Characterization of responses of neonatal sinus and AV nodes to critically timed, brief vagal stimuli

1991 ◽  
Vol 260 (2) ◽  
pp. H459-H464 ◽  
Author(s):  
S. Yamasaki ◽  
A. Stolfi ◽  
A. S. Pickoff
Keyword(s):  
Cycle Length ◽  
Cardiac Cycle ◽  
Gradual Increase ◽  
Latency Period ◽  
Atrial Pacing ◽  
Response Curves ◽  
Stimulus Train ◽  
Sinus Cycle Length ◽  
The Right

We studied the responses of sinus cycle length and atrioventricular (AV) nodal conduction to brief, critically timed vagal stimuli in 25 neonatal (9.6 +/- 3.1 days) canines. Vagal stimuli were delivered to the right or left decentralized cervical vagosympathetic trunk as either a single, brief stimulus train or a repetitive, phase-coupled train with both stimulation paradigms programmed to scan the entire cardiac cycle. The effects of brief vagal stimuli on cardiac cycle length were measured while the heart was beating spontaneously, and the vagal effects on AV nodal conduction were measured while the cycle length was held constant by atrial pacing at 300 ms. Neither changes in sinus cycle length nor AV nodal conduction demonstrated classical phase dependency, i.e., a gradual increase in the magnitude of the vagal response as stimuli are delivered progressively later in the cardiac cycle until the latency period (that point in the cardiac cycle at which vagal stimulation no longer affects the next cardiac cycle) is reached. Phase-response curves (PRCs) to single and repetitive stimuli typically exhibited either a flat response or a small decrease in magnitude as the latency period of the PRC was approached. Thus the neonatal sinus and AV node PRCs exhibit a different configuration than that reported in the adult.

Effects of vagus nerve on heart rate and ventricular contractility in chicken

1989 ◽  
Vol 256 (5) ◽  
pp. H1295-H1302
Author(s):  
S. A. Lang ◽  
M. N. Levy
Keyword(s):  
Vagus Nerve ◽  
Cycle Length ◽  
Cardiac Cycle ◽  
Ventricular Contractility ◽  
Ventricular Contraction ◽  
Vagus Stimulation ◽  
Constant Frequency ◽  
The Right ◽  
Contraction And Relaxation ◽  
Left Vagus

We determined the effects of vagus nerve stimulation on cardiac cycle length and on ventricular contraction and relaxation in 18 chickens anesthetized with pentobarbital. Right vagus stimulation at a constant frequency of 35 Hz prolonged cycle length by 190%, whereas left vagus stimulation at the same frequency increased cycle length by 136%. When one burst of stimuli was delivered to the right vagus nerve each cardiac cycle, but the timing of the stimuli was changed within the cardiac cycle, the response of the avian pacemaker cells varied substantially with the timing of the stimuli. Right and left vagus stimulation at a constant frequency of 20 Hz depressed ventricular contraction by 62 +/- 6 and 52 +/- 6%, respectively, and depressed ventricular relaxation by 56 +/- 7 and 53 +/- 7%, respectively. These results indicate that in the chicken the chronotropic effects of right vagus stimulation are greater than those of left vagus stimulation, whereas right and left vagus stimulation are approximately equipotent on ventricular contraction and relaxation.

Characterization of sulfidopeptide leukotriene responses in sheep tracheal smooth muscle in vitro

1991 ◽  
Vol 69 (6) ◽  
pp. 805-811 ◽  
Author(s):  
K. Tomioka ◽  
J. T. Jackowski ◽  
W. M. Abraham
Keyword(s):  
Smooth Muscle ◽  
Dose Response ◽  
Tracheal Smooth Muscle ◽  
Response Curves ◽  
Leukotriene Antagonist ◽  
Dose Response Curves ◽  
The Right ◽  
Glutamyl Transpeptidase

We have investigated the effects of leukotrienes (LTs) on isolated tracheal smooth muscle from sheep sensitive to Ascaris suum antigen. LTC4 and LTD4 produced dose-dependent contractions of sheep trachea, but LTE4 was virtually inactive. YM-17690, a non-analogous LT agonist, produced no contractile response up to 100 μM. Indomethacin (5 μM) had no effect on LTC4- and LTD4-induced contractions. L-Serine borate (45 mM), an inhibitor of γ-glutamyl transpeptidase, shifted the dose–response curve of LTC4 to the left by 161-fold, and L-cysteine (6 mM), an inhibitor of aminopeptidase, shifted the dose–response curves of LTC4 and LTD4 to the left by 67- and 23-fold, respectively. YM-16638 (1 μM), an LT antagonist, shifted the dose–response curves of LTC4 and LTD4 to the right with pKB values of 6.57 and 7.13, respectively. YM-16638 did not affect LTC4-induced contractions of L-serine borate-treated tissues, indicating that the compound acts only on LTD4 receptors in sheep trachea. LTE4 (1 μM) shifted the dose–response curves of LTC4 and LTD4 to the right with pKB values of 6.87 and 7.31, respectively. YM-17690 (10 μM) showed effects similar to LTE4, suggesting that the compound acts as an LTE4 agonist in sheep trachea. These results suggest that in sheep tracheal smooth muscle (a) LTC4 and LTD4 produce contractions, (b) these LT-induced contractions are not mediated by cyclooxygenase products, (c) LTC4 is converted to LTD4 and then to LTE4, and (d) the potency of the LTC4- and LTD4-induced contractions is increased when their conversion to LTE4 is inhibited. This potentiation may result from the inability of LTE4 to contract sheep trachea and (or) its antagonist actions.Key words: leukotriene antagonist, receptors, asthma.

Effect of phasic vagal stimulation and atrial pacing site on atrioventricular conduction time

1997 ◽  
Vol 272 (5) ◽  
pp. H2289-H2298 ◽  
Author(s):  
D. A. Igel ◽  
D. W. Wallick ◽  
P. J. Martin ◽  
M. N. Levy
Keyword(s):  
Coronary Sinus ◽  
Cycle Length ◽  
Vagal Stimulation ◽  
Interatrial Septum ◽  
Conduction Time ◽  
Atrial Pacing ◽  
Av Conduction ◽  
Recovery Times ◽  
Anesthetized Dogs ◽  
The Right

We tested the hypothesis that the effect of phasic vagal stimulation on atrioventricular (AV) conduction time is affected by the site of atrial pacing in anesthetized dogs. We paced the right atrium at a constant cycle length from the interatrial septum (IAS), superior coronary sinus (SCS), or inferior coronary sinus (ICS) regions, and we evaluated the time-dependent effects of vagal stimulation on AV conduction at each pacing site. When we stimulated the vagi at stimulus (St)-A phases greater than 136 +/- 40 ms and less than the phase that blocked AV conduction (182 +/- 70 ms), IAS pacing prolonged A-V intervals by 8.6 +/- 8.2 ms more than ICS pacing. A change in pacing site affected the A-V intervals by up to 30 ms when we stimulated the vagus at those times that caused the A-V intervals to prolong maximally. Furthermore, the effect of atrial pacing site on A-V intervals was modulated by AV nodal recovery times during the second or third cycles after the vagal stimulus.

Characterization of receptors for angiotensin in the rat vas deferens

1979 ◽  
Vol 57 (4) ◽  
pp. 417-423 ◽  
Author(s):  
J. Magnan ◽  
D. Regoli
Keyword(s):  
Smooth Muscle ◽  
Vas Deferens ◽  
Proteolytic Enzymes ◽  
Rabbit Aorta ◽  
Rat Vas Deferens ◽  
Converting Enzyme ◽  
Response Curves ◽  
Sympathetic Nerve Stimulation ◽  
The Right

Experiments were performed in the rat vas deferens to characterize the receptor for angiotensin mediating the potentiation of the sympathetic nerve stimulation by this peptide. For this purpose we measured the order of potency of various angiotensins, the affinity of two specific and competitive antagonists, and we compared the effects of several angiotensins in tissues desensitized by angiotensin II.The potency of natural angiotensins follows the order: ATII > ATI > ATIII the relative potency of a few analogues which resist degradation by proteolytic enzymes as well as the potency of three L-Ala analogues of ATII show similar changes as those observed in other smooth muscle preparations (e.g. the rabbit aorta).Affinity of antagonists was evaluated by measuring pA2 and is higher for [Leu8]-ATII than for [des-Asp1, Leu8]-ATII. Both antagonists appear to be competitive since they displace the dose-response curves of ATII and ATIII to the right without changing the slope of the curves. Desensitization with ATII renders the tissues insensitive to ATIII and to other angiotensins without changing the response of the tissues to substance P.ATII does not modify the action of exogenous NA on nonstimulated tissues. ATI has no direct effect since its action is completely blocked in the presence of an inhibitor of the converting enzyme (SQ. 14225), while the responses of the vas deferens to ATII and substance P are unaltered.It is concluded that the receptor for ATII in the rat vas deferens is of the same type as the receptor mediating contraction of the rabbit aorta.

Sustained increases in heart rate induced by timed repetition of vagal stimulation in dogs

1985 ◽  
Vol 249 (4) ◽  
pp. H703-H709
Author(s):  
T. Yang ◽  
M. D. Jacobstein ◽  
M. N. Levy
Keyword(s):  
Cycle Length ◽  
Cardiac Cycle ◽  
Vagal Stimulation ◽  
Sinus Node ◽  
Critical Time ◽  
Critical Value ◽  
Chronotropic Effect ◽  
Chronotropic Response ◽  
The Right ◽  
Positive Chronotropic Effect

We determined the influence of the "free-running cycle length" (tau FR) on chronotropic responses to one burst of right vagal stimuli per cardiac cycle in anesthetized dogs (tau FR, cycle length that prevailed in absence of right vagal stimulation). We varied tau FR by the following methods: 1) tonic left vagal stimulation in pentobarbital-anesthetized animals; 2) tonic left vagal stimulation plus sinus node cooling in pentobarbital-anesthetized animals; and 3) anesthesia with fentanyl, droperidol, and pentobarbital. When tau FR was less than a critical value [1,019 +/- 60 (SE) ms], right vagal stimulus bursts always had the expected negative chronotropic effect. However, when the tau FR was increased beyond critical value, right vagal stimulus bursts delivered within a specific portion of cardiac cycle actually had a positive chronotropic effect; i.e., cycle lengths diminished to values below tau FR. As tau FR was progressively increased beyond critical value, positive chronotropic response became greater and could be evoked by stimulus bursts delivered within a greater fraction of cardiac cycle. The right vagal stimuli that elicited the maximum positive chronotropic effect were those that were given approximately 235 ms prior to beginning of next atrial depolarization. This critical time probably occurs near the end of the period of phase 4 depolarization of sinus node automatic cells.

Supersensitivity to acetylcholine of canine sinus and AV nodes after parasympathetic denervation

1988 ◽  
Vol 255 (3) ◽  
pp. H534-H539 ◽  
Author(s):  
S. Kaseda ◽  
D. P. Zipes
Keyword(s):  
Dose Response ◽  
Cycle Length ◽  
Vagal Stimulation ◽  
Conduction Time ◽  
Av Block ◽  
Response Curves ◽  
Parasympathetic Ganglia ◽  
Sinus Cycle Length ◽  
Alpha Chloralose ◽  
Complete Av Block

Supersensitivity of the sinus (SAN) and atrioventricular (AVN) nodes to acetylcholine (ACh) after parasympathetic denervation has not been demonstrated conclusively. In this study, we denervated the SAN and AVN by surgically removing parasympathetic ganglia and painting the area with phenol. Sham dogs underwent thoracotomy without denervation. Four to 9 days later, vagal denervation was proved by supramaximal bilateral vagal stimulation, which prolonged the sinus cycle length (SCL) only 32 +/- 7% (mean +/- SE) and the AVN conduction time (AH interval) 15 +/- 7% in denervated dogs. We tested for supersensitivity by obtaining dose-response curves to ACh (1 ml, 10(-8.0) to 10(-4.0) M in 10(0.5) steps) infused over 15 s into the sinus nodal and posterior septal arteries in open chest-denervated (Den) dogs and in sham-operated (Sham) dogs that were anesthetized with alpha-chloralose. ACh concentration (Log[ACh], M) required to prolong SCL 50, 100, and 300% was -5.7 +/- 0.1, -5.6 +/- 0.1, and -5.4 +/- 0.1 in 10 Sham dogs vs. -6.4 +/- 0.1 (P less than 0.001), -6.3 +/- 0.1 (P less than 0.001) and -6.1 +/- 0.1 (P less than 0.001) in 11 Den dogs. ACh concentration necessary to produce second degree and complete AV block was -5.7 +/- 0.1 and -5.3 +/- 0.1 in 11 Sham dogs vs. -6.3 +/- 0.1 (P less than 0.001) and -5.8 +/- 0.1 (P less than 0.01) in 10 Den dogs. Because significantly lower doses of ACh prolonged SCL or produced AV block in Den compared with Sham dogs, we conclude that dogs with vagally denervated SAN and AVN develop a supersensitive response to ACh.

Quantitative comparison of canine right and left ventricular isovolumic pressure waves

1987 ◽  
Vol 253 (2) ◽  
pp. H475-H479 ◽  
Author(s):  
D. Burkhoff ◽  
M. W. Kronenberg ◽  
D. T. Yue ◽  
W. L. Maughan ◽  
W. C. Hunter ◽  
...  
Keyword(s):  
Cardiac Cycle ◽  
Sampling Rate ◽  
Left Ventricular ◽  
Pressure Waves ◽  
Atrial Pacing ◽  
Maximum Value ◽  
Time Courses ◽  
Mean Square Difference ◽  
Developed Pressure ◽  
The Right

The mechanical properties of the right and left ventricles (RV and LV) have previously been studied separately. However, because of differences in RV and LV architecture, geometry, and muscle mass, it is not obvious how the properties of the two chambers would relate to each other. This study compared the time courses of RV and LV isovolumic pressure waves (LVP, RVP, respectively) measured simultaneously in the same heart. We compared RVP and LVP in each of five isolated, supported canine hearts after pentobarbital anesthesia. RV and LV volumes were varied independently so that on various beats peak LVP exceeded, equaled, or was less than peak RVP. There was a delay of approximately 35 ms between the onset of LV and RV pressure waves with atrial pacing, but only 5 ms with ventricular pacing. LVP and RVP were measured and digitized at a sampling rate of 200 Hz. Pressure waves were offset and rescaled by their respective amplitudes so that for each beat the pressure wave had a minimum value of 0% at end diastole and a maximum value of 100% at end systole. RVP was then shifted in time so that its upstroke was synchronous with that of the LVP at the point of 50% of maximal developed pressure. The rescaled, time-shifted RVP was plotted as a function of the rescaled LVP for each point of the cardiac cycle, and the relation between the two was quantified by their root mean square difference (Drms). Drms averaged 2.3 +/- 1.5% (SD) for the first half of contraction, 1.5 +/- 0.4% for the second half of contraction, and 4.6 +/- 1.6% during relaxation.(ABSTRACT TRUNCATED AT 250 WORDS)

New insights into the atrial electrophysiology of rodents using a novel modality: the miniature-bipolar hook electrode

2008 ◽  
Vol 295 (4) ◽  
pp. H1460-H1469 ◽  
Author(s):  
Yoram Etzion ◽  
Michal Mor ◽  
Aryeh Shalev ◽  
Shani Dror ◽  
Ohad Etzion ◽  
...  
Keyword(s):  
Right Atrium ◽  
Cycle Length ◽  
Rate Adaptation ◽  
Right Atrial ◽  
Reverse Remodeling ◽  
Atrial Pacing ◽  
Anesthetized Rats ◽  
Atrial Electrophysiology ◽  
The Right ◽  
First Time

Studies of atrial electrophysiology (EP) in rodents are challenging, and available data are sparse. Herein, we utilized a novel type of bipolar electrode to evaluate the atrial EP of rodents through small lateral thoracotomy. In anesthetized rats and mice, we attached two bipolar electrodes to the right atrium and a third to the right ventricle. This standard setup enabled high-resolution EP studies. Moreover, a permanent implantation procedure enabled EP studies in conscious freely moving rats. Atrial EP was evaluated in anesthetized rats, anesthetized mice (ICR and C57BL6 strains), and conscious rats. Signal resolution enabled atrial effective refractory period (AERP) measurements and first time evaluation of the failed 1:1 atrial capture, which was unexpectedly longer than the AERP recorded at near normal cycle length by 27.2 ± 2.3% in rats ( P < 0.0001; n = 35), 31.7 ± 8.3% in ICR mice ( P = 0.0001; n = 13), and 57.7 ± 13.7% in C57BL6 mice ( P = 0.015; n = 4). While AERP rate adaptation was noted when 10 S1s at near normal basic cycle lengths were followed by S2 at varying basic cycle length and S3 for AERP evaluation, such rate adaptation was absent using conventional S1S2 protocols. Atrial tachypacing in rats shortened the AERP values on a timescale of hours, but a reverse remodeling phase was noted thereafter. Comparison of left vs. right atrial pacing in rats was also feasible with the current technique, resulting in similar AERP values recorded in the low right atrium. In conclusion, our findings indicate that in vivo rate adaptation of the rodent atria is different than expected based on previous ex vivo recordings. In addition, atrial electrical remodeling of rats shows unique remodeling-reverse remodeling characteristics that are described here for the first time. Further understanding of these properties should help to determine the clinical relevance as well as limitations of atrial arrhythmia models in rodents.

scholarly journals Phenotypical features of long Q-T syndrome in transgenic mice expressing human Na-K-ATPase α3-isoform in hearts

2000 ◽  
Vol 279 (5) ◽  
pp. H2133-H2142 ◽  
Author(s):  
Sharon E. O'Brien ◽  
Michael Apkon ◽  
Charles I. Berul ◽  
H. T. Patel ◽  
Kurt Saupe ◽  
...  
Keyword(s):  
Transgenic Mice ◽  
Atpase Activity ◽  
Sinus Rhythm ◽  
Cycle Length ◽  
Human Heart ◽  
Sodium Pump ◽  
Atrial Pacing ◽  
Adult Human ◽  
Sinus Cycle Length ◽  
Perfused Hearts

To understand why the adult human heart expresses three isoforms of the sodium pump, we generated transgenic mice (TGM) with 2.3- to 5.5-fold overexpression of the human α3-isoform of Na-K-ATPase in the heart. Hearts from the TGM had increased maximal Na-K-ATPase activity and ouabain affinity compared with control hearts, even though the density of Na-K-ATPase pump sites (of all isoforms) was similar to that of control mice. In perfused hearts, contractility both at baseline and in the presence of ouabain tended to be greater in TGM than in controls. Surface electrocardiograms in anesthetized TGM had a steeper dependence of Q-T on sinus cycle length, and Q-T intervals measured during atrial pacing were significantly longer in TGM. Q-T dispersion during sinus rhythm also tended to be longer in TGM. Thus TGM overexpressing human α3-isoform have several of the phenotypical features of human long Q-T syndrome, despite the absence of previously described mutations in Na+ or K+channels.

Ridogrel Inhibits Systemic and Renal Formation of Thromboxane A2 and Antagonizes Platelet Thromboxane A2/Prostaglandin Endoperoxide Receptors upon Chronic Administration to Man

1992 ◽  
Vol 68 (02) ◽  
pp. 214-220 ◽  
Author(s):  
C Weber ◽  
J R Beetens ◽  
F Tegtmeier ◽  
P Van Rooy ◽  
E Vercammen ◽  
...  
Keyword(s):  
Uric Acid ◽  
Potent Inhibitor ◽  
Ex Vivo ◽  
Thromboxane A2 ◽  
Chronic Administration ◽  
Response Curves ◽  
Clinically Significant ◽  
Synthase Inhibitor ◽  
The Right ◽  
Steady State Plasma Level

SummaryThe effects of ridogrel, a dual thromboxane A2 (TXA2) synthase inhibitor and TXA2/prostaglandin (PG) endoperoxide receptor antagonist, on systemic and renal production of prostaglandins and on platelet TXA2/PG endoperoxide receptors was evaluated upon chronic administration (300 mg b. i. d. orally, for 8 and 29 days) to man. Such a medication with ridogrel inhibits the systemic as well as the renal production of TXA2 as measured by the urinary excretion of 2,3-dinor-TXB2 and TXB2 respectively without inducing significant changes in systemic or renal PGI2 production. Simultaneously with the latter effects, the production of TXB2 by spontaneously coagulated whole blood ex vivo is inhibited (>99%) while that of PGE2 and PGF2α is largely increased. Administration of ridogrel causes a three- to five-fold shift to the right of concentration-response curves for U46619 in eliciting platelet aggregation; no tachyphylaxis is observed after 29 days of treatment in this respect. Apart from a reduction of serum uric acid levels with a concomitant increase in urinary uric acid excretion during the first days of treatment, no clinically significant changes in hematological, biochemical, hemodynamic and coagulation parameters occur during the 8 days or 29 days study. The study demonstrates that ridogrel is a potent inhibitor of the systemic as well as renal TXA2 synthase and an antagonist of platelet TXA2/PG endoperoxide receptor in man, covering full activity during 24 h at steady-state plasma level conditions without tachyphylaxis during 29 days of medication. The compound is well tolerated, at least during 1 month of administration.

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