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Biomedical subjects

W H Barry

Publications and source records attributed to W H Barry.

At least 91 records · Page 5Linked to original sources
PubMed1987

Effects of ryanodine and caffeine on contractility, membrane voltage, and calcium exchange in cultured heart cells.

To investigate the mechanisms of action of ryanodine and caffeine, changes in mechanical and electrical activity caused by these agents were correlated with alterations in 45Ca fluxes and cell Ca contents in chick embryo ventricular cell monolayer cultures. Ryanodine (10(-10)-10(-5) M) irreversibly decreased contraction amplitude by 10-70% relative to control in a concentration-dependent manner with minimal effects on electrical activity. Ryanodine caused a slight decrease in rapid 45Ca uptake, but no change in total exchangeable calcium content or rapid 45Ca efflux. Caffeine (1-20 mM) caused a transient (less than 10 seconds) 5-12% increase in contraction amplitude followed by a sustained 9-76% decrease in contraction amplitude and a 10 mV decrease in diastolic membrane voltage. Caffeine caused a decrease in rapid 45Ca uptake, a decrease in total exchangeable calcium content, and an increase in rapid 45Ca efflux. These results suggest that caffeine produces a decrease in sarcoplasmic reticulum (SR) Ca2+ uptake, and/or an increase in SR Ca2+ release that eventually depletes the SR of Ca2+, presumably accounting for the negative inotropic effect. The ryanodine effects on contraction are more difficult to account for solely in terms of alterations of transsarcolemmal Ca2+ fluxes and Ca2+ contents. Our data indicate an important role for the SR in excitation-contraction coupling in cultured chick embryo ventricular cells and suggest that SR Ca2+ is part of the rapidly exchanging Ca2+ compartment noted in 45Ca flux studies.

Alkaloids↗
PubMed1987

Role of changes in [Ca2+]i in energy deprivation contracture.

Mechanisms of energy deprivation contracture were investigated in cultured chick embryo ventricular cells. In the presence of zero-extracellular-Na+, (choline chloride substitution)-nominal-zero-Ca2+ [( Ca2+] approximately 5 microM), exposure of ventricular cells to 1 mM cyanide (CN) and 20 mM 2-deoxyglucose (2-DG)-zero-glucose solution resulted in the development of a contracture (video motion detector) in 5.9 +/- 0.5 minutes. Early after contracture development, the resupply of extracellular Na+, in the continued presence of CN + 2-DG, resulted in a rapid partial relaxation (t1/2 = 1.9 +/- 0.3 seconds), associated with an increase in 45Ca efflux, presumably due to transsarcolemmal Ca2+ extrusion due to Na+-Ca2+ exchange. Resupply of glucose and removal of CN + 2-DG, in the continued absence of Na+, resulted in an initially slower (t1/2 = 11.6 +/- 2.5 seconds), but more complete relaxation of contracture, which was not associated with increased Ca2+ efflux. Pretreatment with 20 mM caffeine delayed the onset of contracture (9.2 +/- 1.1 minutes) and resulted in a contracture that could not be relaxed by resupply of external Na+ only. Studies using the fluorescent Ca2+ probe indo 1 demonstrated that in zero-Na+-zero-Ca2+ solutions, contracture due to CN + 2-DG was associated with an initial rise in [Ca2+]i but that this did not account for all of contracture force development. In cells exposed to CN + 2-DG in the presence of normal extracellular Na+ and Ca2+ concentrations, a small rise in [Ca2+]i was associated with initial contracture development, consistently preceding the development of a larger accelerated contracture presumably due to ATP depletion.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Triphosphate↗
PubMed1987

Acute coronary occlusion and reperfusion. Reliability of angiographic classification and grading.

93 patients with acute myocardial infarction entered into a multicentre, randomised fibrinolytic therapy study underwent coronary angiography prior to treatment with intracoronary streptokinase or intravenous anisoylated plasminogen streptokinase activator complex (APSAC). Subsequent to administration of fibrinolytic therapy, coronary arteriography of the infarct-related artery was also performed at 15, 30, 45, 60, 75 and 90 minutes. Angiographically defined coronary perfusion was graded as follows: grade 0--no perfusion; grade 1--vessel penetration by contrast without perfusion; grade 2--partial perfusion with delayed flow and/or clearance; grade 3--normal flow and clearance. Two independent readers at separate sites reviewed all serial angiograms with consensus achieved with a third reader. Disagreement potentially affecting therapeutic outcome (grades 1 vs 2, 0 vs 2, 0 vs 3, and 1 vs 3) occurred for only 15 angiographic views. Evaluation of agreement by the K index demonstrated a reasonable level of agreement for all grades (K = 0.73). In order to assess the effect of angiographic classification and timing upon reperfusion percentage rates, 4 reperfusion criteria were applied to these serial angiograms: group A = grade 2 or 3 flow at 90 minutes; group B = grade 2 or 3 flow at any time; group C = grade 1, 2 or 3 flow at any time in patients with control grade 0 or 1 flow; group D = grade 1, 2 or 3 flow at any time in patients with only grade 0 flow at control. Percentage reperfusion varied widely depending upon reperfusion criteria: group A: streptokinase 49%, APSAC 44%; group B: streptokinase 70%, APSAC 50%; group C: streptokinase 86%, APSAC 67%; group D: streptokinase 79%, APSAC 59%.(ABSTRACT TRUNCATED AT 250 WORDS)

Anistreplase↗
PubMed1986

External Na-independent Ca extrusion in cultured ventricular cells. Magnitude and functional significance.

The relative magnitudes and functional significance of Ca extrusion by Na-Ca exchange and by an Nao-independent mechanism were investigated in monolayer cultures of chick embryo ventricular cells. Abrupt exposure of cells in 0-Nao, nominally 0-Cao solution to 20 mM caffeine produced a large contracture (3.94 +/- 0.90 micron of cell shortening) that relaxed with a t1/2 of 8.60 +/- 1.22 s. An abrupt exposure to caffeine plus 140 mM Na resulted in a contracture that was smaller in amplitude (1.53 +/- 0.50 micron) and relaxed much more rapidly (t1/2 = 0.77 +/- 0.09 s). An abrupt exposure to caffeine in 0-Nao solutions produced an increase in 45Ca efflux that persisted for 20 s, and a net loss of Ca content, determined by atomic absorption spectroscopy (AAS), of approximately 4 nmol/mg protein, within 35 s. A comparable net loss of Ca was demonstrated in the presence of 100 microM [Ca]o. The abrupt exposure of cultured cells to 0 Nao in 1.8 mM Ca produced a Ca uptake, estimated with 45Ca, of 3.2 nmol/mg protein X 15 s, but produced no increase in cell Ca content (AAS). In cells in which a 30% increase in Nai was produced by 5 min exposure to 10(-6) M ouabain, the abrupt exposure to 0 Nao produced a Ca uptake of 6 nmol/mg protein X 15 s and an increase in Ca content (AAS) of 4 nmol/mg protein. We conclude that there is an Nao-independent mechanism for Ca extrusion in these cells, presumably a Ca-ATPase Ca pump, with a limited Ca transport capacity of no more than 2 nmol/mg protein X 15 s. This is five times smaller than the demonstrated maximum capacity of the Na-Ca exchanger in these cells. The relaxation of twitch tension in these cells seems to be dependent primarily on sarcoplasmic reticulum uptake of Ca, with a secondary role provided by the Na-Ca exchanger. The Ca pump appears to contribute little to beat-to-beat relaxation.

Animals↗
PubMed1986

Effects of contrast media on cultured myocardial cells.

To quantify and characterize mechanisms of negative inotropic effects of ionic and nonionic angiographic contrast media, spontaneously contracting monolayers of cultured chick ventricular cells were studied using the Renografin-76 and iohexol as characteristic ionic and nonionic contrast agents. Utilizing microscopic video-motion detector techniques the effect of each contrast agent on contraction amplitude was measured. Also, the effect of changes in the ionized calcium concentration and osmolality induced by the contrast agents was evaluated. The study demonstrated a linear depression of contractility by increasing contrast concentrations. The negative inotropic effect of Renografin-76 was significantly greater than that of iohexol. Renografin-76 demonstrated significant calcium binding, whereas iohexol had none. Correction for calcium binding by Renografin-76 partially reversed the negative inotropic effect of this agent. Hypertonic sugar solutions of equivalent osmolality to the contrast agents demonstrated dose-related negative inotropic effects such that, in this preparation, calcium binding by Renografin-76 and its high osmolality accounted for all its negative inotropic effect. In contrast, iohexol demonstrated an intrinsic negative inotropic effect not completely explained by its osmolality.

Animals↗
PubMed1985

Usefulness of transstenotic coronary pressure gradient measurements during diagnostic catheterization.

A difficult problem in coronary arteriography is the assessment of the hemodynamic significance of stenoses that appear angiographically to be of only moderate severity (25 to 75% diameter narrowing). This is particularly important in patients who may be candidates for invasive therapy, such as percutaneous transluminal coronary angioplasty (PTCA) or coronary bypass surgery. To determine the significance of such lesions, we measured transstenotic coronary pressure gradients in 15 patients with angiographically moderate stenoses. For comparison, similar measurements were made in 17 patients with severe stenoses (more than 75% diameter narrowing) being considered for PTCA. The transstenotic pressure gradients were measured with a 2.0Fr polyvinyl chloride catheter cleared of microbubbles of air by flushing with carbon dioxide and degassed saline solution and attached to a low-volume displacement transducer for optimal frequency response. Mean transstenotic pressure gradients greater than 10 mm Hg at rest or more than 20 mm Hg under conditions of high coronary blood flow, as induced by Renografin 76, appeared to be associated with objective evidence of myocardial ischemia and symptomatic relief from PTCA. Smaller pressure gradients occurred in patients whose symptoms probably were not ischemic in nature. Transstenotic pressure gradient determination performed at the time of diagnostic catheterization may provide assistance in clinical decision-making in selected patients with angiographically moderate stenoses.

Angioplasty, Balloon↗
PubMed1985

Inotropic, vascular and neuroendocrine effects of nifedipine in heart failure: comparison with nitroprusside.

To evaluate the short-term hemodynamic and neuroendocrine effects of nifedipine in heart failure, it was compared with nitroprusside, a balanced vasodilator without known inotropic effect, in equihypotensive doses during right and left heart catheterization in nine patients with heart failure. Mean arterial pressure decreased from 89 +/- 12 to 76 +/- 14 mm Hg with nitroprusside, and from 90 +/- 12 to 75 +/- 13 mm Hg with sublingual nifedipine. Right atrial, pulmonary artery, pulmonary capillary wedge and left ventricular end-diastolic pressures decreased significantly with nitroprusside, but not with nifedipine. Cardiac index and stroke volume index increased to a similar extent with both drugs; in contrast, stroke work index increased significantly with nitroprusside, but not with nifedipine. Peak rate of left ventricular pressure development (dP/dt) (measured with a micromanometer-tipped catheter in seven patients) was unchanged with nitroprusside, but decreased significantly with nifedipine (747 +/- 292 to 639 +/- 238 mm Hg/s; p less than 0.002). There was no change in heart rate with either medication. Plasma norepinephrine and epinephrine concentrations were not altered significantly by either drug. Plasma renin activity was not changed by nitroprusside infusion, but was increased after the administration of nifedipine. Thus, in contrast to the balanced vasodilator action of nitroprusside, the effect of nifedipine is predominantly on the arterial circulation. In these patients with heart failure, reflex sympathetic stimulation did not occur in response to a decrease in systemic arterial pressure by either vasodilator. A negative inotropic effect occurred after the administration of nifedipine, but not nitroprusside.

Adult↗
PubMed1985

Attenuation of coronary vascular resistance by selective alpha 1-adrenergic blockade in patients with coronary artery disease.

Alpha-adrenergic-mediated coronary vasoconstriction during stress such as cold pressor testing may contribute to myocardial ischemia by increasing coronary vascular resistance in patients with severe coronary artery disease. Nonselective alpha-receptor blockade with phentolamine abolishes both the peripheral and coronary vasoconstriction during cold pressor testing, but causes reflex tachycardia and increased inotropy. To determine the role of selective alpha 1-receptor blockade, the changes in coronary vascular resistance during cold pressor testing were measured in 18 patients with coronary artery disease before and after intravenous administration of 100 mg of trimazosin. Cold pressor testing was performed at a constant paced subanginal heart rate of 95 +/- 5 beats/min (+/- 1 SD). Before trimazosin, cold pressor testing increased mean arterial pressure by 9 +/- 4% (102 +/- 14 to 111 +/- 14 mm Hg, p less than 0.001) with no change in coronary sinus blood flow, but significantly increased coronary vascular resistance by 15 +/- 19% (1.02 +/- 0.46 to 1.15 +/- 0.57 units, p less than 0.05). Five minutes after trimazosin, cold pressor testing increased mean arterial pressure by 6 +/- 5% (p less than 0.001) with a marked attenuation of the increase in coronary vascular resistance (6 +/- 11%, p = NS), which was significantly less than before trimazosin (p less than 0.02). Trimazosin did not increase plasma norepinephrine concentration at rest, suggesting that in the dosage used trimazosin caused selective alpha 1-receptor blockade.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic alpha-Antagonists↗
PubMed1985

Evaluation of optimized biplane pulmonary cineangiography.

Biplane pulmonary cineangiograms utilizing a short cine pulse width and automatic brightness control were performed in 47 patients during normal respiration. The diagnostic quality of the arteriograms was categorized as good in 33 patients, fair in 12 patients, and poor in two patients. Of the 18 patients in whom pulmonary emboli were identified, cineangiography displayed certain diagnostic features to advantage, including motion of emboli in ten and respiratory scissoring of vessels overcoming vascular superimposition in three. Optimized pulmonary cineangiography is an acceptable alternative to serial film pulmonary angiography for the diagnosis of pulmonary embolism.

Cineangiography↗
PubMed1985

Comparison of negative inotropic potency, reversibility, and effects on calcium influx of six calcium channel antagonists in cultured myocardial cells.

The negative inotropic effects of calcium channel antagonists on the myocardium were used as a standard for the definition and determination of potency of this group of drugs. The effects of six calcium channel antagonists (verapamil, methoxyverapamil (D600), nifedipine, lidoflazine, perhexiline and diltiazem) were compared on cultured chick embryo ventricular cells. Drug concentrations producing 50% inhibition of contractile amplitude, derived from linearized concentration-response curves, varied from 2.8 X 10(-8)M for nifedipine to 8.3 X 10(-7)M for perhexiline. Equipotent negative inotropic concentrations of verapamil, D600, perhexiline, diltiazem and lidoflazine produced a similar inhibitory effect on 45Ca uptake into cultured cells. Nifedipine produced no significant inhibition of 45Ca uptake. The time required for recovery of contractility after cessation of drug superfusion varied in the order lidoflazine greater than perhexiline greater than D600 greater than verapamil greater than nifedipine greater than diltiazem. This relative order accords closely with the reported in vivo half-lives of these drugs. It is concluded that while some inhibition of 45Ca2+ uptake into cardiac cells can be demonstrated with five of the six calcium channel blockers studied, the relationship between the degree of inhibition of calcium influx and negative inotropic effects may not be uniform for all calcium channel antagonists.

Animals↗
PubMed1985

Sodium pump inhibition, enhanced calcium influx via sodium-calcium exchange, and positive inotropic response in cultured heart cells.

The effects of sodium pump inhibition produced by exposure to the cardiac glycosides, ouabain or dihydroouabain, or by reduction in extracellular potassium to 1.0 mM, on contractile state and sodium-calcium exchange were studied in primary monolayer cultures of chick embryo ventricular cells. Ouabain, 10(-6)M, dihydroouabain, 5 X 10(-5)M, and extracellular potassium of 1.0 mM all induced similar and prominent positive inotropic effects. These effects were accompanied, in each case, by 40-50% inhibition of the rate of active uptake of 42K and by similar increases in steady state sodium content. Stimulation of the rate of 45Ca uptake on exposure to zero extracellular sodium occurred in response to extracellular potassium (1.0 mM) or to glycoside concentrations that induced a positive inotropic effect and sodium-potassium pump inhibition. Reactivation of the sodium pump after return from 1.0 to 4.0 mM extracellular potassium was rapid and was associated with membrane hyperpolarization and slowing of spontaneous beating rate. With pump reactivation under these circumstances, the time course of disappearance of stimulation of sodium-calcium exchange on exposure to zero extracellular sodium was similar to the time course of loss of the positive inotropic effect. Under physiological conditions (4.0 mM extracellular potassium), exposure to positively inotropic but nontoxic concentrations of ouabain or dihydroouabain caused a small but consistent increase in unidirectional calcium influx, but had no discernible effect on calcium efflux. Since similar inotropic effects were produced for comparable degrees of glycoside or low extracellular potassium-induced sodium pump inhibition and increases in cellular sodium content, sodium pump inhibition rather than a glycoside-specific change in calcium binding appears to underlie the inotropic response. These findings are further consistent with the view that the primary mechanism of the positive inotropic effects of digitalis and low extracellular potassium in this experimental preparation is sodium pump inhibition resulting in increased intracellular sodium. We suggest that increased calcium influx via sodium-calcium exchange is the principal mechanism whereby increased intracellular sodium results in enhanced calcium availability to the myofibrils, but an additional effect on calcium efflux is not excluded.

Animals↗
PubMed1984

Effects of prostacyclin on coronary hemodynamics at rest and in response to cold pressor testing in patients with angina pectoris.

To assess the effect of prostacyclin on the diseased coronary circulation basally and, in particular, on the coronary responses to the cold pressor test, a small dose of 4 ng/kg/min and a large dose of 8 to 10 ng/kg/min was infused in 11 patients with stable angina pectoris. Coronary blood flow was measured by coronary sinus thermodilution technique. The mean blood pressure decreased from 97 +/- 5 to 89 +/- 5 mm Hg during the low-dose infusion (p less than 0.005) and to 81 +/- 5 mm Hg during the high-dose infusion (p less than 0.001); the heart rate increased from 65 +/- 4 to 69 +/- 4 beats/min during the low-dose infusion (p less than 0.05) and to 78 +/- 5 beats/min during the high-dose infusion (p less than 0.001). Systemic vascular resistance decreased by 11 +/- 4% with small doses (p less than 0.05) and by 38 +/- 4% with large doses (p less than 0.001) of prostacyclin, and coronary vascular resistance decreased by 16 +/- 7% (p less than 0.05) with the small dose and by 29 +/- 6% (p less than 0.001) with the large dose of prostacyclin. Seven of 11 patients showed a baseline vasoconstrictor response to the cold pressor test (increase in coronary vascular resistance of 11 +/- 2%). This increase in coronary vascular resistance was not altered by either the small or the large dose of prostacyclin. Thus, prostacyclin causes marked coronary and systemic vasodilation, with no evidence of selective enhancement of the sensitivity of the diseased coronary circulation.(ABSTRACT TRUNCATED AT 250 WORDS)

Angina Pectoris↗
PubMed1984

Effects of calcium flux inhibitors on contracture and calcium content during inhibition of high energy phosphate production in cultured heart cells.

The effects of inhibition of oxidative phosphorylation by 1 mM cyanide (CN) and of glycolysis by 20 mM 2-deoxyglucose (2DG) on contraction and relaxation of cultured monolayers of chick embryo heart cells were determined. Exposure to these agents first induced a gradual decline in contractility and a transient impairment of relaxation. Spontaneous beating then ceased, associated with increased relaxation, followed by a marked and prolonged contracture. This contracture was completely reversible after washout of metabolic inhibitors. The effects of calcium flux inhibitors on the time course of development of contracture were studied. Verapamil, which inhibits Ca influx via the slow Ca channel, delayed the onset of contracture when used in pretreatment, but had no effect if added to cultures after exposure to CN + 2DG. Lanthanum, which inhibits Ca influx both via the slow Ca channel and via Na-Ca exchange, delayed onset of contracture if added after exposure to CN and 2DG, but accelerated contracture if added prior to treatment with CN + 2DG. Cellular exchangeable calcium content, measured after exposure to CN and 2DG for the same time period that produced contracture, was reduced compared to the control level while unidirectional Ca influx rate was not measurably altered. Exchangeable Ca content was unaffected by pretreatment with verapamil and La, but was reduced if cells were exposed to La after metabolic inhibition. These findings suggest that after metabolic inhibition intracellular storage capacity for Ca+ is reduced in cultured heart cells. Ca influx via the slow Ca channel after metabolic inhibition does not appear to contribute to development of contracture in this model system. However, Ca entry via Na-Ca exchange may accelerate cellular contracture developing after metabolic inhibition of ATP production.

Adenosine Triphosphate↗
PubMed1984

Electrophysiologic and mechanical effects of metabolic inhibition of high-energy phosphate production in cultured chick embryo ventricular cells.

The early electrophysiological and mechanical effects of metabolic inhibition of high energy phosphate production were studied in cultured chick embryo heart cells. Selective inhibition of either glycolysis by 2-deoxyglucose in the presence of acetate or of oxidative phosphorylation by cyanide showed different effects. 2-deoxyglucose induced pronounced reduction in maximal diastolic potential and prolongation of excitation contraction delay, with only a moderate decrease of contractility and with only minimal changes in action potential duration. Cyanide, on the other hand, induced a profound negative inotropic effect and caused slowing of relaxation, shortening of action potential duration, a decrease in the upstroke of the action potential, and only a moderate decrease in the diastolic membrane potential. Exposure to 2-deoxyglucose and cyanide combined produced effects consistent with inhibition of both metabolic pathways. These observations are consistent with the hypothesis that these two metabolic pathways may have specific roles in fueling several energy-demanding functions of the myocardial cell.

Adenosine Triphosphate↗
PubMed1984

Movement of Ca2+ across the sarcolemma: effects of abrupt exposure to zero external Na concentration.

Uncertainty exists regarding the mechanisms of Ca efflux from isolated myocardial cells. Therefore, transmembrane fluxes of Ca, exchangeable Ca content, and contractile behavior were studied in monolayers of cultured chick embryo-ventricle during abrupt exposure to media containing zero [Na]o (choline chloride substitution). Exposure to zero [Na]o induced a transient contracture of cultured heart cells. Rapid Ca influx increased significantly over the first 60 s immersion in zero [Na]o; however, total exchangeable Ca content, measured by labelling with 45Ca, did not change, suggesting that rapid Ca efflux was also increasing under these conditions. When 45Ca in the extracellular space was removed by washing for 16 s in ice cold buffer before 45Ca efflux was measured, an increase in Ca efflux with exposure to zero [Na]o was apparent. Treatment of cells with 10(-3) M cyanide and 20 mM 2-deoxyglucose resulted in a decrease in the Ca efflux in zero [Na]o-zero [Ca]o medium, and in the appearance of significant components of [Na]o and [Ca]o-dependent Ca efflux. These results are consistent with the hypothesis that Ca efflux in these cells normally occurs predominantly by a non-[Na]o-dependent mechanism, probably an ATP-dependent Ca pump. After metabolic blockade of ATP production with a resulting increase in Ca loading of the cytoplasm, increased efflux of Ca via Na Ca and Ca Ca exchange occurs.

Adenosine Triphosphate↗
PubMed1984

Effects of verapamil on contraction and relaxation of cultured chick embryo ventricular cells during calcium overload.

The calcium channel blocking agents verapamil and nifedipine have been reported to lessen abnormalities of left ventricular relaxation in patients with severe left ventricular hypertrophy or coronary artery disease. Whether these effects in human beings are related in part to a direct effect on myocardial calcium metabolism is difficult to determine because of complicating drug influences on ventricular loading via systemic arterial vasodilation, on myocardial blood supply via coronary artery vasodilation and on reflex changes in sympathetic tone. For this reason, the effects of verapamil were investigated in a cellular model of impaired relaxation using spontaneously contracting tissue cultured monolayers of chick embryo ventricular cells exposed to high external calcium ([Ca]o). Under control conditions ([Ca]o, 0.9 mM), verapamil (2 X 10(-8)M) induced a 57 +/- 8% decrease in amplitude of cell contraction monitored with a phase contrast microscope video motion detector system. Elevation of [Ca]o from 0.9 to 8.0 mM resulted in a decrease in amplitude and velocity of contraction and a decrease in velocity of relaxation associated with an upward shift in diastolic cell wall position, suggesting a failure of normal myofilament dissociation. These abnormalities were completely reversible on reperfusion with [Ca]o, 0.9 mM. On re-exposure of the cells to [Ca]o, 8.0 mM, in the presence of verapamil, there was an increase in amplitude of contraction (0.56 +/- 0.11 to 1.03 +/- 0.09 micron, p less than 0.01) and velocity of relaxation (4.97 +/- 0.89 to 9.94 +/- 0.87 micron/s, p less than 0.01) compared with exposure to [Ca]o, 8.0 mM, alone, and an attenuation of the upward shift in diastolic cell wall position.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗