THE EFFECT OF CERTAIN HORMONE-LIKE SUBSTANCES ON THE ISOLATED HEART OF THE SKATE

1932 ◽  
Vol 7 (1) ◽  
pp. 31-43 ◽  
Author(s):  
M. ELINOR HUNTSMAN

The excised hearts of spinal skates (Raja spp.) were employed, using a modified Straub method with Smith's perfusion fluid. Adrenaline, when added to the perfusion fluid, produced both acceleration and augmentation of the heart beats, but after atropine adrenaline had scarcely any effect. Acetyl choline diminished the rate and decreased the amplitude of the heart beat but on addition of atropine the beat returned to normal. Histamine produced augmentation and a slight acceleration of the heart beat. It was concluded that the skate heart reacts to this substance in much the same way as does the mammalian heart but in the case of the skate there is a rather poorly developed sympathetic innervation.

1964 ◽  
Vol 41 (4) ◽  
pp. 689-700
Author(s):  
HILARY F. BROWN

1. With an external hook electrode placed upon the ganglionic nerve trunk of the isolated heart of Squilla mantis a burst of a small number (3-12) of nerve impulses was recorded at each heart beat. 2. The number of impulses per burst showed a direct correlation with interval between bursts. 3. The only consistent feature of impulse pattern within the bursts was a lengthening of the intervals between impulses towards the ends of the bursts. 4. Electrodes at two points on the ganglionic nerve trunk each recorded the same number of impulses at a burst. The delay between the two recording points was the same for all impulses, and usually all the impulses were, in a given heart, recorded travelling in the same direction, though this could be either forwards or backwards along the chain. 5. It is suggested that each cell in the chain of 16 fires in succession the same number of times during a burst and that the impulses travel along the same ‘firing channel’ within the ganglionic nerve trunk. 6. Cells near the two ends of the chain showed the greatest spontaneity when isolated by transverse cuts or ligatures. Coupled with the records obtained from two points, this suggests that the bursts are initiated in the front or back regions of the chain, but not invariably by the same one of the 16 cells.


1999 ◽  
Vol 202 (19) ◽  
pp. 2595-2607 ◽  
Author(s):  
D. Willoughby ◽  
M.S. Yeoman ◽  
P.R. Benjamin

We have used a combination of biochemical and pharmacological techniques to investigate the role of the cyclic nucleotides, 3′, 5′-cyclic adenosine monophosphate (cyclic AMP) and 3′,5′-cyclic guanosine monophosphate (cyclic GMP), in mediating the cardioregulatory effects of FMRFamide and other neuropeptides encoded on exon II of the FMRFamide gene of Lymnaea stagnalis. The ‘isoleucine’ peptides (EFLRIamide and pQFYRIamide) produced complex biphasic effects on the frequency, force of contraction and tonus of the isolated heart of L. stagnalis, which were dependent on adenylate cyclase (AC) activity of the heart tissue. At a control rate of cyclic AMP production of less than or equal to 10 pmoles min(−)(1)mg(−)(1) protein, the ‘isoleucine’ peptides produced a significant increase in AC activity in heart membrane preparations. This suggested that the enhanced AC activity is responsible for the stimulatory effects of the ‘isoleucine’ peptides on frequency and force of contraction of heart beat. This excitation sometimes followed an initial ‘inhibitory phase’ where the frequency of beat, force of contraction and tonus of the heart were reduced by the ‘isoleucine’ peptides. Hearts that showed the inhibitory phase of the ‘isoleucine’ response, but characteristically lacked the delayed excitatory phase, were found to have high levels of membrane AC activity (breve)10 pmoles min(−)(1)mg(−)(1) protein in controls. Application of the ‘isoleucine’ peptides to membrane homogenate preparation from these hearts failed to increase AC activity. The addition of FMRFamide produced significant increases in the rate of cyclic AMP production in the heart membrane preparations, which could account, at least in part, for the cardioexcitatory effects of this peptide in the isolated whole heart. A membrane-permeable cyclic AMP analogue (8-bromo-cyclic AMP) and an AC activator (forskolin) were also cardioexcitatory. The peptide SEEPLY had no effects on the beat properties of the isolated heart and did not alter AC activity. The activity of the membrane-bound (particulate) guanylate cyclase (GC) was not significantly affected by any of the peptides.


2003 ◽  
Vol 284 (6) ◽  
pp. H2384-H2392 ◽  
Author(s):  
A. Rosa ◽  
J.-P. Maury ◽  
J. Terrand ◽  
X. Lyon ◽  
P. Kucera ◽  
...  

Recently, rapid and transient cardiac pacing was shown to induce preconditioning in animal models. Whether the electrical stimulation per se or the concomitant myocardial ischemia affords such a protection remains unknown. We tested the hypothesis that chronic pacing of a cardiac preparation maintained in a normoxic condition can induce protection. Hearts of 4-day-old chick embryos were electrically paced in ovo over a 12-h period using asynchronous and intermittent ventricular stimulation (5 min on-10 min off) at 110% of the intrinsic rate. Sham ( n = 6) and paced hearts ( n= 6) were then excised, mounted in vitro, and subjected successively to 30 min of normoxia (20% O2), 30 min of anoxia (0% O2), and 60 min of reoxygenation (20% O2). Electrocardiogram and atrial and ventricular contractions were simultaneously recorded throughout the experiment. Reoxygenation-induced chrono-, dromo-, and inotropic disturbances, incidence of arrhythmias, and changes in electromechanical delay (EMD) in atria and ventricle were systematically investigated in sham and paced hearts. Under normoxia, the isolated heart beat spontaneously and regularly, and all baseline functional parameters were similar in sham and paced groups (means ± SD): heart rate (190 ± 36 beats/min), P-R interval (104 ± 25 ms), mechanical atrioventricular propagation (20 ± 4 mm/s), ventricular shortening velocity (1.7 ± 1 mm/s), atrial EMD (17 ± 4 ms), and ventricular EMD (16 ± 2 ms). Under anoxia, cardiac function progressively collapsed, and sinoatrial activity finally stopped after ∼9 min in both groups. During reoxygenation, paced hearts showed 1) a lower incidence of arrhythmias than sham hearts, 2) an increased rate of recovery of ventricular contractility compared with sham hearts, and 3) a faster return of ventricular EMD to basal value than sham hearts. However, recovery of heart rate, atrioventricular conduction, and atrial EMD was not improved by pacing. Activity of all hearts was fully restored at the end of reoxygenation. These findings suggest that chronic electrical stimulation of the ventricle at a near-physiological rate selectively alters some cellular functions within the heart and constitutes a nonischemic means to increase myocardial tolerance to a subsequent hypoxia-reoxygenation.


1897 ◽  
Vol 2 (4) ◽  
pp. 391-404 ◽  
Author(s):  
W. T. Porter

1. The cause of the rhythmic contraction of the ventricle lies within the ventricle itself. 2. The cause of the rhythmic contraction is not a single, localized, co-ordination centre; the co-ordination mechanism, whatever it may be, is present in all parts of the ventricle. 3. The integrity of the whole ventricle is not essential to the coordinated contractions of a part of the ventricle. 4. The apex of the mammalian heart possesses spontaneous, rhythmic contractility. 5. Assuming that the general belief in the absence of nerve cells from the apical part of the ventricle is correct, these experiments demonstrate that nerve cells are not essential to spontaneous, long-continued, co-ordinated contractions of the ventricle.


1972 ◽  
Vol 56 (1) ◽  
pp. 239-247
Author(s):  
G. W. CIVIL ◽  
T. E. THOMPSON

1. Isolated hearts of Helix pomatia could be maintained for 3-4 days at 19 °C in physiological saline. Co-ordination was soon lost, but irregular twitches could be observed for up to 115 h. 2. A perfusion apparatus was designed which supplied a simulated venous return pressure of 8 cm saline and enabled in vitro survival of pericardium-free hearts for up to 2 days at 15 °C. Cessation of perfusion led immediately to a reversible stoppage of heart-beat. 3. An artificial pericardium apparatus (APA) allowed the role of the pericardium to be studied. In the APA measurable translocation of fluid was effected by the heart, even when the simulated venous return pressure was negative. 4. If the APA was transformed into an open system by opening up a simulated reno-pericardial canal, the effectiveness of the heart was greatly reduced. 5. In the APA the greater the dilation of the heart (in consequence of decreased volume of pericardial fluid) the greater was the stroke volume for a given simulated venous return pressure. 6. Results obtained with the APA give support to the theory that in the gastropod heart the filling of the auricle is hydrodynamically coupled (through the pericardial fluid) to the emptying of the ventricle.


1999 ◽  
Vol 202 (19) ◽  
pp. 2581-2593 ◽  
Author(s):  
D. Willoughby ◽  
M.S. Yeoman ◽  
P.R. Benjamin

This paper examines the importance of the calcium-mobilizing inositol phosphate pathway in mediating the effects of FMRFamide and its gene-related neuropeptides on the myogenic heart beat of the pond snail Lymnaea stagnalis. These peptides are encoded on a single exon of the FMRFamide gene and mediate diverse physiological effects in the isolated heart. The rate of production of inositol-1,4, 5-trisphosphate [Ins(1,4,5)P(3)] and inositol-1,3,4, 5-tetrakisphosphate [Ins(1,3,4,5)P(4)], measured using an HPLC method, were both significantly elevated in a concentration-dependent manner by FMRFamide (and were also elevated by FLRFamide). The threshold for increasing inositol phosphate production was low (100 pmol l(−1)) with a peak response occurring at 1 micromol l(−1) FMRFamide. The shape of the dose-response curve for FMRFamide-induced elevation of heart-beat frequency, obtained in pharmacological experiments on the isolated whole heart, was similar to that for stimulation of inositol phosphate levels in homogenized heart tissue. FMRFamide and Ins(1,4,5)P(3) produced similar effects on the rate of heart beat in permeabilized whole hearts. In addition, the phospholipase C inhibitor, neomycin (2.5 mmol l(−)(1)), blocked the stimulatory effects of FMRFamide on Ins(1, 4,5)P(3) production in heart homogenate, and attenuated the excitatory effects of this neuropeptide in the isolated heart. The ‘isoleucine’ pentapeptides, EFLRIamide and pQFYRIamide, also encoded by the FMRFamide gene, produced no significant effects on inositol phosphate production when applied alone or in combination with FMRFamide. These results suggested that FMRFamide (and FLRFamide), but not EFLRIamide and pQFYRIamide, mediated their main effects on heart beat via the inositol phosphate pathway. The fifth peptide, SEQPDVDDYLRDVVLQSEEPLY (‘SEEPLY’) had no effect when applied alone but appeared to modulate the effects of FMRFamide by delaying the time-to-peak of the Ins(1,4,5)P(3) response from 5 s to 20 s by an unknown mechanism.


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