Effect of carotid or aortic baroreceptor denervation on arterial pressure during hemorrhage in conscious dogs

2001 ◽  
Vol 280 (6) ◽  
pp. R1642-R1649 ◽  
Author(s):  
Terry N. Thrasher ◽  
Cassandra Shifflett
Keyword(s):  
Heart Rate ◽  
Standard Deviation ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Conscious Dogs ◽  
Carotid Baroreceptors ◽  
Intact Condition ◽  
Aortic Baroreceptors

We studied the effect of chronically denervating aortic baroreceptors (ABR; n = 6) or carotid baroreceptors (CBR; n= 7) on mean arterial pressure (MAP) and heart rate (HR) responses to hemorrhage in the dog. Neither denervation had a significant effect on basal MAP, the variability (standard deviation) of MAP, or resting HR. However, the breakpoint of MAP (defined as the volume of blood removed when MAP fell more than 10% below control and declined monotonically thereafter) was significantly reduced in dogs with only ABR functional (12.4 ± 1.4 ml/kg) compared with the volume in the intact condition (18.9 ± 1.8 ml/kg). In contrast, there was no difference in the breakpoint or the MAP at any time during hemorrhage in dogs with both CBR functional compared with their intact responses. In a different group of dogs ( n = 6), responses were determined with both CBR operating and again after unilateral denervation, leaving only one CBR (1CBR) functional. Basal MAP and the variability of MAP were not altered in dogs with only 1CBR functional, but the breakpoint (11.7 ± 1.4 ml/kg) during hemorrhage was significantly different compared with responses with two CBR (21.2 ± 2.3 ml/kg), and MAP fell to much lower levels. These results indicate that the CBR can compensate fully for loss of ABR during hemorrhage but not vice versa; and bilateral CBR inputs are required for normal responses to hemorrhage.

Sinovagal interaction in arterial pressure restoration after 10% hemorrhage

1979 ◽  
Vol 237 (3) ◽  
pp. R203-R209 ◽  
Author(s):  
H. Hosomi ◽  
K. Sagawa
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Pressure Measurement ◽  
Carotid Sinus ◽  
Open Loop ◽  
Baroreceptor Reflex ◽  
Conscious Dogs ◽  
Intact Condition ◽  
Reflex System ◽  
Additive Summation

The summation between the carotid sinus baroreceptor reflex system (CS system) and the vagally mediated reflex system (V system) was studied as they restore mean arterial pressure (MAP) after 10% quick hemorrhage in splenectomized conscious dogs chronically instrumented with catheters for pressure measurement and hemorrhage. The experiment was repeated under nerve-intact condition (intact), with cold block of the vagi ([V]), after carotid sinus denervation (CS), and CS plus [V] situations. MAP falls at 1.5 min after the hemorrhage were 7.2 in intact, 24.7 in [V], 36.0 in CS, and 67.6 in CS + [V] mmHg. When we calculated the open-loop gains of CS and V systems assuming a simply additive summation between them a self-contradiction occurred. To avoid this contradiction, it was necessary to assume that CS and V systems interact in a facilitatory manner. Mean open-loop gains calculated under this assumption were 1.64 for the CS system alone, 0.89 for the V system alone, and 6.59 for the interacting component between them. These intriguing results warrant further analysis of the summation between the two reflex systems.

Corticotropin-releasing factor, sauvagine, and urotensin I: effects on blood flow

1985 ◽  
Vol 249 (1) ◽  
pp. R85-R90
Author(s):  
H. J. Lenz ◽  
L. A. Fisher ◽  
W. W. Vale ◽  
M. R. Brown
Keyword(s):  
Heart Rate ◽  
Blood Flow ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Plasma Concentrations ◽  
Peripheral Circulation ◽  
Corticotropin Releasing Factor ◽  
Conscious Dogs ◽  
Central Administration ◽  
Mesenteric Blood Flow

Corticotropin-releasing factor (CRF), sauvagine (SVG), and urotensin I (UI) were tested for their effects on superior mesenteric blood flow in conscious dogs. Intravenous (iv) administration of CRF, SVG, and UI induced an immediate rise of mesenteric blood flow that was associated with a decrease in mean arterial pressure and an increase in heart rate. Intracerebroventricular (ICV) injection of SVG and UI, but not CRF, rapidly (within 5 min after injection) elicited a long (90 min) elevation of mesenteric blood flow. Central administration of these peptides induced a delayed rise in heart rate and slightly elevated mean arterial pressure. The finding that CRF given ICV did not increase mesenteric blood flow could not be explained by the release of vasoactive agents such as vasopressin, epinephrine, or norepinephrine. After injection of CRF, SVG, and UI, plasma concentrations of CRF-, SVG-, and UI-like immunoreactivity did not increase as determined by radioimmunoassay. These results indicate that SVG and UI, but not CRF, administered ICV produce a long increase of mesenteric blood flow in conscious dogs. Because iv SVG and UI decrease mean arterial pressure and ICV SVG and UI increase mean arterial pressure and do not cause an increase in SVG- and UI-like immunoreactivity in the peripheral circulation, it is proposed that SVG and UI injected into the third cerebral ventricle act within the central nervous system to increase superior mesenteric blood flow in the dog.

Baroreflex mechanisms buffering alpha-adrenergic agonists in conscious dogs

1987 ◽  
Vol 253 (4) ◽  
pp. H728-H736
Author(s):  
A. M. Fujii ◽  
S. F. Vatner
Keyword(s):  
Heart Rate ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Total Peripheral Resistance ◽  
Adrenergic Receptor ◽  
Peripheral Resistance ◽  
Conscious Dogs ◽  
Receptor Blockade ◽  
Receptor Agonists ◽  
Alpha Adrenergic Receptor

To determine the relative importance of the mechanisms utilized by the arterial baroreflex in buffering the pressor and vasoconstrictor responses to alpha-adrenergic receptor agonists, we studied responses to norepinephrine and phenylephrine in conscious dogs. The dogs were studied 2-8 wk after instrumentation with aortic catheters and aortic electromagnetic flow probes to measure arterial pressure and cardiac output. Total peripheral resistance was calculated on-line by a digital computer. The dogs were studied after beta-adrenergic receptor blockade (propranolol 1.0 mg/kg) to eliminate the complicating inotropic effects of the agonists studied. Norepinephrine (0.2 microgram/kg bolus) increased mean arterial pressure by 30 +/- 3 mmHg, total peripheral resistance by 51 +/- 4 mmHg . l-1 . min-1, and decreased heart rate by 26 +/- 3 beats/min. After arterial baroreceptor denervation, norepinephrine increased mean arterial pressure by 69 +/- 8 mmHg, total peripheral resistance by 48 +/- 6 mmHg . l-1 . min-1, and heart rate did not change. After ganglionic blockade (hexamethonium 40 mg/kg), norepinephrine increased mean arterial pressure by 76 +/- 3 mmHg, total peripheral resistance by 47 +/- 4 mmHg X l-1 X min-1, and heart rate did not change. Only after elimination of the buffering by heart rate by use of cholinergic receptor blockade (atropine 0.1 mg/kg) or ventricular pacing could buffering of the vasoconstrictor responses to alpha-adrenergic receptor agonists be demonstrated. Thus in conscious dogs the primary mechanism for buffering increases in arterial pressure induced by alpha-adrenergic receptor agonists is compensatory changes in heart rate and cardiac output with little buffering of total peripheral resistance.

Role of the vasoconstrictor and antidiuretic activities of vasopressin in inhibition of renin secretion in conscious dogs

1986 ◽  
Vol 250 (1) ◽  
pp. F92-F96 ◽  
Author(s):  
J. Schwartz ◽  
I. A. Reid
Keyword(s):  
Heart Rate ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Plasma Renin Activity ◽  
Arginine Vasopressin ◽  
Plasma Renin ◽  
Renin Secretion ◽  
Conscious Dogs ◽  
Specific Antagonist

The nature of the activity of vasopressin that is responsible for the inhibition of renin secretion was studied in normally hydrated conscious dogs using intravenous infusions of vasopressin and analogues of vasopressin with selective antidiuretic and vasoconstrictor activity. Vasopressin (1.0 ng . kg-1 . min-1) increased mean arterial pressure (MAP) from 106 +/- 2 to 115 +/- 3 mmHg (P less than 0.05) and decreased heart rate (HR) from 81 +/- 6 to 56 +/- 5 beats/min (P less than 0.001). Plasma renin activity (PRA) decreased from 4.4 +/- 1.1 to 2.4 +/- 0.8 ng . ml-1 . 3 h-1 (P less than 0.05). A specific antagonist of the vasoconstrictor activity of vasopressin, d(CH2)5MeTyrAVP (10 micrograms/kg), completely blocked the cardiovascular and renin responses to vasopressin. A selective vasoconstrictor agonist, 2-phenylalanine-8-ornithine oxytocin (1.0 ng . kg-1 . min-1), increased MAP from 112 +/- 4 to 128 +/- 6 mmHg (P less than 0.001) and decreased HR from 69 +/- 3 to 47 +/- 4 beats/min (P less than 0.001). PRA decreased from 5.5 +/- 1.1 to 2.7 +/- 0.2 ng . ml-1 X 3 h-1 (P less than 0.001). In contrast, a selective antidiuretic agonist, 1-deamino-8-D-arginine vasopressin (1.0 ng . kg-1 . min-1) did not alter PRA, MAP, or HR. These results demonstrate that the acute inhibition of renin secretion by vasopressin in normally hydrated conscious dogs is due to vasoconstrictor rather than antidiuretic activity.

Chronic Lability of Arterial Pressure in the Rat Does Not Evolve into Hypertension

1980 ◽  
Vol 59 (s6) ◽  
pp. 405s-407s ◽  
Author(s):  
W. T. Talman ◽  
D. R. Alonso ◽  
D. J. Reis
Keyword(s):  
Heart Rate ◽  
Standard Deviation ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Histopathological Changes ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Electrolytic Lesions ◽  
The Mean ◽  
Catecholamine Neurons

1. In rats, electrolytic lesions of the A2 group of catecholamine neurons result in lability of arterial pressure without hypertension. 2. To establish whether labile arterial pressure, when chronic, will lead to fixed hypertension, we placed lesions in the A2 area of adult male Sprague-Dawley rats and measured mean arterial pressure, heart rate and their variability (expressed as the standard deviation) 11 months later. Controls were age-matched, unoperated or sham-operated rats. 3. In rats with A2 lesions: (a) the mean arterial pressure was lower (103 ± 7.5 mmHg; n = 6; P<0.05) than in sham-operated (123 ± 4.7 mmHg; n = 4) or unoperated (120 ± 3.1 mmHg; n = 9) controls; (b) the standard deviation of mean arterial pressure was higher (16 ± 1.8 mmHg; P<0.001) than in sham-operated (5 ± 0.7 mmHg) or unoperated controls (7 ± 0.6 mmHg); (c) the mean and standard deviation of heart rate did not differ between groups. No histopathological changes were detected in the A2 group. 4. Chronic lability of arterial pressure does not evolve into sustained hypertension nor does it induce systemic lesions.

Dual adrenergic control of renin during nonhypotensive hemorrhage in conscious dogs

1991 ◽  
Vol 260 (6) ◽  
pp. E910-E919 ◽  
Author(s):  
M. L. Blair ◽  
H. Hisa ◽  
C. D. Sladek ◽  
K. J. Radke ◽  
F. M. Gengo
Keyword(s):  
Heart Rate ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Plasma Renin Activity ◽  
Plasma Renin ◽  
Conscious Dogs ◽  
Beta Adrenoceptors ◽  
Alpha Adrenoceptors ◽  
Adrenergic Control ◽  
Arterial Plasma

These experiments evaluated the contribution of renal alpha-adrenoceptors, renal beta-adrenoceptors, and extrarenal beta-adrenoceptors to increased plasma renin activity (PRA) during nonhypotensive hemorrhage in conscious dogs. Blood withdrawal at a rate of 16 g/kg body wt over 20 min increased PRA to nearly threefold control levels without decreasing mean arterial pressure. The PRA response to hemorrhage was reduced to a greater extent by simultaneous direct renal arterial (ira) infusion of phenoxybenzamine and propranolol than by propranolol alone. Phenoxybenzamine infusion ira did not block alpha-adrenoceptors located outside of the kidney. The PRA and heart rate responses to hemorrhage were both significantly reduced when propranolol was infused either ira or intravenously (iv) at a rate of 2 micrograms.kg-1.min-1 for 20 min followed by 0.5 microgram.kg-1.min-1 continuous infusion. Propranolol infusion at a lower rate (0.5 microgram.kg-1.min-1 for 20 min followed by 0.12 microgram.kg-1.min-1) had little effect on the magnitude of increase in PRA when infused either iv or ira. The calculated renal arterial plasma propranolol concentration was at least fivefold higher or more during ira than during iv propranolol infusion at each rate and was approximately the same during ira infusion at the lower rate (17.5 +/- 0.7 ng/ml) as during iv infusion at the higher rate (16.7 +/- 2.4 ng/ml). These data indicate that the hemorrhage-induced increase in PRA is mediated by renal alpha-adrenoceptors and extrarenal beta-adrenoceptors, whereas renal beta-adrenoceptors appear to play little or no role.

V1 vs. combined V1+V2 vasopressin blockade after hemorrhage in conscious dogs

1988 ◽  
Vol 255 (6) ◽  
pp. H1325-H1329
Author(s):  
J. F. Liard
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Peripheral Resistance ◽  
Electromagnetic Flowmeter ◽  
Conscious Dogs ◽  
Hemodynamic Changes ◽  
Significant Difference ◽  
V2 Antagonist

We examined the hypothesis that V2-like receptors might contribute to the hemodynamic response seen after blockade of the vasoconstrictor (V1) effect of arginine vasopressin (AVP) in nonhypotensive hemorrhage. Seven chronically instrumented dogs were bled 15 ml/kg within 15 min on two different days, at least 3 days apart, and then injected either with the V1 antagonist [1-(beta-mercapto-beta,beta-cyclopentamethylenepropionic acid)2-(O-methyl)tyrosine]AVP [d(CH2)5Tyr(Me)AVP, 10 micrograms/kg] or with the combined V1+V2 antagonist [1(beta-mercapto-beta,beta-cyclopentamethylenepropionic acid)2-(O-ethyl)-D-tyrosine)4-valine]AVP [d(CH2)5-D-Tyr-(Et)VAVP (10 micrograms/kg)]. Mean arterial pressure, heart rate, and cardiac output (electromagnetic flowmeter) were measured before as well as after hemorrhage and for 10 min after antagonist administration. Both antagonists given after hemorrhage significantly decreased mean arterial pressure as well as total peripheral resistance and increased cardiac output. The V1 antagonist also increased heart rate significantly. No significant hemodynamic changes were measured in another group of six dogs in the absence of antagonist treatment. Although hemodynamic changes tended to be greater with the V1 antagonist than with the combined V1+V2 antagonist, a significant difference between the two analogues was established only for heart rate. These results indicate that in hemorrhage interaction with V2-like receptors plays only a modest role in the hemodynamic changes after V1 blockade in conscious dogs, contrary to what was found in dehydration.

Blood Pressure Variability in Man: Its Relation to High Blood Pressure, Age and Baroreflex Sensitivity

1980 ◽  
Vol 59 (s6) ◽  
pp. 401s-404s ◽  
Author(s):  
G. Mancia ◽  
A. Ferrari ◽  
L. Gregorini ◽  
G. Parati ◽  
G. Pomidossi ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Standard Deviation ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Blood Pressure Variability ◽  
Baroreflex Sensitivity ◽  
Variation Coefficient ◽  
Arterial Blood ◽  
Normotensive Subjects

1. Intra-arterial blood pressure and heart rate were recorded for 24 h in ambulant hospitalized patients of variable age who had normal blood pressure or essential hypertension. Mean 24 h values, standard deviations and variation coefficient were obtained as the averages of values separately analysed for 48 consecutive half-hour periods. 2. In older subjects standard deviation and variation coefficient for mean arterial pressure were greater than in younger subjects with similar pressure values, whereas standard deviation and variation coefficient for heart rate were smaller. 3. In hypertensive subjects standard deviation for mean arterial pressure was greater than in normotensive subjects of similar ages, but this was not the case for variation coefficient, which was slightly smaller in the former than in the latter group. Normotensive and hypertensive subjects showed no difference in standard deviation and variation coefficient for heart rate. 4. In both normotensive and hypertensive subjects standard deviation and even more so variation coefficient were slightly or not related to arterial baroreflex sensitivity as measured by various methods (phenylephrine, neck suction etc.). 5. It is concluded that blood pressure variability increases and heart rate variability decreases with age, but that changes in variability are not so obvious in hypertension. Also, differences in variability among subjects are only marginally explained by differences in baroreflex function.

scholarly journals Effect of Dexmedetomidine on Perioperative Stress Response and Immune Function in Patients With Tumors

2020 ◽  
Vol 19 ◽  
pp. 153303382097754
Author(s):  
Lihong Zheng ◽  
Juan Zhao ◽  
Likun Zheng ◽  
Shuangfeng Jing ◽  
Xiaoting Wang
Keyword(s):  
Heart Rate ◽  
Stress Response ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Immune Function ◽  
Spontaneous Respiration ◽  
General Anesthetics ◽  
Ifn Γ ◽  
Group D ◽  
Perioperative Stress

Objective: This study aims to investigate the effect of dexmedetomidine on perioperative stress response and immune function in patients with tumors. Methods: Sixty patients who underwent selective radical gastrectomy for cancer were randomly divided into 3 groups: remifentanil group (group R), dexmedetomidine group (group D), and sufentanil group (group S). Remifentanil, dexmedetomidine, and sufentanil were used as general anesthetics. Endotracheal intubation and mechanical ventilation were performed after the spontaneous respiration disappeared. Then, the data were recorded, and blood samples were collected at all time points. Results: The heart rate significantly increased ( P < 0.05) at T1 in group S, and both heart rate and mean arterial pressure significantly increased ( P < 0.05) in group R when compared to group D. The heart rate significantly increased ( P < 0.05) at T2 in group S and group R. Furthermore, the heart rate significantly increased ( P < 0.05) at T3 and T4 in group S and group R. Intra-group comparison: The heart rate at T1–T4 and mean arterial pressure at T1–T4 significantly increased ( P < 0.05) in group S, and the heart rate at T1 and T4, and mean arterial pressure at T2–T4 significantly increased ( P < 0.05) in group R when compared to T0. The serum IL-6, IFN-γ, and β-EP significantly increased ( P < 0.05) at T0’ in group S and group R when compared to group D. Blood glucose, and serum IL-10, IFN-γ, and β-EP significantly increased ( P < 0.05), while IL-18 significantly decreased ( P < 0.05) at T1’ in group S and group R. Conclusion: Continuous infusion of dexmedetomidine in combination with the inhalation of sevoflurane is superior to sevoflurane + remifentanil or sufentanil in patients undergoing tumor surgery.

scholarly journals Preclinical Pharmacology in the Rhesus Monkey of CW 1759-50, a New Ultra-short Acting Nondepolarizing Neuromuscular Blocking Agent, Degraded and Antagonized by L-Cysteine

2018 ◽  
Vol 129 (5) ◽  
pp. 970-988 ◽  
Author(s):  
John J. Savarese ◽  
Hiroshi Sunaga ◽  
Jeff D. McGilvra ◽  
Matthew R. Belmont ◽  
Matthew T. Murrell ◽  
...  
Keyword(s):  
Heart Rate ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Neuromuscular Blockade ◽  
Blocking Agent ◽  
Neuromuscular Blocking ◽  
Neuromuscular Blocking Agent ◽  
Duration Of Action ◽  
Short Acting ◽  
Circulatory Effects

Abstract Editor’s Perspective What We Already Know about This Topic What This Article Tells Us That Is New Background Structure–activity studies were performed to identify a new neuromuscular blocking agent retaining the ultra-short acting characteristics of gantacurium, including degradation and reversal by l-cysteine, but lacking its histaminoid properties in man. CW 1759-50 has emerged from this program. Methods Adduction of CW 1759-50 with l-cysteine was studied by high-performance liquid chromatography and mass spectrometry. Institutional Animal Care and Use Committee–approved comparisons of CW 1759-50 to gantacurium were performed in rhesus monkeys. ED95 for neuromuscular blockade was established. Spontaneous recovery was compared to reversal by l-cysteine in paired studies of boluses or infusions. In addition, changes in mean arterial pressure and heart rate after very large doses of 15 to 60 × ED95 were compared. Results The half-time of adduction of l-cysteine to CW 1759-50 in vitro was 2.3 min. The ED95 of CW 1759-50 was 0.069 ± 0.02 mg/kg; ED95 of gantacurium was 0.081 ± 0.05 mg/kg (P = 0.006). Duration of action (recovery to 95% twitch height after 98 to 99% blockade) was as follows: CW 1759-50, 8.2 ± 1.5 min; and gantacurium, 7.4 ± 1.9 min; (n = 8 and 9, P = 0.355). Administration of l-cysteine (30 mg/kg) shortened recovery (i.e., induced reversal) from CW 1759-50 after boluses or infusions (P always less than 0.0001). Recovery intervals (5 to 95% twitch) ranged from 6.1 to 6.7 min (and did not differ significantly) after boluses of 0.10 to 0.50 mg/kg, as well as control infusions (P = 0.426 by analysis of variance). Dose ratios comparing changes of 30% in mean arterial pressure or heart rate to ED95 for neuromuscular blockade (ED 30% Δ [mean arterial pressure or heart rate]/ED95) were higher for CW 1759-50 than for gantacurium. Conclusions CW 1759-50, similar to gantacurium, is an ultra-short acting neuromuscular blocking agent, antagonized by l-cysteine, in the monkey. The circulatory effects, however, are much reduced in comparison with gantacurium, suggesting a trial in humans.

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