Reflexes In Dogs Research Articles

Carotid sinus baroreceptor reflex in dogs with experimental heart failure.

We have previously demonstrated a decrease in baroreceptor discharge sensitivity in dogs with experimental heart failure. In the present study, we determined the sensitivity of the carotid sinus baroreceptor reflex in dogs with pacing-induced heart failure. The carotid sinus baroreceptor reflex sensitivity was determined by pressurizing one carotid sinus with all other baroreceptor and cardiopulmonary receptor inputs removed. The data were analyzed by plotting carotid sinus pressure-mean arterial pressure curves and carotid sinus pressure-renal sympathetic nerve activity curves in the two groups of dogs. The peak arterial pressure during carotid hypotension was significantly depressed in dogs with heart failure compared with normal dogs (107.1 +/- 5.7 versus 139.8 +/- 7.0 mm Hg, p less than 0.001). Mean arterial pressure range, renal sympathetic nerve activity range, and peak slope were significantly decreased in the heart-failure group. To determine if this depression was completely due to depression of baroreceptor discharge per se, or to alterations in central or end-organ responsiveness, similar experiments were performed by stimulating the carotid sinus nerve and evaluating frequency, voltage, and duration of stimulation on the resultant mean arterial pressure and renal sympathetic nerve activity. As was the case with carotid sinus pressurization, electrical stimulation caused a significantly smaller change in mean arterial pressure in heart-failure dogs compared with the normal dogs. However, there was no significant difference between normal and heart-failure dogs for the renal sympathetic nerve activity-electrical stimulation curves. These data strongly suggest that the depressed carotid sinus baroreceptor reflex in heart failure is not solely the result of depressed baroreceptor responsiveness but may be related to poor end-organ responses and normal central control of renal sympathetic outflow.

Effect of midline laparotomy on the cough reflex in dogs

The present studies were designed to test the hypothesis that midline laparotomy promotes selective inhibition of the transversus abdominis muscle during cough as it does during expiratory threshold loading. Anesthetized dogs were studied in the supine posture, and cough was induced by mechanical stimulation of the airways. Midline laparotomy had virtually no effect on the cough-induced activation of the triangularis sterni or the external oblique. On the other hand, the activation of the transversus abdominis was markedly reduced in all animals. Despite this marked inhibition, however, peak pleural pressure and expiratory flow were preserved. This suggests that this inhibition does not play a significant role in determining the occurrence of bronchopulmonary infection after abdominal surgery.

Alimentary conditioned reflexes in dogs on activation and blockage of the cholinoreactive amygdaloid system.

1. Chemical stimulation of the basolateral area of the amygdala by acetylcholine at a dose of 300 μg, carbocholine at a dose of 0.5 μg, and atropine at a dose of 60 μg changes the production of the secretory component of alimentary reactions but has no effect on the production of the instrumental component. 2. Activation of the cholinoreactive system of the amygdaloid complex in dogs has an inhibiting action and blockage an activating action on the production of alimentary secretory conditioned reflexes; in the case of a decrease in the value of the total conditioned reflex salivation, differentiation is improved, while in the case of an increase in this value it is impaired. 3. On blockage and activation of the cholinoreactive system of the basolateral area of the amygdala, the ratio of the conditioned reflex salivation in response to different stimuli presented in a stereotype order (dynamic stereotype) changes.

Nonalgebraic interaction between pressor and depressor reflexes in dogs: evidence for a central site of action.

In a previous study (Kendrick, JE and Matson, G 1979, Amer J Physiol 327:H662-H667) we demonstrated that the vascular responses in dogs to electrical stimulation of aortic nerve (AN) pressor and carotid sinus nerve (CSN) depressor afferents did not sum algebraically. We suggest this results from a reflex interaction which occurs in the central nervous system. The present study extends earlier studies by recording sympathetic vasomotor in chloralose-anesthetized dogs. Stimulation of the CSN reduced sympathetic activity by 51 +/- 20 (SD)%. AN stimulation (2 Hz) caused a 17 +/- 12% increase in sympathetic activity. Combined stimulation of the ipsilateral CSN and AN caused 0 +/- 28% change rather than a 34% decrease expected by an additive interaction. The interaction recorded in this study from the sympathetic outflow is therefore consistent with the previously reported vascular responses (cited above) and implicates central nervous site(s) of action. A conditioning stimulus train to CSN inhibited sympathetic discharges to AN test stimuli. This inhibition was prevented by pairing an AN stimulus with the CSN stimulus train. The AN pressor reflexes act in part by increasing sympathetic activity and in part by suppressing the baroreflexes.

Stimulation techniques and response characteristics of the M and F waves and H reflex in dogs.

The voltage and duration of electrical rectangular pulsed stimuli needed to produce an F wave and a monosynaptic reflex (H wave) and the characteristics of these responses were recorded in clinically normal dogs. Optimal stimulus to produce H waves was 0.1 to 0.2 ms and less than 80 volts. F waves were variable in appearance and were most evident following 0.5 ms and 125 to 150 volt stimulation. F waves had shorter latency than comparable H waves.

Conditioned and unconditioned food reflexes in dogs during electrical stimulation of the orbital cortex.

1. Low-frequency (1 Hz) subthreshold stimulation of the orbital cortex induces a significant decrease in the spontaneous and conditioned secretion of saliva, doubles the latent periods of the conditioned reflex, but is not reflected in the volume of unconditioned secretion. 2. High-frequency (100 Hz) electrical stimulation of the same points of the orbital cortex has a more marked inhibitory effect on spontaneous and conditioned secretion and lengthens the latent period by 1.5 times. The unconditioned secretion has a tendency to increase. 3. Internal inhibition (differential and extinctive) has a tendency toward disinhibition during low-frequency stimulation; high-frequency stimulation has no such effect.

Effect of low-frequency stimulation of the head of the caudate nucleus on an instrumental defensive reflex in dogs.

1. Experiments on dogs using a model of an instrumental defensive reflex showed the inhibitory effect of low-frequency stimulation of the head of the caudate nucleus on the EMG and mechanographic components of the response determining its coordination program. The greatest changes affected the initial EMG components of the instrumental reflex. Inhibitory effects increased proportionally to the intensity of the stimulating current. 2. The motor solution to the instrumental problem (avoiding the action of the electric current) was characterized by resistance to the inhibitory effect of stimulation of the head of the caudate nucleus. 3. The results are evidence that the head of the caudate nucleus is involved in monitoring the realization of the motor program of a behavioral task that is important in the given situation.

Effect of Anesthetics on the Interaction between Pressor and Depressor Reflexes in Dogs

AbstractThe interaction between the pressor reflex to aortic nerve (AN) stimulation and the depressor reflex to carotid sinus nerve (CSN) stimulation was studied in the perfused hind limbs of dogs using different anesthetic agents commonly used in physiological studies. With chloralose, pentobarbital, or a combination of urethane and chloralose, stimulation of the depressor reflexes augmented the vasoconstrictor effects of the pressor reflex. Animals anesthetized with urethane alone did not demonstrate this interaction between these reflexes. The results suggest that chloralose and pentobarbital enhance the aortic nerve pressor reflexes rather than suppress the carotid sinus nerve depressor reflexes.

The influence of perfusate temperature on the responses of a superficial vein in the carotid baroreceptor reflex in dogs.

In chloralose-anaesthetised dogs, both vagus nerves were cut and both carotid sinuses vascularly isolated and perfused with blood. The left hind limb was vascularly isolated and the femoral artery and the central end of a superficial metatarsal vein were perfused at constant flows with blood from an oxygenator. Femoral venous pressure was held constant. Arterial and venous responses were determined by measuring changes in arterial perfusion pressure and in the pressure gradient between the superficial metatarsal and femoral veins. Large step increases in carotid sinus pressure resulted in an average decrease in venous gradient of 5.6% when the temperature of the venous perfusate was 38 degrees C and a significantly (P less than 0.01) greater response (8.8%) when the perfusate was at 31 degrees C. When the venous perfusate was cooled from 38 to 31 degrees C, venous gradient increased by averages of 89% when carotid pressure was low, 64% when carotid pressure was high and 32% after lumbar sympathectomy. These responses are significantly different from each other (P less than 0.05). It is concluded that the reflex responses of the superficial vein to maximal stimulation of the baroreceptors were small but they were significantly protentiated by cooling the perfusate. The venous constriction in response to cooling was reduced by raising the carotid pressure and further reduced by surgical sympathectomy.

Conditioned taste aversions: Vagal and circulatory mediation of the toxic unconditioned stimulus

In these experiments we tested the hypothesis that the same afferent systems which mediate vomiting reflexes also participate in conditioned taste aversions which are formed when ingestion of a taste cue is paired with subsequent internal malaise. Borison and Wang have shown that emetic reflexes in dogs and cats are integrated in a brainstem center which responds to local gastric irritation mediated by the vagus or to bloodborne toxins monitored by brain stem chemoreceptors. This same afferent system may mediate taste-illness conditioning since the emetic center is anatomically associated with the relay nucleus for primary taste afferents. We have shown that subdiaphragmatic vagotomy in rats disrupts the acquisition of a saccharin aversion induced by repeated conditioning trials with low doses of intragastric or intraperitoneal copper sulfate. In contrast, there is little effect on the aversion produced by a single, larger dose of copper sulfate injected directly into the blood via the tail vein, although vagotomized rats displayed an accelerated extinction pattern. These results parallel reports on the effect of vagotomy on vomiting reflexes in dogs and suggest a functional relationship between acute vomiting reflexes in dogs and suggest a functional relationship between acute vomiting reflexes which eject poison and chronic conditioned taste aversions which inhibit subsequent ingestion of poison; further, they provide evidence that these responses are subserved, at least in part, by similar neural mechanisms.

I. Pulmonary-CO 2 ventilatory reflex in dogs: Effective range of CO 2 and results of vagal cooling

Bartoli et al. (1974) found in dogs with constant Pa CO 2 that an increase in P CO 2 in the vascularly isolated lungs increased ventilatory drive by a vagal reflex. We have examined the range of lung P CO 2 over which the reflex operates. In anesthetized dogs we ventilated the lungs separately with O 2, maintaining gas exchange with the right lung. When we occluded the left pulmonary artery, left lung P CO 2 fell to 2–4 mm Hg, and phrenic nerve firing decreased significantly. Phrenic activity increased again when left lung P CO 2 was raised in steps to 19, 32 and finally to 50 mm Hg. Pa CO 2 was unchanged. Phrenic responses were abolished by cutting the left vagus nerve or by cooling it to 7–8°C. The largest increase in phrenic activity occurred when left lung P CO 2 was increased from 2 to 19 mm Hg, and the smallest when P CO 2 was raised from 32 to 50 mm Hg. Hence the significance of the pulmonary-CO 2 ventilatory relfex may lie in depression of ventilatory drive when pulmonary CO 2 falls below normal, rather than in stimulation of breathing when pulmonary CO 2 increases above normal.

The effect of tracheostomy on the laryngeal closure reflex.

The clinical observation of aspiration following prolonged tracheostomy prompted a neurophysiologic investigation of the glottic closure reflex in dogs longitudinally evaluated after permanent tracheostomy. The data support significant alterations in the central organization of the protective closure reflex heretofore considered phylogenetically primitive and therefore physiologically stable over wide ranges of functional demand. The data indicate that chronic upper airway bypass results in: 1. increased threshold of the evoked adductor response; 2. random shifts in its latency; 3. rapid attenuation of the primary evoked response to repetitive SLN stimulation; and 4. reduced after-discharge activity, all of which contribute to a weakened, ill-coordinated closure respons.

Carotid sinus reflex in dogs with low- to high-sodium intake

ARTICLESCarotid sinus reflex in dogs with low- to high-sodium intakeA. P. Rocchini, J. R. Cant, and A. C. BargerA. P. Rocchini, J. R. Cant, and A. C. BargerPublished Online:01 Aug 1977https://doi.org/10.1152/ajpheart.1977.233.2.H196MoreSectionsPDF (1 MB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInEmailWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformationCited ByInteraction between angiotensin II and the baroreceptor reflex in the control of adrenocorticotropic hormone secretion and heart rate in conscious dogs.Circulation Research, Vol. 58, No. 6Catecholamines in discrete kidney regions. Changes in salt-sensitive Dahl hypertensive rats.Hypertension, Vol. 4, No. 6Hemodynamic effects of n-acetylprocainamide compared with procainamide in conscious dogs.Circulation, Vol. 64, No. 6 More from this issue > Volume 233Issue 2August 1977Pages H196-H202 Copyright & PermissionsCopyright © 1977 the American Physiological Societyhttps://doi.org/10.1152/ajpheart.1977.233.2.H196PubMed196510History Published online 1 August 1977 Published in print 1 August 1977 Metrics

Interplay among carotid sinus, cardiopulmonary, and carotid body reflexes in dogs.

Interactions among vascular reflexes evoked from carotid sinuses, carotid bodies, and cardiopulmonary region were examined in anesthetized, atropinized, and respired dogs with aortic nerves cut. The carotid sinuses were perfused at 220, 150, and 40-50 mmHg; the chemoreceptors were stimulated by perfusion with hypoxic hypercapnic blood. Cardiopulmonary vasomotor inhibition was interrupted by vagal cold block. Measurements were made of arterial blood pressure and of kidney and hindlimb vascular resistance. At sinus pressures less than 170-160 mmHg, cardiopulmonary vasomotor inhibition increased with increase in blood volume. At high sinus pressure, interruption of this augmented cardiopulmonary inhibition was as ineffective in changing vascular resistance as interruption of the lesser inhibition present during normovolemia. Chemoreceptor stimulation increased the response to vagal block at intermediate but not at high or low sinus pressure. The studies demonstrate the dominant role of the carotid sinus reflex when the three systems interact and the ineffectiveness of chemoreceptor stimulation when carotid or cardiopulmonary inhibition is maximal.

KETAMINE CATALEPSY AND ANESTHESIA IN DOGS PRETREATED WITH ANTISEROTONERGIC OR ANTIDOPAMINERGIC NEUROLEPTICS OR WITH ANTICHOLINERGIC AGENTS

Summary Pretreatment with methiothepin or chlorpromazine prevents catalepsy, prolongs duration of anesthesia and recovery, prevents apneustic respiration, and favors disappearance of limb-withdrawal and jaw reflexes in dogs injected intramuscularly with a minimum anesthetic dose of ketamine. These effects relate to degree of sedation produced by the neuroleptics, and therefore may be nonspecific. A subsedative dose of pimozide antagonizes ketamine anesthesia and potentiates catalepsy, respiratory apneusis, and emergent delirium. Sedative doses of pimozide are less effective in these regards. Mecamylamine enhances ketamine catalepsy and respiratory apneusis, and lightens (but does not shorten) anesthesia. Atropine prevents ketamine catalepsy and antagonizes respiratory apneusis, but potentiates muscle jerking, prolongs recovery time, and greatly prolongs emergent delirium. The results seem to implicate dopaminergic, nicotinic cholinoceptive, and muscarinic cholinoceptive mechanisms in a complex system of mediation and modulation of canine responses to ketamine. This system is different from one previously proposed for the cat. Weingarten (1972) postulated that ketamine catalepsy might be due to stimulation of the monoaminergic component of a balanced cholinergic-monoaminergic system in the brain. In rabbits, the anticholinergic agent procyclidine enhanced ketamine catalepsy ( Authier & others, 1972 ). In cats, the antiserotonergic neuroleptic agent methiothepin ( Monachon & others, 1972 ) prevented ketamine catalepsy, but pimozide 9an antidopaminergic neuroleptic, Anden & others, 1970 ) and chlorpromazine 9a neuroleptic of mixed antimonoamine activity) did not affect ketamine catalepsy ( Hatch, 1973 ). Thus, it appeared that ketamine catalepsy may indeed relate to a cholinergic-monoaminergic imbalance, and that the monoamine of interest in this regard might be serotonin. The purpose of the present study was to examine the validity of the proposed cholinergic-serotonergic mechanism of ketamine catalepsy in dogs. This species is particularly susceptible to the cataleptic and deliriant effects of ketamine.

The Effect of Local Anaesthesia of the Airway on Respiratory Reflexes in Dog and Man

Conference Abstract| February 01 1975 The Effect of Local Anaesthesia of the Airway on Respiratory Reflexes in Dog and Man Sietske Archer; Sietske Archer 1Department of Medicine, Charing Cross Hospital Medical School; Department of Anaesthesia, Charing Cross Hospital; and Department of Pharmacology and Therapeutics, St Thomas's Hospital Medical School, London Search for other works by this author on: This Site PubMed Google Scholar Brenda A. Cross; Brenda A. Cross 1Department of Medicine, Charing Cross Hospital Medical School; Department of Anaesthesia, Charing Cross Hospital; and Department of Pharmacology and Therapeutics, St Thomas's Hospital Medical School, London Search for other works by this author on: This Site PubMed Google Scholar A. Guz; A. Guz 1Department of Medicine, Charing Cross Hospital Medical School; Department of Anaesthesia, Charing Cross Hospital; and Department of Pharmacology and Therapeutics, St Thomas's Hospital Medical School, London Search for other works by this author on: This Site PubMed Google Scholar S. K. Jain; S. K. Jain 1Department of Medicine, Charing Cross Hospital Medical School; Department of Anaesthesia, Charing Cross Hospital; and Department of Pharmacology and Therapeutics, St Thomas's Hospital Medical School, London Search for other works by this author on: This Site PubMed Google Scholar Felicity Reynolds; Felicity Reynolds 1Department of Medicine, Charing Cross Hospital Medical School; Department of Anaesthesia, Charing Cross Hospital; and Department of Pharmacology and Therapeutics, St Thomas's Hospital Medical School, London Search for other works by this author on: This Site PubMed Google Scholar J. H. Stevens J. H. Stevens 1Department of Medicine, Charing Cross Hospital Medical School; Department of Anaesthesia, Charing Cross Hospital; and Department of Pharmacology and Therapeutics, St Thomas's Hospital Medical School, London Search for other works by this author on: This Site PubMed Google Scholar Clin Sci Mol Med (1975) 48 (2): 18P. https://doi.org/10.1042/cs048018Pa Views Icon Views Article contents Figures & tables Video Audio Supplementary Data Peer Review Share Icon Share Twitter LinkedIn Cite Icon Cite Get Permissions Citation Sietske Archer, Brenda A. Cross, A. Guz, S. K. Jain, Felicity Reynolds, J. H. Stevens; The Effect of Local Anaesthesia of the Airway on Respiratory Reflexes in Dog and Man. Clin Sci Mol Med 1 February 1975; 48 (2): 18P. doi: https://doi.org/10.1042/cs048018Pa Download citation file: Ris (Zotero) Reference Manager EasyBib Bookends Mendeley Papers EndNote RefWorks BibTex toolbar search Search Dropdown Menu toolbar search search input Search input auto suggest filter your search All ContentAll JournalsClinical Science Search Advanced Search This content is only available as a PDF. © 1975 The Biochemical Society and the Medical Research Society1975 Article PDF first page preview Close Modal You do not currently have access to this content.

Ketamine catalepsy and anesthesia in dogs pretreated with antiserotonergic or antidopaminergic neuroleptics or with anticholinergic agents

Summary Pretreatment with methiothepin or chlorpromazine prevents catalepsy, prolongs duration of anesthesia and recovery, prevents apneustic respiration, and favors disappearance of limb-withdrawal and jaw reflexes in dogs injected intramuscularly with a minimum anesthetic dose of ketamine. These effects relate to degree of sedation produced by the neuroleptics, and therefore may be nonspecific. A subsedative dose of pimozide antagonizes ketamine anesthesia and potentiates catalepsy, respiratory apneusis, and emergent delirium. Sedative doses of pimozide are less effective in these regards. Mecamylamine enhances ketamine catalepsy and respiratory apneusis, and lightens (but does not shorten) anesthesia. Atropine prevents ketamine catalepsy and antagonizes respiratory apneusis, but potentiates muscle jerking, prolongs recovery time, and greatly prolongs emergent delirium. The results seem to implicate dopaminergic, nicotinic cholinoceptive, and muscarinic cholinoceptive mechanisms in a complex system of mediation and modulation of canine responses to ketamine. This system is different from one previously proposed for the cat. Weingarten (1972) postulated that ketamine catalepsy might be due to stimulation of the monoaminergic component of a balanced cholinergic-monoaminergic system in the brain. In rabbits, the anticholinergic agent procyclidine enhanced ketamine catalepsy ( Authier & others, 1972 ). In cats, the antiserotonergic neuroleptic agent methiothepin ( Monachon & others, 1972 ) prevented ketamine catalepsy, but pimozide 9an antidopaminergic neuroleptic, Anden & others, 1970 ) and chlorpromazine 9a neuroleptic of mixed antimonoamine activity) did not affect ketamine catalepsy ( Hatch, 1973 ). Thus, it appeared that ketamine catalepsy may indeed relate to a cholinergic-monoaminergic imbalance, and that the monoamine of interest in this regard might be serotonin. The purpose of the present study was to examine the validity of the proposed cholinergic-serotonergic mechanism of ketamine catalepsy in dogs. This species is particularly susceptible to the cataleptic and deliriant effects of ketamine.

Effect of hyperthermia and Pa CO2 on the slowly adapting pulmonary stretch receptor.

Effect of hyperthermia and Pa CO2 on the slowly adapting pulmonary stretch receptor.

Heart rate in relation to sympathetic efferentation associated with the Bainbridge reflex in dogs.

Acta Physiologica ScandinavicaVolume 83, Issue 4 p. 571-573 Heart Rate in Relation to Sympathetic Efferentation Associated with the Bainbridge Reflex in Dogs R. M. Bergström, R. M. Bergström Institute of Physiology, University of Helsinki, FinlandSearch for more papers by this authorM. O. K. Hakumäki, M. O. K. Hakumäki Institute of Physiology, University of Helsinki, FinlandSearch for more papers by this authorH. S. S. Sarajas, H. S. S. Sarajas Institute of Physiology, University of Helsinki, FinlandSearch for more papers by this author R. M. Bergström, R. M. Bergström Institute of Physiology, University of Helsinki, FinlandSearch for more papers by this authorM. O. K. Hakumäki, M. O. K. Hakumäki Institute of Physiology, University of Helsinki, FinlandSearch for more papers by this authorH. S. S. Sarajas, H. S. S. Sarajas Institute of Physiology, University of Helsinki, FinlandSearch for more papers by this author First published: December 1971 https://doi.org/10.1111/j.1748-1716.1971.tb05115.xCitations: 10AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Citing Literature Volume83, Issue4December 1971Pages 571-573 RelatedInformation

Relationship between phrenic nerve activity and ventilation.

Relationship between phrenic nerve activity and ventilation.