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PubMed1976

Repetitive extrasystole as an index of vulnerability to ventricular fibrillation.

The assessment of ventricular vulnerability by inducing ventricular fibrillation (VF) presents limitations when neural activity is being investigated, especially in the unanesthetized animal. As repetitive extrasystoles (RE) have been observed to precede the occurrence of VF, it was relevant to determine whether the RE threshold provides a reliable index of cardiac susceptivility to fibrillation. The RE and VF threshold relationships were studied in 32 chloralose-anesthetized dogs during left stellate ganglion stimulation, vagus nerve stimulation, and beta-adrenergic blockage with practolol. The vulnerable period was scanned at 1-ms intervals and at 2-mA increments with a single, 2-ms, constant-current cathodal stimulus; RE and multiple RE were induced reproducibly when 66% and 82%, respectively, of the fibrillatory current was administered. The nadirs for RE and multiple RE were coincident in the cardiac cycle with the vulnerable-period threshold for VF. Stellate and vagal stimulation and beta-adrenergic blockade resulted in comparable changes in RE and VF thresholds and produced equivalent shifts in the cardiac cycle of the RE and VF vulnerable-period nadirs. These observations suggest that RE and VF phenomena share a common electrophysiologic basis and that the RE threshold can be used as an end point for measuring ventricular vulnerability to VF.

Animals↗

PubMed1992

Substance P modulates autonomic nerve activity in canine hearts.

We examined the hypothesis that substance P (SP) acts as an "afferent neuromodulator" in the heart regulating the response of the cardiac autonomic nerves to reflexes originating in the heart. We employed the acute, isovolumic canine heart preparation in which the amplitude of the chamber pressure accurately reflects changes in contractility. The heart was decentralized except for one-half of the right vagus, which was left intact to permit afferent communication with the central nervous system, while the remaining one-half was tightly ligated so that the distal part could be used for efferent stimulation. SP was injected in doses of 2-10 micrograms ic. There were no significant inotropic responses to 2 and 5 micrograms SP, whereas 10 micrograms produced positive inotropy of 5-15%. When vagal tone was elevated with sustained vagal stimulation, the same doses of SP increased contractility by 12-28%. Similarly, during right stellate ganglion stimulation (SS), SP decreased contractility 8-22%. After the intact half of the right vagus was sectioned, SP modulation of vagal responses was unaffected, while modulation of atrial, but not ventricular, responses to SS was significantly attenuated. When tested on a series of cardiac-denervated dogs, SP had no effect on cardiac inotropy at any dose. However, when contractility was increased with isoproterenol infusion, SP caused a small decrease in ventricular contractility. These results suggest that SP acts as a modulator of cardiac autonomic neural tone. It is possible that the neuropeptide is released from intramyocardial afferent collateral fibers and inhibits the elevation in vagal or sympathetic nerve activity initiated by activation of cardiac primary afferent nerves.

Animals↗

PubMed1983

Vagal modulation of adrenergic effects on canine sinus and atrioventricular nodes.

Vagal stimulation modulates adrenergic neurotransmission at pre- and postjunctional sites. The purpose of this study was to test whether such multilevel cholinergic inhibition depressed sinus nodal automaticity and atrioventricular (AV) nodal conduction (A-H interval) in open-chest dogs anesthetized with chloralose. We compared the inhibitory effects of vagal stimulation when sinus nodal automaticity and AV nodal conduction were enhanced by bilateral stellate ganglia stimulation with comparable degrees of enhanced automaticity and conduction achieved by infusing norepinephrine and isoproterenol. We found that vagal stimulation prolonged in a frequency-dependent fashion sinus nodal cycle length and A-H interval more during stellate ganglion stimulation than during norepinephrine or isoproterenol infusion. Atropine eliminated all effects of vagal stimulation. These data provide functional evidence to support the concept that muscarinic modulation of adrenergic effects on sinus nodal cycle length and AV nodal conduction occurs at site(s) in addition to the postjunctional effector cell.

Animals↗

PubMed1984

Intestinal peristalsis associated with release of immunoreactive substance P.

The release of immunoreactive substance P into the vascular bed of the isolated small intestine of the guinea-pig was investigated. Raising the intraluminal pressure to 5 mbar for 5 min initiated peristalsis and stimulated the release of substance P. The substance P releasing effect of pressure stimulation was reduced by 46% when hexamethonium (240 microM) was added to the perfusion solution. The ganglion stimulant drug dimethylphenylpiperazinium (32 microM) also stimulated the release of substance P; its effect was completely prevented by hexamethonium (240 microM). Intraarterial infusion of capsaicin (22 microM), a neurotoxin known to act on sensory substance P-containing neurones, stimulated the release of substance P and caused intestinal contractions. The motor effect of capsaicin in the gut can thus be explained by release of substance P from sensory nerve endings in the gut. Systemic pretreatment of the guinea-pigs with capsaicin abolished the release of substance P due to capsaicin, whereas that evoked by elevated intraluminal pressure or dimethylphenylpiperazinium was not reduced. This means that substance P released in the course of peristalsis or by dimethylphenylpiperazinium originates from neurones intrinsic to the intestine. These findings indicate that intestinal peristalsis is associated with the release of substance P from enteric neurones. Substance P is likely to be a neurotransmitter involved in the coordination of the peristaltic reflex.

Animals↗

PubMed1976

Regional shortening patterns in canine right ventricle.

The right ventricular outflow tract (OT) is a functionally distinct area of the right ventricle. However, there is little information on the contrdingly, inflow tract (IT) and OT chords and right ventricular free wall segmental changes were measured with implanted ultrasound crystals. The timing and extent of shortening of IT and OT chords and free wall segments were determined both at rest and after stellate ganglion stimulation. At rest, IT chord shortening began 51 ms before OT shortening. OT expansion occurred during this period. IT chord shortening began 51 ms before OT shortening. OT expansion occurred during this period. IT chord shortening was 38% while OT shortening was 34%. In contrast, OT segments did not show systolic expansion. IT segment shortening was 13% while OT shortening was 21%. With stellate stimulation, IT-OT gradients of 15-25 mmHg developed. The lag between IT and OT shortening decreased to 30 ms and segmental shortening increased. We conclude that the OT is a physiologically distinct region which contracts later and remains contracted longer than the IT. Both septal and free wall movements contribute to these changes.

Animals↗

PubMed1997

Developmental changes in modulation of cardiac repolarization by sympathetic stimulation: the role of beta- and alpha-adrenergic receptors.

INTRODUCTION: Our goals were to study the role of development in determining the cardiac effects of sympathetic neural activation, and to identify the roles of alpha- and beta-adrenergic receptor-mediated pathways in modulating the effects of sympathetic stimulation. METHODS AND RESULTS: We compared responses of young and adult canine hearts in situ to right, left, and bilateral stellate ganglion stimulation. We focused on changes in heart rate, rhythm, QT interval, rate-corrected QT interval (QTc), and T wave amplitude. Right stellate stimulation (RSS) induced more pronounced sinus tachycardia in adult than young animals. Left stellate stimulation (LSS) induced junctional tachycardia in adult more than young animals. In adults, LSS and RSS prolonged QTc (LSS > RSS), whereas 1-week-olds manifested QTc shortening with RSS. LSS also increased T wave amplitude, most markedly in adults. In all studies, bilateral stellate stimulation induced responses intermediate between those seen with RSS and LSS. beta-Adrenergic blockade (propranolol) abolished all responses to LSS in adult hearts, but alpha-blockade (prazosin) attenuated only the LSS-induced prolongation in QTc. CONCLUSION: In the postnatal modulation of cardiac rhythm, rate, and repolarization by the sympathetic nervous system, beta-adrenergic receptors play a major role at all ages, whereas alpha-adrenergic receptors play a lesser role, which is manifested only in adults. Moreover, expression of junctional tachycardias, which are beta-adrenergically modulated, is seen only in the adults.

Animals↗

PubMed1984

The large fourth abdominal intersegmental interneuron: a new type of wind-sensitive ventral cord interneuron in locusts.

A large interneuron in Locusta migratoria is described that extends from the fourth abdominal ganglion to the brain. The morphology was revealed by injection of cobaltous ions or Lucifer yellow into the cell. As its cell body lies within the fourth abdominal ganglion it is named A4I1, the first-identified intersegmental interneuron of the fourth abdominal ganglion. This neuron receives input from highly flexible, wind-sensitive hairs on the prosternum, the pronotum, and the head (field 1). Sensory connections with A4I1 are made within the prothoracic ganglion. Stimulation of the receptive field initiates spikes in A4I1 which travel anteriorly and posteriorly from the prothoracic ganglion. Intracellular recording from the axon and the soma shows that the cell membrane becomes inactive within the fourth abdominal ganglion. Spikes could be generated within the fourth abdominal ganglion by current injection into the soma. Occasionally excitatory postsynaptic potentials were observed in a soma recording, but up to now there is no evidence for a second spike initiation site. By intracellular current injection into the soma of the left and right A4I1 cell it is shown that the two cells are not electrically coupled.

Afferent Pathways↗

PubMed1988

Cardiovascular effects of 1-methyl-4-(1-naphthylvinyl)piperidine hydrochloride.

1-Methyl-4-(1-naphthylvinyl)piperidine (B-120) produced a dose related decrease in blood pressure in cats. B-120 did not alter the cardiovascular response to acetylcholine or vagal stimulation. It did not affect the response of the nictitating membrane to both pre- and post-ganglionic stimulation. In isolated cortical synaptosomes, B-120 decreased calcium flux below basal levels. Thus, the blockade of calcium channels appeared to be related to the production of hypotension and may be the mechanism by which B-120 protected against organophosphate toxicity.

Animals↗

PubMed1986

Interaction between the adrenergic and renin-angiotensin-aldosterone-systems.

In congestive heart failure (CHF) both the sympathetic nervous system (SNS) and the renin-angiotensin-aldosterone-system (RAAS) are activated. Both phenomena are only of short-term benefit and inevitably detrimental with prolonged activation. There are many possibilities for interaction between the systems, in particular when they are both in the activated state as in CHF. Renin release from the renal juxtaglomerular cells is stimulated by the SNS via beta 1-adrenoceptors. At a higher level of renal nerve stimulation there is recruitment of antinatriuretic and finally vasoconstrictor activity, mediated by alpha 1-adrenoceptors. The vasoconstrictor potency of angiotensin II (AII) involves both postsynaptic angiotensin II-receptors and also various processes stimulating sympathetic activity and its sequelae. The following sympathetic components may contribute to the effect of angiotensin II:ganglionic stimulation; enhanced release of noradrenaline (tyramine-like effect); inhibited noradrenaline re-uptake; facilitation of noradrenaline release via presynaptic AII-receptors; sensitization of postsynaptic alpha-adrenoceptors. The presynaptic AII-mechanism is probably the most sensitive and relevant process, which is also involved in the vasodilator activity of ACE-inhibitors.

Angiotensin II↗

PubMed2005

Blunted functional responses to pre- and postjunctional sympathetic stimulation in hibernating myocardium.

Regional reductions in norepinephrine-tracer uptake are found in pigs with hibernating myocardium. Clinical studies would suggest that this is evidence for denervation; however, the functional responses to sympathetic stimulation have not been evaluated, and our previous studies with beta-adrenergic stimulation have not suggested denervation hypersensitivity. Therefore, pigs were chronically instrumented to produce hibernating myocardium characterized by chronic regional dysfunction and histological viability. Open-chest studies were performed to determine changes in regional function in response to both pre- and postjunctional stimulation. Regional segment shortening was reduced at rest in hibernating myocardium compared with controls (13 +/- 3% vs. 27 +/- 3%, P = 0.004). During stellate ganglion stimulation, regional function increased in both groups of animals (P = 0.008 vs. baseline), but the increase in hibernating myocardium was blunted compared with controls (Delta%, 3 +/- 2% vs. 8 +/- 3%, P = 0.04). Similar results occurred with intracoronary tyramine (10 mug/kg). Functional improvement during intravenous epinephrine infusion (0.35 mug.kg(-1).min(-1)) was also blunted in hibernating myocardium compared with controls (Delta%, 7 +/- 1% vs. 15 +/- 2%, P = 0.04). Even when the improvement in function was expressed relative to the reduced baseline, there was no evidence for catecholamine-mediated hypersensitivity in hibernating myocardium. We therefore conclude that functional responses to both pre- and postjunctional sympathetic stimulation are blunted in pigs with hibernating myocardium. In contrast to previous studies of infarcted, denervated, and acutely stunned myocardium, there is no catecholamine-induced hypersensitivity in hibernating myocardium. These data suggest a downregulation in functional responses to stimulation that would protect hibernating myocardium from demand-induced ischemia at the expense of contractile reserve during sympathetic stimulation.

Animals↗

PubMed1984

A comparison of the antimuscarinic effects of pirenzepine and N-methylatropine on ganglionic and vascular muscarinic receptors in the rat.

The antimuscarinic properties of pirenzepine and N-methylatropine were evaluated in two intact preparations by measuring A) the inhibition of increase in mean arterial pressure evoked by McN-A-343 in pithed rats through activation of ganglionic muscarinic receptors and B) the inhibition of fall in arterial pressure evoked by methacholine in anaesthetized rats through activation of vascular muscarinic receptors. To characterize the antimuscarinic potencies of pirenzepine and N-methylatropine, for both antagonists doses were calculated that produce a 10-fold shift to the right of the dose-response curves for A) the pressor response to McN-A-343 (i.v. administration) in pithed rats (D10-p.r.) and B) for the depressor effect to methacholine (i.v. administration) in anaesthetized rats (D10-an.r.), respectively. Whereas N-methylatropine was virtually equieffective in blocking both muscarinic responses (D10-an.r./D10-p.r. approximately equal to 1), pirenzepine, however, was considerably more potent at ganglionic than at vascular muscarinic receptors (D10-an.r./D10-p.r. approximately equal to 16). These data confirm the existence of excitatory ganglionic muscarinic receptors with high affinity for pirenzepine (M1) and provide evidence for the presence of M2 receptors - receptors which show a low sensitivity to pirenzepine - on vascular smooth muscle cells. To further characterize the anticholinergic properties of pirenzepine, its effect on the pressor response to DMPP, a nicotinic ganglionic stimulant, was investigated in pithed rats. A high dose of pirenzepine (1.13 mumol/kg), given i.v., did not affect nicotinic ganglionic transmission.

Animals↗

PubMed1993

Does isoflurane alter mesenteric venous capacitance in the intact rabbit?

Volatile anesthetics act at a number of sites to alter cardiovascular function and the response of the cardiovascular system to barostatic reflexes. We examined the effects of isoflurane on reflex regulation of mesenteric venous capacitance vessels. To determine whether isoflurane alters mesenteric venous capacitance, continuous direct observations of mesenteric vein diameter, intravenous pressure, and mesenteric sympathetic efferent nerve activity (SENA) were made in 31 chloralose-anesthetized New Zealand white rabbits. Simultaneous measurements were obtained for aortic pressure and heart rate. The responses to changes in baroreceptor activation by means of either bilateral carotid occlusion (BCO) or aortic nerve stimulation (ANS) were studied in one group of 18 rabbits, while the response to direct electric activation by means of celiac ganglion stimulation (CGS) was studied in another group of 13 rabbits. In both groups, isoflurane vapor was administered at levels of 0.75% or 1.5%, and superfused isoflurane was administered directly to the vessel in doses of either 3% or 5% equilibrated with physiologic salt solution. Anesthetic levels were verified by mass spectrometry for expired gas and by gas chromatography for blood and superfusate levels. Inhaled isoflurane reduced hemodynamic variables and SENA in a dose-dependent fashion, but these same variables were unaffected by superfused isoflurane. One and one-half percent inhaled isoflurane abolished all reflex responses to baroreceptor stimulation in mesenteric capacitance veins and in SENA, but superfused isoflurane produced no corresponding attenuation of reflex responses to baroreceptor stimulation. Neither inhaled nor superfused isoflurane suppressed the reflex venoconstriction in response to CGS. Both inhaled and superfused isoflurane dilated the baseline vein diameter before stimulation. These results indicate that isoflurane dose increase the diameter of mesenteric venous capacitance vessels and inhibits reflex-induced constriction of mesenteric veins, whereas mesenteric sympathetic efferent nerve activity decreases and the reflex responses to activation of the carotid sinus and aortic baroreceptors are attenuated by inhaled isoflurane. The mechanism of this action appears to be primarily through the inhibition of central or peripheral sympathetic ganglionic transmission of barostatic control.

Animals↗

PubMed1993

Conformationally restricted sumatriptan analogues, CP-122,288 and CP-122,638 exhibit enhanced potency against neurogenic inflammation in dura mater.

CP-122,288 and CP-122,638 blocked plasma protein extravasation response within dura mater following trigeminal ganglion stimulation. The threshold (1 and 0.1 pmol/kg, respectively) was remarkably lower than for sumatriptan (7 nmol/kg), as was the dose at maximum response. As with sumatriptan, substance P-induced plasma leakage was unaffected by either compound, and metergoline only partially (27%) reversed the effects of CP-122,288. The data suggest the importance of modifications at the aminoethyl side chain to the actions of sumatriptan and possibly to the treatment of migraine headache.

Animals↗

PubMed1978

Neural control of renal tubular sodium reabsorption of the dog.

The evidence supporting a role for direct neurogenic control of renal tubular sodium reabsorption is reviewed. Electron microscopic and fluorescence histochemical studies demonstrate adrenergic nerve terminals in direct contact with basement membranes of mammalian renal tubular epithelial cells. Low level direct or baroreceptor reflex stimulation of renal sympathetic nerves produces an increase in renal tubular sodium reabsorption without alterations in glomerular filtration rate, renal blood flow, or intrarenal distribution of blood flow. The antinatriuresis is prevented by prior treatment of the kidney with guanethidine or phenoxybenzamine. Possible indirect mediation of the antinatriuresis by other humoral agents known to be released from the kidney upon renal nerve stimulation (angiotensin II, prostaglandin) was excluded by experiments with appropriate blocking agents. Reflex diminutions in renal nerve activity (left atrial distention, stellate ganglion stimulation) produce a decrease in renal tubular sodium reabsorption independent of glomerular filtration rate or renal blood flow. The anatomically described adrenergic innervation of the renal tubules participates in the direct regulation of renal tubular sodium reabsorption.

Animals↗

PubMed1996

Unilateral changes of sympathetic tone to the heart impair left ventricular function.

BACKGROUND: Different regions within the left ventricle are preferentially supplied by the left or right sympathetic system. In order to characterize different influences of left vs right sympathetic lateralization on LV function, haemodynamic effects of right and left stellate ganglion stimulations (RSGS and LSGS) as well as a right sympathetic block (RSB) were compared. METHODS: Seven alpha-chloralose anaesthetized open chest dogs were instrumented for measurement of LV pressure (tip manometers) and regional LV wall thickness (WT, sonomicrometry) in the antero-apical wall (AW, innervated by right stellate ganglion) and postero-basal wall (PW, left stellate ganglion). Timing of regional myocadial wall motion was evaluated by the phase of the first Fourier transform of the WT signals, LV asynchrony by the phase difference (phi) between both regions, and LV diastolic function by the time constant of isovolumic relaxation (tau). Measurements were performed before and after RSB (5 ml of lidocaine 1%); in 6 dogs of this group, RSGS and LSGS (4 V, 0.2 ms, 20 Hz) were performed before RSB. In order to investigate a regional inotropic stimulation without systemic effect, 6 additional dogs received intracoronary noradrenaline injections (NIC, 0.25 microgram) into the left circumflex artery perfused myocardium. RESULTS: LSGS and NIC led to an earlier PW-motion within the cardiac cycle (phase reduction by 40.0 +/- 15.0 degree (SEM) and 55.5 +/- 11.2 degrees) and RSGS induced an earlier AW-motion (by 33.7 +/- 15.2 degrees). After RSB, AW-motion was delayed (38.1 +/- 9.2 degrees). The consequence was an asynchronous wall motion pattern after all interventions (change in phi: LSGS-64.7 +/- 18.7 degrees, RSGS 41.1 +/- 15.7 degrees, NIC -74.5 +/- 17.4 degrees, RSB -52.6 +/- 14.6 degrees), and a prolonged relaxation (tau increase: RSGS 9.4 +/- 1.9, NIC 8.3 +/- 1.5, RSB 3.7 +/- 0.8 ms). CONCLUSION: Unilateral increases as well as decreases of sympathetic tone to the heart result in an asynchronous wall motion pattern and an impaired LV relaxation.

Animals↗

PubMed1984

Evidence that GABAA receptors mediate relaxation of rat duodenum by activating intramural nonadrenergic-noncholinergic neurones.

GABA produced rapid and transient relaxation of rat duodenum. Homotaurine (3-aminopropansulphonic acid) but not (+/-)-baclofen had a GABA-like effect. GABA-induced relaxation was almost completely inhibited by tetrodotoxin but was unaffected by atropine. Cross desensitization developed between GABA and homotaurine but not between GABA and (+/-)-baclofen. The concentration response curve to the relaxant effects of GABA was shifted to the right by both bicuculline and picrotoxin. However maximal relaxation was still produced by GABA in the presence of bicuculline but not in the presence of picrotoxin. GABA-induced relaxation was not affected by prazosin, yohimbine, propranolol or reserpine pretreatment. Field stimulation (0.1 Hz) of rat isolated duodenum in the presence of atropine and guanethidine produced relaxation similar to that produced by GABA. The ganglionic stimulant DMPP produced a similar effect. Neither Met-enkephalin, noradrenaline, 5-HT, histamine, VIP or arachidonic acid could be held responsible for GABA-induced neurogenic relaxation of rat duodenum. ATP produced relaxations which closely mimicked those produced by either GABA or field stimulation. Exposure to ATP desensitized responses to both GABA and field stimulation to about the same extent. ATP, GABA and field stimulation-induced relaxation was unaffected by either theophylline or indomethacin, but was significantly and selectively antagonized by apamin. In conclusion, GABA-induced relaxation of rat isolated duodenum is largely dependent upon activation of intra-mural nonadrenergic-noncholinergic neurones. The GABA receptor involved appears to be of the GABAA subtype. Circumstantial evidence is provided indicating that ATP might be the endogenous substance released by GABA.

Animals↗

PubMed1985

Metabolic activation of specific postsynaptic elements in superior cervical ganglion by antidromic stimulation of external carotid nerve.

Using the rat superior cervical ganglion in vivo as a model of the central nervous system, we have sought to determine whether postsynaptic elements as well as terminal processes are metabolically activated during impulse activity. The rate of glucose utilization in the ganglion was found to be stimulated by antidromic stimulation of the external carotid nerve. This stimulation was frequency-dependent and was confined only to the region in the caudal portion of the ganglion corresponding to the location of the cell bodies of origin of the external carotid nerve.

Animals↗

PubMed1997

Functional connectivity in the rodent trigeminal pathway grown in vitro.

In explant cocultures of the rat trigeminal pathway, embryonic trigeminal ganglion cells grow their axons into peripheral cutaneous and central nervous system targets (R.S. Erzurumlu, S. Jhaveri, Target influences on the morphology of trigeminal axons, Exp. Neurol, 135 (1995) 1-16; R.S. Erzurumlu, S. Jhaveri, H. Takahashi, R.D.G. McKay, Target-derived influences on axon growth modes in explant cocultures of trigeminal neurons, Proc. Natl. Acad. Sci. USA 90 (1993) 7235-7239). In heterochronic cocultures, composed of embryonic trigeminal ganglion, embryonic whisker pad and postnatal brainstem slice, trigeminal axons develop arbors and terminal boutons in the brainstem trigeminal nuclei. To determine whether these terminal arbors establish functional connections with the brainstem neurons, we examined the electrophysiological properties of brainstem neurons and their responsiveness to trigeminal ganglion stimulation. Intracellular recordings were done in vitro on cells of the trigeminal subnucleus interpolaris (SPI) in trigeminal pathway cocultures (E15 whisker pad, E15 trigeminal ganglion, and postnatal day (PND) 0-2 brainstem slice) or in the SPI of acutely prepared brainstem slices. Electrophysiological properties of SPI cells in both preparations were virtually identical. The voltage responses of SPI neurons to intracellular current injection were highly linear suggesting they lacked a number of voltage-dependent conductances. Depolarizing current injection produced trains of action potentials with a frequency that varied with stimulus intensity. In explant cocultures, electrical activation of the trigeminal ganglion evoked EPSPs, and EPSPs coupled with IPSPs in SPI cells. Bicuculline blockade of IPSP activity resulted in long lasting EPSPs whose duration increased with membrane depolarization. These results show that brainstem trigeminal neurons can retain their functional properties in culture and establish functional connections with primary sensory afferents.

Animals↗