Effect of blood pressure on medial medulla-induced muscle atonia

1987 ◽  
Vol 252 (6) ◽  
pp. H1249-H1257 ◽  
Author(s):  
Y. Y. Lai ◽  
J. M. Siegel ◽  
W. J. Wilson
Keyword(s):  
Blood Pressure ◽  
Carotid Sinus ◽  
Muscle Tone ◽  
Blood Pressure Reduction ◽  
Base Line ◽  
Cervicothoracic Junction ◽  
Medullary Reticular Formation ◽  
Muscle Atonia ◽  
6 Hydroxydopamine ◽  
Stimulation Of

Stimulation of the medial medullary reticular formation (MMRF) has long been reported to produce generalized inhibition of skeletal muscle activity. However, several studies have reported that in most cases MMRF stimulation produces only increases in muscle tone. In the present investigation we have found that blood pressure is a critical variable, determining whether MMRF stimulation will produce muscle excitation or inhibition. When mean arterial pressure (MAP) was greater than 80 mmHg but less than 148 mmHg, MMRF stimulation produced muscle antonia. Reductions of blood pressure by pharmacological or mechanical techniques induced a reversal of response to MMRF stimulation; stimulation that produced inhibition in base-line conditions produced excitation after MAP reduction. MAP reductions of as little as 10% could cause the reversal response. In contrast, the EMG reduction to MMRF stimulation was not changed or was augmented when MAP was raised. MMRF induced atonia, and its reversal by blood pressure reduction persisted after bilateral isolation of the carotid sinus combined with vagotomy, and in the 6-hydroxydopamine-treated cat. Spinal transection at the cervicothoracic junction did not block atonia or the reversal response. It is suggested that the reversal is mediated centrally.

Acute Device-Based Blood Pressure Reduction: Electrical Activation of the Carotid Baroreflex in Patients Undergoing Elective Carotid Surgery

Vascular ◽  
2007 ◽  
Vol 15 (2) ◽  
pp. 63-69 ◽  
Author(s):  
Jürg Schmidli ◽  
Hannu Savolainen ◽  
Friedrich Eckstein ◽  
Eric Irwin ◽  
Tim K. Peters ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Carotid Sinus ◽  
Blood Pressure Reduction ◽  
Acute Effect ◽  
Carotid Surgery ◽  
Proof Of Concept ◽  
Sinus Wall ◽  
Carotid Baroreflex ◽  
Voltage Dependent ◽  
Stimulation Of

Carotid sinus baroreceptors are involved in controlling blood pressure (BP) by providing input to the cardiovascular regulatory centers of the medulla. The acute effect of temporarily placing an electrode on the carotid sinus wall to electrically activate the baroreflex was investigated. We studied 11 patients undergoing elective carotid surgery. Baseline BP was 146+30/66±17 mm Hg and heart rate (HR) 72±7 bpm (mean ± standard deviation). An electrode was placed upon the carotid sinus and after obtaining a steady state baseline of BP and HR, an electric current was applied and increased in 1-volt increments. A voltage dependent and highly significant reduction in BP was observed which averaged 18±26* and 8.0±12 mm Hg for systolic BP and diastolic BP, respectively. Maximal reductions occurred at 4.4±1.2 V: 23±24 mm Hg*, 16±10 mm Hg* and 7±12 bpm* for systolic BP, diastolic BP and HR, respectively (= p <.05). Thus, electrical stimulation of the carotid sinus activates the carotid baroreflex resulting in a reduction in BP and HR. This presents a proof of concept for device based baroreflex modulation in acute BP regulation and adds to the available data which provide a rationale for evaluating this system in the context of chronic BP reduction in hypertensive patients.

Effect of baroreceptor denervation on stimulation of drinking by angiotensin II in conscious dogs

1991 ◽  
Vol 260 (3) ◽  
pp. E333-E337 ◽  
Author(s):  
C. K. Klingbeil ◽  
V. L. Brooks ◽  
E. W. Quillen ◽  
I. A. Reid
Keyword(s):  
Blood Pressure ◽  
Drinking Water ◽  
Angiotensin Ii ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Carotid Sinus ◽  
Plasma Osmolality ◽  
Plasma Angiotensin ◽  
High Doses ◽  
Stimulation Of

Angiotensin II causes marked stimulation of drinking when it is injected centrally but is a relatively weak dipsogen when administered intravenously. However, it has been proposed that the dipsogenic action of systemically administered angiotensin II may be counteracted by the pressor action of the peptide. To test this hypothesis, the dipsogenic action of angiotensin II was investigated in dogs, in which low and high baroreceptor influences had been eliminated by denervation of the carotid sinus, aortic arch, and heart. In five sham-operated dogs, infusion of angiotensin II at 10 and 20 ng.kg-1.min-1 increased plasma angiotensin II concentration to 109.2 +/- 6.9 and 219.2 +/- 38.5 pg/ml and mean arterial pressure by 20 and 29 mmHg, respectively, but did not induce drinking. In four baroreceptor-denervated dogs, the angiotensin II infusions produced similar increases in plasma angiotensin II concentration and mean arterial pressure but, in contrast to the results in the sham-operated dogs, produced a dose-related stimulation of drinking. Water intake with the low and high doses of angiotensin II was 111 +/- 44 and 255 +/- 36 ml, respectively. The drinking responses to an increase in plasma osmolality produced by infusion of hypertonic sodium chloride were not different in the sham-operated and baroreceptor-denervated dogs. These results demonstrate that baroreceptor denervation increases the dipsogenic potency of intravenous angiotensin II and provides further support for the hypothesis that the dipsogenic action of intravenous angiotensin II is counteracted by the rise in blood pressure.

Nutrient control of cardiac rate in infant rats: role of arterial baroreceptors

1985 ◽  
Vol 249 (4) ◽  
pp. R443-R448 ◽  
Author(s):  
M. A. Hofer
Keyword(s):  
Blood Pressure ◽  
Carotid Sinus ◽  
Nutrient Deprivation ◽  
Base Line ◽  
Cardiac Rate ◽  
Suckling Rats ◽  
Arterial Baroreceptors ◽  
Infant Rats ◽  
And Control

A surgical procedure is described for the deafferentation of carotid sinus (CS) and aortic depressor (AD) baroreceptors in 2-wk suckling rats. Baroreflex testing in unanesthetized pups showed that cardiac rate responses to acute elevations of blood pressure were reduced to less than 9% of controls after combined denervation (CSAD), 28% after AD and 47% after CS denervation at 4 h. After 24 h of nutrient deprivation, resting cardiac rates of sham operated controls fell a mean of -148 beat/min, significantly more than CS, AD, or CSAD groups (P less than 0.01). Baroreflex test responses in individuals correlated significantly with their later responses to nutrient deprivation (r = 0.67, P less than 0.01). There were no significant differences in base-line cardiac rate, systolic blood pressure, or cardiac rate during 24 h intragastric milk infusion between deafferented and control pups. These experiments suggest that arterial baroreceptors are important in the cardiovascular adjustments after nutrient deprivation in suckling rats.

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.

Elevations in plasma ADH levels during PEEP ventilation in the dog: mechanisms involved

1980 ◽  
Vol 239 (6) ◽  
pp. E474-E481 ◽  
Author(s):  
H. Bark ◽  
D. Le Roith ◽  
M. Nyska ◽  
S. M. Glick
Keyword(s):  
Blood Pressure ◽  
Intracranial Pressure ◽  
Carotid Sinus ◽  
Plasma Renin ◽  
Base Line ◽  
Positive End Expiratory Pressure ◽  
Physiological Factors ◽  
Bilateral Vagotomy ◽  
Propranolol Administration ◽  
Peep Ventilation

In an attempt to define more precisely the various mechanisms involved in antidiuretic hormone (ADH) release during positive end-expiratory pressure ventilation (PEEP), experiments were performed on seven groups of dogs. PEEP-10 and PEEP-15 cmH2O caused significant elevations of plasma ADH from basal values of 24.9 +/- 5.2 pg/ml (mean +/- SE) to 64.6 +/- 14.2 and 106.0 +/- 20.6, respectively (P < 0.02, P < 0.005). The ADH levels returned to basal values after cessation of PEEP. This rise in ADH levels was prevented by an infusion of dextran prior to PEEP. The fall in blood pressure and cardiac output that occurred during PEEP was also prevented by the dextran infusion. Changes in ADH levels were unrelated to lung volume, left transmural pressure, and serum osmolality. Bilateral vagotomy and carotid sinus denervation was followed by an attenuated rise in ADH levels in terms of the percent rise above base line, but it did not significantly alter the absolute rise in ADH during PEEP. ADH levels were, however, reduced significantly by decreasing intracranial pressure by the removal of cerebrospinal fluid during PEEP. Propranolol administration prior to PEEP completely blocked plasma renin activity. Although the peak ADH levels were unaffected by propranolol, the rise was delayed. The results obtained indicate that a number of physiological factors may affect plasma ADH levels during PEEP. These include the carotid body and aortic arch baroreceptors as wells as sensors of intracranial pressure.

Reflux mechanisms involved in cardiac arrhythmias induced by hypothalamic stimulation

1978 ◽  
Vol 234 (2) ◽  
pp. H199-H209
Author(s):  
D. E. Evans ◽  
R. A. Gillis
Keyword(s):  
Blood Pressure ◽  
Cardiac Arrhythmias ◽  
Carotid Sinus ◽  
Vagal Afferents ◽  
Vagal Activity ◽  
Vagus Nerves ◽  
Stretch Receptors ◽  
Vagal Nerve Activity ◽  
Afferent Vagal ◽  
Stimulation Of

Electrical stimulation of widespread areas in the CNS has been shown to cause cardiac arrhythmias, which occur most frequently after cessation of stimulation. To determine the reflex and autonomic mechanism responsible for the poststimulation arrhythmias, we anesthetized cats with chloralose, and recorded arterial pressure, ECG, and cardiac vagal nerve activity. Stimulation of the hypothalamus consistently caused increases in blood pressure and heart rate during stimulation and caused arrhythmias, accompanied by vagal hyperactivity, immediately following stimulation. The arrhythmias were mediated solely by the vagus nerves because vagotomy or propantheline administration prevented them, whereas propranolol did not. Administration of either phentolamine or spinal cord transection prevented both the rise in blood pressure during stimulation and the poststimulation arrhythmias, but sectioning the carotid sinus and aortic depressor nerves had no preventative effect. However, when this denervation was combined with sectioning of vagal afferents, bursts of vagal activity (used as an index of cardiac rhythm disturbances) were prevented in three of six animals. Subsequent administration of phentolamine prevented the bursts in the remaining animals. It is concluded that poststimulation arrhythmias are elicited by the rise in blood pressure occurring during stimulation causing a sudden surge in parasympathetic outflow to the heart. The reflexogenic areas involved appear to be stretch receptors innervated by afferent vagal fibers.

The Central Hypotensive Action of Clonidine and BAY 1470 in Cats and Rats

1974 ◽  
Vol 48 (s2) ◽  
pp. 273s-276s ◽  
Author(s):  
L. Finch
Keyword(s):  
Blood Pressure ◽  
Cardiovascular Responses ◽  
Intraventricular Administration ◽  
Dopaminergic Receptors ◽  
Hypertensive Rats ◽  
Hypotensive Action ◽  
Cardiovascular Actions ◽  
Small Doses ◽  
6 Hydroxydopamine ◽  
Stimulation Of

1. Intraventricular clonidine and BAY 1470, administered in small doses to conscious renal hypertensive cats, produced a fall in mean blood pressure lasting for a period of 3 h. This fall in blood pressure was accompanied by a marked bradycardia. 2. Pretreatment with intraventricular phentolamine (0.3–6 μmol), piperoxan (0.18–0.74 μmol) or tolazoline (0.35–1 μmol) abolished the hypotensive effects of intraventricular clonidine (74 nmol), whereas pretreatment with haloperidol (2.6 μmol/kg, intraperitoneally), or desmethylimipramine (3.3 μmol/kg, intraperitoneally, or 1.7 μmol, intraventricularly) did not modify the cardiovascular responses to clonidine. 3. Emesis was observed 1 min after intraventricular administration of clonidine (18–112 nmol) or BAY 1470 (0.07–0.14 μmol), which always preceded the cardiovascular actions and was still observed after pretreatment with haloperidol, desmethylimipramine, phentolamine, piperoxan or tolazoline. 4. In conscious hypertensive rats clonidine (0.6 μmol/kg, intraperitoneally) produced a marked fall in blood pressure that was antagonized by centrally acting α-adrenoreceptor blocking agents but not modified by pretreatment with either 6-hydroxydopamine (three doses of 1 μmol, intraventricularly) or 5,6-dihydroxytryptamine (0.1 μmol). 5. It is concluded that the anti-hypertensive responses to clonidine are mediated via stimulation of central α-adrenoreceptors and are independent of central dopaminergic receptors, intact central serotonergic neurons and intact adrenergic uptake mechanisms.

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