Responses of on and off cells in the rostral ventral medulla to stimulation of vagal afferents and changes in mean arterial blood pressure in intact and cardiopulmonary deafferented rats

Pain ◽  
1995 ◽  
Vol 62 (1) ◽  
pp. 19-38 ◽  
Author(s):  
C. L. Thurston ◽  
A. Randich
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Mean Arterial Blood Pressure ◽  
Vagal Afferents ◽  
Arterial Blood ◽  
Ventral Medulla ◽  
On And Off Cells ◽  
Stimulation Of

Interactions between brain acetylcholine and prostaglandins in control of vasopressin release

1991 ◽  
Vol 261 (2) ◽  
pp. R420-R426
Author(s):  
M. Inoue ◽  
J. T. Crofton ◽  
L. Share
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Arterial Blood Pressure ◽  
Mean Arterial Blood Pressure ◽  
Cardiovascular Responses ◽  
Vasopressin Release ◽  
Arterial Blood ◽  
Plasma Vasopressin ◽  
Vasopressin Secretion ◽  
Stimulation Of

We have examined in conscious rats the interaction between centrally acting prostanoids and acetylcholine in the stimulation of vasopressin secretion. The intracerebroventricular (icv) administration of carbachol (25 ng) resulted in marked transient increases in the plasma vasopressin concentration and mean arterial blood pressure and a transient reduction in heart rate. Central cyclooxygenase blockade by pretreatment icv with either meclofenamate (100 micrograms) or indomethacin (100 micrograms) virtually completely blocked these responses. Prostaglandin (PG) D2 (20 micrograms icv) caused transient increases in the plasma vasopressin concentration (much smaller than after carbachol) and heart rate, whereas mean arterial blood pressure rose gradually during the 15-min course of the experiment. Pretreatment with the muscarinic antagonist atropine (10 micrograms icv) decreased the peak vasopressin response to icv PGD2 by approximately one-third but had no effect on the cardiovascular responses. We conclude that the stimulation of vasopressin release by centrally acting acetylcholine is dependent on increased prostanoid biosynthesis. On the other hand, stimulation of vasopressin release by icv PGD2 is partially dependent on activation of a cholinergic pathway.

Bradykinin in reflex cardiovascular responses to static muscular contraction

1986 ◽  
Vol 61 (1) ◽  
pp. 271-279 ◽  
Author(s):  
C. L. Stebbins ◽  
J. C. Longhurst
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Mean Arterial Blood Pressure ◽  
Cardiovascular Response ◽  
Time Derivative ◽  
Cardiovascular Responses ◽  
Carboxypeptidase B ◽  
Arterial Blood ◽  
Static Contraction ◽  
Stimulation Of

We examined the contribution of bradykinin to the reflex hemodynamic response evoked by static contraction of the hindlimb of anesthetized cats. During electrical stimulation of ventral roots L7 and S1, we compared the cardiovascular responses to hindlimb contraction before and after the following interventions: inhibition of converting enzyme (kininase II) with captopril (3–4 mg/kg, n = 6); inhibition of kallikrein activity with aprotinin (Trasylol, 20,000–30,000 KIU/kg, n = 8); and injection of carboxypeptidase B (500–750 U/kg, n = 7). Treatment with captopril augmented the rise in mean arterial blood pressure and maximal time derivative of pressure (dP/dt) caused by static contraction from 21 +/- 3 to 39 +/- 7 mmHg and 1,405 +/- 362 to 2,285 +/- 564 mmHg/s, respectively. Aprotinin attenuated the contraction-induced rise in mean arterial blood pressure (28 +/- 4 to 9 +/- 2 mmHg) and maximal dP/dt (1,284 +/- 261 to 469 +/- 158 mmHg/s). Carboxypeptidase B reduced the cardiovascular response to static contraction. Thus the mean arterial blood pressure response was decreased from 36 +/- 12 to 24 +/- 11 mmHg, maximal dP/dt from 1,618 +/- 652 to 957 +/- 392 mmHg/s, and heart rate from 12 +/- 2 to 7 +/- 1 beats/min. These data suggest that stimulation of muscle afferents by bradykinin contributes to a portion of the reflex cardiovascular response to static contraction.

Cardiovascular effects of atrial extracts in anesthetized rats

1984 ◽  
Vol 62 (7) ◽  
pp. 819-826 ◽  
Author(s):  
Uwe Ackermann ◽  
Terumi G. Irizawa ◽  
Susan Milojevic ◽  
Harald Sonnenberg
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Mean Arterial Blood Pressure ◽  
Cardiovascular Effects ◽  
Hypotensive Effect ◽  
Vagal Afferents ◽  
Sprague Dawley ◽  
Direct Stimulation ◽  
Arterial Blood ◽  
Cardiopulmonary Receptors

Tissue extracts derived from atria or ventricles of Sprague–Dawley rats were injected into Inactin-anesthetized assay rats. Compared with ventricular extracts, atrial extracts produced a 20 mmHg (1 mmHg = 133.322 Pa) fall in mean arterial blood pressure. This fall resulted from failure to increase cardiac output in compensation for peripheral vasodilation. Two factors were responsible: depression of heart rate (by 25 beats/min) and failure to increase cardiac performance. The time patterns and magnitudes of changes in cardiovascular parameters after cardiac extracts were not changed by prior atropinization. However, assay rats that were vagotomized showed no cardiac slowing after atrial extract and showed a significantly smaller decrease in mean arterial blood pressure than did sham-vagotomized or intact rats. Another group of assay rats was vagotomized as well as carotid-sinus-denervated before extract injection. In these rats the degree of hypotension caused by atrial extract was significantly greater than that observed after vagotomy alone and was not significantly different from that observed in rats with intact innervation. The results suggest that the hypotension that is caused by atrial extract, but not by ventricular extracts, results in part from the reflex effects of direct stimulation of chemosensitive cardiopulmonary receptors with vagal afferents and partly from the reflex effects of baroreceptor unloading. Ventricular extract had no hypotensive effect in any group of assay rats.

Effects of vagal afferent stimulation on ON and OFF cells in the rostroventral medulla: relationships to nociception and arterial blood pressure

1992 ◽  
Vol 67 (1) ◽  
pp. 180-196 ◽  
Author(s):  
C. L. Thurston ◽  
A. Randich
Keyword(s):  
Blood Pressure ◽  
Firing Rate ◽  
Arterial Blood Pressure ◽  
Neural Activity ◽  
Pressor Response ◽  
Vagal Afferents ◽  
Tail Flick ◽  
Threshold Intensity ◽  
Arterial Blood ◽  
On And Off Cells

1. Extracellular recordings of 125 neurons in the rostroventral medulla (RVM) were performed in 35 rats that were maintained in a light plane of anesthesia with methohexital. The neurons were classified as ON, OFF, or NEUTRAL cells, depending on their response to noxious heat applied to the tail. ON cells showed an increase in firing rate just before the tail flick (TF), OFF cells showed a decrease in firing rate just before the TF, and NEUTRAL cells showed no correlation between neural activity and the TF. 2. The effects of electrical stimulation of cervical vagal afferents (VAS) on 1) the activity of ON, OFF, and NEUTRAL cells, 2) TF latency, and 3) arterial blood pressure (ABP) were determined at intensities less than or equal to the intensity of VAS necessary to inhibit the TF reflex to a cutoff latency of 10 s. VAS excited 70.8% of the ON cells and inhibited 77.8% of the OFF cells at greater intensities, including intensities that inhibited the TF. However, 55.6% of the OFF cells inhibited by the threshold intensity of VAS to inhibit the TF reflex were excited by lesser intensities of VAS (less than 50% of the intensity that inhibited the TF) that facilitated the TF reflex, and 14.3% of the ON cells excited by the threshold intensity of VAS to inhibit the TF reflex were inhibited by lesser intensities of VAS. VAS had mixed effects on NEUTRAL cells. VAS excited 23.7% and inhibited 10.5% of the NEUTRAL cells that had somatic receptive fields. VAS excited 12.9% and inhibited 9.7% of the NEUTRAL cells that had no identified somatic receptive field. The excitation of ON cells and inhibition of OFF cells produced by VAS at the intensity to inhibit the TF are opposite to predicted outcomes on the basis of current theories on the function of ON and OFF cells in nociception. 3. VAS produced a depressor response at intensities ranging from approximately 50% to 100% of the VAS intensity necessary to inhibit the TF reflex to the cutoff latency. At lesser intensities, VAS occasionally produced a small pressor response. 4. ON and OFF cells generally showed marked fluctuations in background activity, shifting between active and inactive states. The levels of background neural activity were correlated with mean ABP. ABP levels were lower when ON cells were active and OFF cells were inactive than when ON cells were inactive and OFF cells active.(ABSTRACT TRUNCATED AT 250 WORDS)

Role of Vagal Afferents and the Rostral Ventral Medulla in Intravenous Serotonin-Induced Changes in Nociception and Arterial Blood Pressure

1999 ◽  
Vol 67 (5) ◽  
pp. 753-767 ◽  
Author(s):  
Cindy L Thurston–Stanfield ◽  
James T Ranieri ◽  
Raviprasad Vallabhapurapu ◽  
Dorcas Barnes–Noble
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Vagal Afferents ◽  
Arterial Blood ◽  
Ventral Medulla ◽  
Induced Changes

Liberal vs. conservative vasopressor use to maintain mean arterial blood pressure during resuscitation of septic shock: an observational study

2007 ◽  
Vol 34 (1) ◽  
pp. 157-162 ◽  
Author(s):  
Sanjay Subramanian ◽  
Murat Yilmaz ◽  
Ahmer Rehman ◽  
Rolf D. Hubmayr ◽  
Bekele Afessa ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Septic Shock ◽  
Observational Study ◽  
Arterial Blood Pressure ◽  
Mean Arterial Blood Pressure ◽  
Arterial Blood ◽  
Vasopressor Use

Cerebral hemorrhage and edema following brain biopsy in rats: significance of mean arterial blood pressure

2000 ◽  
Vol 92 (1) ◽  
pp. 100-107 ◽  
Author(s):  
Helene Benveniste ◽  
Katie R. Kim ◽  
Laurence W. Hedlund ◽  
John W. Kim ◽  
Allan H. Friedman
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Mean Arterial Blood Pressure ◽  
Neurosurgical Procedures ◽  
Shr Rats ◽  
Mr Microscopy ◽  
Content Type ◽  
Wky Rats ◽  
Arterial Blood ◽  
Fine Print

Object. It is taken for granted that patients with hypertension are at greater risk for intracerebral hemorrhage during neurosurgical procedures than patients with normal blood pressure. The anesthesiologist, therefore, maintains mean arterial blood pressure (MABP) near the lower end of the autoregulation curve, which in patients with preexisting hypertension can be as high as 110 to 130 mm Hg. Whether patients with long-standing hypertension experience more hemorrhage than normotensive patients after brain surgery if their blood pressure is maintained at the presurgical hypertensive level is currently unknown. The authors tested this hypothesis experimentally in a rodent model.Methods. Hemorrhage and edema in the brain after needle biopsy was measured in vivo by using three-dimensional magnetic resonance (MR) microscopy in the following groups: WKY rats, acutely hypertensive WKY rats, spontaneously hypertensive rats (SHR strain), and SHR rats treated with either sodium nitroprusside or nicardipine. Group differences were compared using Tukey's studentized range test followed by individual pairwise comparisons of groups and adjusted for multiple comparisons.There were no differences in PaCO2, pH, and body temperature among the groups. The findings in this study indicated that only acutely hypertensive WKY rats had larger volumes of hemorrhage. Chronically hypertensive SHR rats with MABPs of 130 mm Hg did not have larger hemorrhages than normotensive rats. There were no differences in edema volumes among groups.Conclusions. The brains of SHR rats with elevated systemic MABPs are probably protected against excessive hemorrhage during surgery because of greater resistance in the larger cerebral arteries and, thus, reduced cerebral intravascular pressures.

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