Convergence of sympathetic, vagal, and other sensory inputs onto neurons in feline ventrolateral medulla

1991 ◽  
Vol 260 (6) ◽  
pp. H1918-H1928 ◽  
Author(s):  
R. W. Blair
Keyword(s):  
Blood Pressure ◽  
Reticular Formation ◽  
Sensory Input ◽  
Vagal Stimulation ◽  
Stellate Ganglion ◽  
Ventrolateral Medulla ◽  
Multiple Sources ◽  
Pressure Sensitive ◽  
Alpha Chloralose ◽  
Stimulation Of

Responses of 80 neurons in rostral and caudal ventrolateral medulla to multiple sources of sensory input were assessed in cats anesthetized with alpha-chloralose. Sixty-one of eighty-one neurons (76%) were excited by stimulation of the stellate ganglion, and one neuron exhibited inhibition followed by excitation. In response to vagal stimulation, 12% of the neurons were excited and 29% inhibited. Vagal stimulation reduced the responses of 13 of 39 (33%) neurons to sympathetic stimulation. Overall, one-third of the neurons responded to both sympathetic and vagal stimulation. There was no difference in proportion of responsive neurons in rostral versus caudal ventrolateral reticular formation. Cells were also tested for auditory, visual, and natural somatic stimuli. Ten percent of the neurons responded to all five stimuli, and another 25% responded to four stimuli. Twelve percent of neurons were unresponsive to any stimulus. Twenty cells were tested for responses to changes in blood pressure elicited with phenylephrine and nitroglycerin. Seven neurons were inhibited by increases or excited by decreases in pressure, four had the opposite responses, and nine were unresponsive. In general, blood pressure-sensitive cells exhibited comparable convergence of other inputs as the overall cell population. However, three times as many pressure-insensitive neurons received vagal input as did pressure sensitive neurons. In conclusion, neurons in the ventrolateral medulla, including the vasopressor and vasodepressor regions, receive and integrate convergent input from multiple sensory origins. Since the regions of the reticular formation studied are functionally heterogeneous, the precise functions of these neurons are not known.

Differential cardiorespiratory control elicited by activation of ventral medullary sites in mice

2000 ◽  
Vol 89 (2) ◽  
pp. 437-444 ◽  
Author(s):  
F. P. Tolentino-Silva ◽  
M. A. Haxhiu ◽  
P. Ernsberger ◽  
S. Waldbaum ◽  
I. A. Dreshaj
Keyword(s):  
Blood Pressure ◽  
Adrenergic Receptors ◽  
Excitatory Amino Acid ◽  
Signal Transduction Pathway ◽  
Ventrolateral Medulla ◽  
Respiratory Drive ◽  
Breathing Frequency ◽  
Cardiorespiratory Control ◽  
Blood Pressure Responses ◽  
Stimulation Of

We studied the respiratory and blood pressure responses to chemical stimulation of two regions of the ventral brainstem in mice: the rostral and caudal ventrolateral medulla (RVLM and CVLM, respectively). Stimulation of the RVLM by microinjections of the excitatory amino acid l-glutamate induced increases in diaphragm activity and breathing frequency, elevation of blood pressure (BP), and a slight increase in heart rate (HR). However, activation of the CVLM induced a decrease in breathing frequency, mainly due to prolongation of expiratory time (Te), and hypotension associated with a slight slowing of HR. Because adrenergic mechanisms are known to participate in the control of respiratory timing, we examined the role of α2-adrenergic receptors in the RVLM region in mediating these inhibitory effects. The findings demonstrated that blockade of the α2-adrenergic receptors within the RVLM by prior microinjection of SKF-86466 (an α2-adrenergic receptor blocker) significantly reduced changes in Te induced by CVLM stimulation but had little effect on BP responses. These results indicate that, in mice, activation of the RVLM increases respiratory drive associated with an elevation of BP, but stimulation of CVLM induces prolongation of Te via an α2-adrenergic signal transduction pathway.

Myocardial catecholamines and stimulation of the stellate ganglion in hemorrhagic shock

1965 ◽  
Vol 209 (4) ◽  
pp. 751-756 ◽  
Author(s):  
Vincent V. Glaviano ◽  
Mary Ann Klouda
Keyword(s):  
Blood Pressure ◽  
Hemorrhagic Shock ◽  
Stellate Ganglion ◽  
Myocardial Contraction ◽  
Cardiac Contraction ◽  
Cardiac Responses ◽  
Left Stellate Ganglion ◽  
Anesthetized Dogs ◽  
The Right ◽  
Stimulation Of

Cardiac responses to electrical stimulation of the right or left stellate ganglion were recorded from 16 open-chest anesthetized dogs in hemorrhagic shock. Shock was induced by bleeding the animals to a mean blood pressure of 40 mm Hg. This level of pressure was maintained for 4 hr, during which time blood pressure, heart rate, force of myocardial contraction, and intraventricular pressures were recorded. Stimulation of the stellate ganglion for 15–40 sec every 30 min after hemorrhage showed a gradual decrease in these parameters to levels below control. The reinfusion of blood and the infusion of exogenous l-norepinephrine did not restore an increase in force of cardiac contraction to stellate stimulation. Myocardial epinephrine and norepinephrine levels in shock were found not to differ from those in 14 normal dog hearts. In contrast to almost complete myocardial refractoriness to stellate stimulation in hemorrhagic shock, stimulation of the vagus nerve elicited bradycardia and eventual cardiac arrest. The decrease observed in force of cardiac contraction to stimulation of the stellate ganglion in hemorrhagic shock may be due to depletion of norepinephrine stores in the heart.

Renal and somatic input to spinal neurons antidromically activated from the ventrolateral medulla

1988 ◽  
Vol 60 (6) ◽  
pp. 1967-1981 ◽  
Author(s):  
W. S. Ammons
Keyword(s):  
Reticular Formation ◽  
Receptive Fields ◽  
Ventrolateral Medulla ◽  
Reticular Nucleus ◽  
Lateral Reticular Nucleus ◽  
Spinal Neurons ◽  
C Fiber ◽  
Somatic Input ◽  
Fiber Stimulation ◽  
Stimulation Of

1. Studies were done to characterize responses of spinal neurons backfired from the ventrolateral medulla to renal and somatic stimuli. Experiments were performed on 31 cats that were anesthetized with alpha-chloralose. Sixty-six spinal neurons were antidromically activated from the area of the lateral reticular nucleus or the ventrolateral reticular formation just rostral to the lateral reticular nucleus contralateral to the recording site. These cells could not be backfired from the medial reticular formation or from the spinothalamic tract just caudal to the thalamus. 2. Cells were located in laminae I, V, and VII of the T12-L2 segments. Antidromic conduction velocities averaged 35.9 +/- 7.2 m/s. Conduction velocities were unrelated to the projection site or laminar location of the cells. Termination sites of 21 cells were located in antidromic mapping experiments. Terminals were localized to the ventrolateral reticular formation, including the lateral reticular nucleus. 3. Responses to electrical stimulation of the renal nerves were always excitatory. Stimulation of renal A-delta-fibers excited 33 cells. These cells failed to respond to stimulation of renal C-fibers. The other 33 cells responded to both A-delta- and C-fiber stimulation. Latencies to A-delta-fiber stimulation averaged 9 +/- 2 ms, whereas latencies to C-fiber stimulation averaged 57 +/- 10 ms. 4. Renal mechanoreceptors were activated by occlusion of the renal vein or upper portion of the ureter. Renal vein occlusion excited 14 of 32 cells tested. Activity increased from 6 +/- 2 to 14 +/- 4 spike/s. Ureteral occlusion increased activity of 19 of 32 cells from 7 +/- 2 to 16 +/- 5 spikes/s. Cells responding to one of the mechanical stimuli were significantly more likely to receive A-delta-and C-fiber input compared with nonresponding cells. Nonresponders were more likely than responders to receive only A-delta input. 5. All cells received somatic input in addition to renal input. Twelve cells were classified as wide dynamic range, 46 as high threshold, and 8 as Deep. Somatic receptive fields most often included skin and muscle of the left flank and abdomen. Thirty-two cells had bilateral receptive fields, and 22 had inhibitory fields in addition to excitatory fields. 6. These data show that spinal neurons projecting to the ventrolateral medulla receive convergent inputs from the kidney and somatic structures. These cells may participate in a variety of functions including autonomic reflexes of renal origin.

Responses of medullary raphespinal neurons to electrical stimulation of thoracic sympathetic afferents, vagal afferents, and to other sensory inputs in cats

1991 ◽  
Vol 66 (6) ◽  
pp. 2084-2094 ◽  
Author(s):  
R. W. Blair ◽  
A. R. Evans
Keyword(s):  
Electrical Stimulation ◽  
Neuronal Activity ◽  
Vagal Stimulation ◽  
Discharge Rate ◽  
Stellate Ganglion ◽  
Cell Activity ◽  
Conditioning Stimulus ◽  
Vagal Afferents ◽  
Early Peak ◽  
Stimulation Of

1. Medullary raphespinal neurons antidromically activated from the T2-T5 segments were tested for responses to electrical stimulation of cervical vagal and thoracic sympathetic afferents (by stimulating the left stellate ganglion), somatic probing, auditory stimuli, and visual stimuli in cats anesthetized with alpha-chloralose. A total of 99 neurons in the raphe nuclei were studied; the locations of 76 cells were histologically confirmed. Neurons were located in raphe magnus (RM, 65%), raphe obscurus (RO, 32%), and raphe pallidus (RPa, 4%). The mean conduction velocity of these neurons was 62 +/- 2.9 (SE) m/s with a range of 1.1-121 m/s. 2. A total of 60/99 tested neurons responded to electrical stimulation of sympathetic afferents. Quantitation of responses was obtained for 55 neurons. With one exception, all responsive neurons were excited and exhibited an early burst of spikes with a mean latency of 16 +/- 1.2 ms. From a spontaneous discharge rate of 5.2 +/- 1.2 spikes/s, neuronal activity increased by 2.9 +/- 0.3 spikes/stimulus. In addition to an early peak, 15 neurons (25%) exhibited a late burst of spikes with a latency of 182 +/- 12.9 ms; neuronal activity increased by 5.0 +/- 1.3 spikes/stimulus. Duration of the late peak (130 +/- 18.5 ms) was longer than for the early peak (18 +/- 0.7 ms), but threshold voltages for eliciting each peak were comparable. Sixteen of 29 spontaneously active neurons exhibited a postexcitatory depression of activity that lasted for 163 +/- 19.1 ms. All but one tested neuron in RO responded to stimulation of sympathetic afferents, but 65% of neurons in RM responded to this stimulus. 3. In response to vagal afferent stimulation, 19% of 57 neurons exhibited inhibition only, 11% were only excited, and 9% were either excited or inhibited, depending on the stimulus paradigm used; the remaining 61% of neurons were unresponsive. From a spontaneous rate of 7.9 +/- 3.8 spikes/s, excited cells increased their discharge rate by 1.6 +/- 0.3 spikes/stimulus. Activity of inhibited cells was reduced from 21.3 +/- 5.8 to 7.8 +/- 3.1 spikes/s. The conditioning-test (CT) technique was used to assess 11 neurons' responses. Stellate ganglion stimulation was the test stimulus, and vagal stimulation the conditioning stimulus. Vagal stimulation reduced the neuronal responses to stellate ganglion stimulation by an average of 50% with a CT interval of 60-100 ms, and cell responses returned to control after 300 ms. With spontaneous cell activity, low frequencies of vagal stimulation were generally excitatory, and high frequencies (10-20 Hz) inhibitory.(ABSTRACT TRUNCATED AT 400 WORDS)

Responses of the canine myocardium to stimulation of thoracic cardiac nerves

1977 ◽  
Vol 232 (5) ◽  
pp. H485-H494 ◽  
Author(s):  
J. E. Norris ◽  
W. C. Randall
Keyword(s):  
Blood Pressure ◽  
Systemic Blood Pressure ◽  
Type Ii ◽  
Systemic Blood ◽  
Type Iv ◽  
The Right ◽  
Alpha Chloralose ◽  
Canine Myocardium ◽  
Cardiac Nerves ◽  
Stimulation Of

The thoracic cardiac nerves were stimulated in each of 21 dogs anesthetized with alpha chloralose. Recordings were made of heart rate, blood pressure, and contractile force from all four cardiac chambers. Walton-Brodie strain-gauge arches were sutured to both atria, and to three locations of each ventricle, representing both anterior and posterior surfaces. The functional autonomic components of each nerve were summarized and classified into four basic types. Types I and II were both located medial to the thoracic vagi. These were shown to contain both sympathetic and parasympathetic components traveling to all four chambers of the heart. The sympathetic componnent of the type II nerves produced reflex changes in force of contraction and systemic blood pressure. Nerves classified as types III and IV produced no parasympathetic effect on the heart. These were all located lateral to the thoracic vagi. While the type III nerves carried sympathetic efferent fibers to all four chambers, the type IV nerve carried sympathetic fibers predominantly to the right atrium.

Mechanisms of action of sodium cromoglycate

1985 ◽  
Vol 63 (6) ◽  
pp. 760-765 ◽  
Author(s):  
D. F. Biggs ◽  
V. Goel
Keyword(s):  
Blood Pressure ◽  
Sodium Cromoglycate ◽  
Arterial Blood Pressure ◽  
Vagal Stimulation ◽  
Cardiovascular Responses ◽  
Bilateral Stimulation ◽  
Vagus Nerves ◽  
Arterial Blood ◽  
Efferent Pathways ◽  
Stimulation Of

The effects of sodium cromoglycate (SCG) on cardiovascular and pulmonary responses to phenylbiguanide, capsaicin, and vagal stimulation were studied in anesthetized guinea pigs. Phenylbiguanide had no bronchospastic activity but induced reflex changes in arterial blood pressure which were reduced or abolished by SCG. Capsaicin induced nonreflex bronchospasm, and decreases in arterial blood pressure that were unaffected by SCG. Sodium cromoglycate, given before or after atropine, had no effect on the bronchospasm and cardiovascular responses to unilateral or bilateral stimulation of the vagus nerves. We conclude that SCG may influence both the afferent and efferent pathways of responses to drugs.

Ventilatory effects of stimulation of phrenic afferents

1987 ◽  
Vol 63 (3) ◽  
pp. 1063-1069 ◽  
Author(s):  
J. D. Road ◽  
N. H. West ◽  
B. N. Van Vliet
Keyword(s):  
Blood Pressure ◽  
Pressor Response ◽  
Sensory Innervation ◽  
Respiratory Muscle Fatigue ◽  
Pentobarbital Sodium ◽  
Arterial Blood ◽  
Afferent Activation ◽  
Ventilatory Drive ◽  
Alpha Chloralose ◽  
Stimulation Of

The diaphragm, a ventilatory muscle, has abundant sensory innervation. The effects of phrenic afferent activation on ventilation have been varied. In this study the proximal end of the phrenic nerve was electrically stimulated, and the effects on ventilation were measured in supine dogs anesthetized with either alpha-chloralose or pentobarbital sodium. We found a maximum increase in ventilation of 45 +/- 4% in the alpha-chloralose group and an increase in mean arterial blood pressure of 18 +/- 4%. This response was obtained at high stimulus intensities (60 times twitch threshold). Stimulation of the proximal end of the gastrocnemius nerve produced a similar ventilatory response (61 +/- 10%) but at lower stimulus intensities. During pentobarbital sodium anesthesia both the hyperventilation and the pressor response were produced; however, ventilation was increased by an increase in respiratory frequency. The reflex was abolished by sectioning of the cervical dorsal roots (C4-C7). Proximal cold blockade of the nerve abolished the response at a perineural temperature of 1.35 +/- 0.64 degrees C. The main effect of activation of phrenic afferents was an increase in ventilation and blood pressure that was mediated by unmyelinated fibers and possibly thin myelinated fibers. This response is similar to skeletal muscle afferent activation and may play a role in ventilatory drive during such conditions as exercise and respiratory muscle fatigue.

Cardiovascular reflexes following lesions in medullary reticular formation

1965 ◽  
Vol 208 (2) ◽  
pp. 283-288 ◽  
Author(s):  
John W. Manning
Keyword(s):  
Blood Pressure ◽  
Reticular Formation ◽  
Tissue Injury ◽  
Cardiac Activity ◽  
Cardiovascular Reflexes ◽  
Medullary Reticular Formation ◽  
Cardiovascular Reflex ◽  
Vascular Reflex ◽  
Inferior Olivary ◽  
Stimulation Of

In 19 anesthetized cats acute destruction of large portions of the medullary reticular formation was achieved with the aid of a radio-frequency lesion maker. Midline structures were spared by confining the lesions to the dorsolateral medulla. Tissue injury extended from a level rostral to the inferior olivary complex to the obex. These lesions in the medullary vasomotor area did not alter significantly the cardiovascular reflex adjustments to bilateral occlusion of the carotid arteries or to the stimulation of the central end of the cut sciatic nerve. In addition, an increase in contractile force, heart rate, and blood pressure evoked by stimulation of pressor areas in the posterior hypothalamus could be obtained following the lesions. The preparations were critically dependent upon supramedullary connections to maintain vascular tone and circulatory reflex adjustments, for decerebration in the lesioned animal brought about a reduction in blood pressure and a loss of vascular reflex responses. These findings suggest that supramedullary centers exert tonic as well as phasic influences on vascular and cardiac activity that is independent of the medullary vasomotor area.

Effects of catecholamines on cardiac chronotropic response to vagal stimulation in the dog

1983 ◽  
Vol 245 (5) ◽  
pp. H721-H724 ◽  
Author(s):  
C. Chassaing ◽  
P. Duchene-Marullaz ◽  
M. J. Veyrac
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Vagus Nerve ◽  
Neurotransmitter Release ◽  
Acetylcholine Release ◽  
Vagal Stimulation ◽  
Norepinephrine Release ◽  
Chronotropic Response ◽  
Anesthetized Dogs ◽  
Stimulation Of

The influence of isoproterenol, norepinephrine, and dopamine on the cardiomoderator effects of moderate vagal stimulation was studied in anesthetized dogs. The drugs were administered at increasing doses in successive perfusions. Stimulation of the vagus nerve, the parameters of which remained constant throughout each experiment, was performed immediately before each sequence of perfusion and after 10-min perfusion. Isoproterenol at 0.025, 0.05, 0.1, and 0.2 microgram X kg-1 X min-1 raised heart rate dose relatedly but did not alter heart rate under vagal stimulation. Thus the amplitude of vagal bradycardic effects increased dose relatedly. Norepinephrine at 0.125, 0.25, 0.5, and 1 microgram X kg-1 X min-1 lowered heart rate through reflex hypertension. Heart rate under vagal stimulation remained constant. Thus the effects of vagal stimulation decreased as dose increased, finally becoming null. Dopamine at 0.5, 1, 2.5, and 5 micrograms X kg-1 X min-1 did not significantly alter heart rate, but at 10 and 20 micrograms X kg-1 X min-1, like norepinephrine, it raised blood pressure, causing a reflex fall in heart rate. At all doses, heart rate under vagal stimulation remained stable. Consequently, at the highest doses, the net effects of vagal stimulation were slight. These results suggest the simultaneous involvement of sympathetic-parasympathetic interactions both post- and prejunctionally. In the latter case, different mechanisms of regulation of neurotransmitter release are involved during vagal stimulation according to the sympathomimetic used. With isoproterenol, norepinephrine release seems more particularly affected, whereas with norepinephrine and dopamine, acetylcholine release is apparently inhibited.

The release of vasopressin without oxytocin in response to haemorrhage

1967 ◽  
Vol 166 (1005) ◽  
pp. 443-458 ◽  
Keyword(s):  
Blood Pressure ◽  
Mammary Gland ◽  
Guinea Pig ◽  
Arterial Blood Pressure ◽  
Vagal Stimulation ◽  
Critical Value ◽  
Inhibitory Substance ◽  
Blood Samples ◽  
Arterial Blood ◽  
Stimulation Of

Blood samples were collected from anaesthetized cats during haemorrhage or stimulation of the peripheral end of the vagus. Vasopressin and oxytocin were estimated in the samples by assaying alcohol extracts for antidiuretic activity in the water loaded rat and for milk-ejecting activity in the lactating guinea-pig. Haemorrhage caused vasopressin to be released into the blood with out detectable amounts of oxytocin. A similar result was obtained with vagal stimulation provided that the fall of blood pressure which it produced exceeded a critical value of about 80 mmHg. Failure to detect oxytocin in blood samples containing vasopressin was not due to the presence of adrenaline or any other inhibitory substance in the extracts blocking the response of the mammary gland to oxytocin. The stimulus for the independent release of vasopressin by haemorrhage appears to be the associated fall in arterial blood pressure.

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