz, indicating an absence of hysteresis in the relation. The results suggest that an increase in aiNa is an important factor involved in the force staircase. As stimulation rate was increased from 0.5 to higher rates (5 or 6 Hz) and then decreased back to 0.5 Hz, a hysteresis phenomenon was observed in the relation between twitch force and aiNa. This suggests that some secondary factor may alter the relation between twitch force and aiNa. As stimulation rate increased and aiNa rose, the steady-state diastolic membrane potential hyperpolarized. This result is consistent with the view that an increase in aiNa enhances the electrogenic Na+-K+ pump and hyperpolarizes the cell membrane.

Action Potentials↗
PubMed1987

Intracellular pH in sheep Purkinje fibres and ferret papillary muscles during hypoxia and recovery.

1. The changes of intracellular pH (pHi) of papillary muscles from ferret and Purkinje fibres from sheep heart during hypoxia and recovery from hypoxia were recorded with pH-sensitive micro-electrodes filled with neutral H+ carrier. 2. Hypoxia was produced by replacement of O2 with N2 in the superfusing solutions. When oxidative phosphorylation was prevented, developed tension fell within 20 min to about 16 and 21% of its control value for papillary muscle and Purkinje fibres respectively. On restoration of O2, recovery of developed tension in ferret papillary muscle is preceded by a transient additional decrease. 3. In ferret papillary muscle, the pHi first increased by a mean value of 0.11 pH units after 3 min hypoxia, then decreased by about 0.24 pH units after 20 min. In sheep Purkinje fibres, the initial alkalosis was small or absent, and after 5-9 min, the pHi started to fall reaching 0.17 pH units after 20 min of hypoxia. On return to oxygenated solution, a transient additional intracellular acidification occurred. This acidification reached its peak of 0.31 pH units in papillary muscle and of 0.13 pH units in Purkinje fibres. In both preparations hypoxia was accompanied by a depolarization of a few millivolts. 4. The presence of cyanide (1-2 mM) or fluorodinitrobenzene (20-40 microM) prevented the additional intracellular acidification occurring on return to oxygenated solution. Removal of cyanide itself produced a transient but smaller and slower acidification. 5. On both preparations, exposure to a Tyrode solution containing 10 mM-L-lactate produced a transient intracellular acidification. After recovery from this acidification the acidification produced by hypoxia was increased without affecting the extra acidification on reintroduction of O2. 6. After reduction of the rate of glycolysis by removal of glucose and application of 2-deoxyglucose, the transient intracellular acidification, occurring on return to oxygenated solution after hypoxia, was inhibited in both preparations. In ferret papillary muscle, insulin (100 mU/ml) potentiated the changes of pHi occurring during hypoxia. 7. Using Na+-sensitive glass micro-electrodes it was found that the intracellular Na+ activity rose slightly during the later stages of hypoxia and rose transiently on readdition of O2. These results are consistent with a Na+-H+ exchange being stimulated by acidosis. 8. The origins of the pH changes during and after hypoxia are discussed as are the differences between the responses of sheep Purkinje fibres and ferret papillary muscle.

Animals↗