The Effects of Halothane on Cardiovascular Responses in the Neuraxis of Cats 

1995 ◽  
Vol 82 (1) ◽  
pp. 153-165 ◽  
Author(s):  
Neil E. Farber ◽  
Enric Samso ◽  
John P. Kampine ◽  
William T. Schmeling
Keyword(s):  
Arterial Pressure ◽  
Reticular Formation ◽  
Cardiovascular Responses ◽  
Artery Occlusion ◽  
Carotid Artery Occlusion ◽  
Implanted Electrodes ◽  
Bilateral Carotid Occlusion ◽  
Pressor Responses ◽  
Bilateral Carotid ◽  
Cns Stimulation

Background This study examined the effects of halothane on arterial pressure after central nervous system (CNS) pressor site stimulation in anesthetized cats, cats rendered unconscious by midcollicular transection, and conscious cats. Methods Two anesthetized groups and two nonanesthetized groups were used. Cats were anesthetized with either alpha-chloralose and urethane or pentobarbital. Nonanesthetized groups were cats with midcollicular transections or conscious cats with chronically implanted electrodes. Stimulating electrodes were placed into vasomotor areas of the hypothalamus (HYP), reticular formation (RF), and medulla, and arterial pressure responses to increasing stimulus currents were examined during different halothane concentrations. Two groups of cats were also anesthetized with either pentobarbital or urethane and underwent bilateral carotid artery occlusion. Results Stimulation at each CNS site produced increases in arterial pressure and heart rate. Halothane attenuated pressor responses evoked by stimulation of all loci in all groups of cats. The inhibition by halothane on these cardiovascular responses was greatest at HYP and RF sites, while the medulla was more resistant to the effects of halothane in the anesthetized animals. Midcollicular transection decreased this medullary resistance. The inhibition of pressor responses by halothane was also greater in pentobarbital-than chloralose urethane-anesthetized animals. In contrast, pressor responses elicited by bilateral carotid occlusion were attenuated by halothane similarly in both anesthetic groups. Reticular formation stimulation in conscious animals resulted in "altering responses" in addition to pressor effects, both of which were attenuated by halothane. Conclusions Modulation of CNS cardiovascular control centers contribute to halothane-induced hemodynamic alterations. Baseline anesthesia, CNS stimulation site, and the suprabulbar system influence the effects of halothane.

Systemic responses to carotid occlusion in the anesthetized rat

1992 ◽  
Vol 72 (4) ◽  
pp. 1247-1254 ◽  
Author(s):  
J. M. Lash ◽  
E. Haase ◽  
A. A. Shoukas
Keyword(s):  
Pressor Response ◽  
Cardiovascular Responses ◽  
Artery Occlusion ◽  
Carotid Artery Occlusion ◽  
Carotid Occlusion ◽  
Male Rats ◽  
Bilateral Carotid Occlusion ◽  
Bilateral Common Carotid Artery ◽  
Bilateral Carotid ◽  
Common Carotid Artery Occlusion

We evaluated the effects of four standard anesthetization regimens on the systemic cardiovascular responses to bilateral common carotid artery occlusion in 28 adult male rats. Rats were randomly assigned to anesthesia groups: thiopental sodium (PT; 100 mg/kg ip), alpha-chloralose (CH; 100 mg/kg iv), ketamine hydrochloride plus acepromazine (KA; 135 mg/kg and 1.5 mg/kg sc), and pentobarbital sodium (PB; 50 mg/kg ip). PT and PB animals had similar baseline heart rates (HR; 333 and 345 beats/min, respectively) and arterial pressures (MAP; 126 and 118 mmHg, respectively), whereas both were lower in CH and KA (314 and 288 beats/min, 92 and 85 mmHg). During bilateral carotid occlusion, PT demonstrated the largest change in MAP (dMAP; +27 mmHg) but the smallest change in HR (dHR; +8 beats/min). CH and PB demonstrated similar dHR (+24 and +16 beats/min) and dMAP (+20 and +19 mmHg). KA demonstrated a significant dHR (+14 beats/min), but the average dMAP was not statistically significant (+3 mmHg). Therefore, carotid occlusion in rats anesthetized with PT, PB, or CH consistently elicits a systemic arterial pressor response comparable with that reported for conscious animals. When the magnitude and stability of baseline HR and MAP are also considered, PT and PB anesthetization seem to be the most reliable for evaluation of the carotid occlusion pressor response in rats.

Vasopressin potentiation of catecholamine actions in dog, rat, cat, and rat aortic strip

1965 ◽  
Vol 208 (4) ◽  
pp. 754-762 ◽  
Author(s):  
Herbert J. Bartelstone ◽  
Peter A. Nasmyth
Keyword(s):  
Artery Occlusion ◽  
Carotid Artery Occlusion ◽  
Aortic Strip ◽  
Pressor Responses ◽  
Pithed Rats ◽  
Bilateral Carotid ◽  
Anesthetized Dogs ◽  
Bilateral Carotid Artery Occlusion ◽  
Physiological Dose ◽  
Bilateral Carotid Artery

This study was undertaken to determine whether arginine vasopressin, infused or injected in doses within known physiological ranges, can alter pressor responses to injected or endogenously liberated catecholamines. In 8 pentobarbital-anesthetized dogs, 14 pithed rats, and 7 spinal cats, the pressor responses to catecholamine injections were definitely potentiated by administration of nonpressor doses of vasopressin. In eight dogs anesthetized with N2O-O2, readily reproducible pressor responses to bilateral carotid artery occlusion were subsequently potentiated by infusions of vasopressin. Vasopressin also potentiated both isometric and isotonic responses of 37 rat aortic strip preparations to norepinephrine or epinephrine added to the Krebs-bicarbonate bath. Vasopressin, in physiological dose ranges, potentiates pressor responses to catecholamines by a direct rather than a central action. Endogenously liberated vasopressin may play a role in the responsiveness of vascular smooth muscle to endogenously liberated catecholamines in dog, rat, and cat.

Adrenergic and pressure-dependent vascular regulation in sedentary and trained rats

1993 ◽  
Vol 265 (4) ◽  
pp. H1064-H1073 ◽  
Author(s):  
J. M. Lash ◽  
T. Reilly ◽  
M. Thomas ◽  
H. G. Bohlen
Keyword(s):  
Steady State ◽  
Exercise Training ◽  
Aerobic Exercise ◽  
Vascular Resistance ◽  
Artery Occlusion ◽  
Carotid Artery Occlusion ◽  
Aerobic Exercise Training ◽  
Vascular Regulation ◽  
Pressor Responses ◽  
Bilateral Carotid

In this study, we determined if aerobic exercise training alters adrenergic or pressure-dependent vascular regulation in the rat hindlimb or intestine. Pressor responses to bilateral carotid artery occlusion and systemic phenylephrine (PE) infusion were not altered by training. During occlusion, peak and steady-state changes in hindlimb vascular resistance (HLR) were significantly greater in trained (24 and 13%) than in sedentary (8 and -3%) rats; a similar trend existed for intestinal vascular resistance (IR). The pressure-dependent contribution was consistent between groups (HLR: peak 55-85%, steady state 25-45%; IR: peak and steady state 40-65%). During PE infusion, increases in IR and HLR were similar between groups. The increase in HLR was substantially pressure dependent in both groups (approximately 50% at highest dose) as was the change in IR in trained rats. However, the IR response to PE was not pressure dependent in sedentary rats. The direct effects of PE were similar between sedentary and trained rats in the hindlimb but were suppressed in the intestine of trained rats compared with sedentary rats. Therefore, aerobic exercise training altered adrenergic and pressure-dependent vasoregulatory mechanisms in both skeletal muscle and intestinal tissues.

Stimulatory and inhibitory reflexes from somatic receptors: effect on renin release

1984 ◽  
Vol 246 (6) ◽  
pp. R1005-R1010 ◽  
Author(s):  
H. Holdaas ◽  
G. F. DiBona
Keyword(s):  
Sciatic Nerve ◽  
Arterial Pressure ◽  
Nerve Stimulation ◽  
Cardiovascular Responses ◽  
Renin Release ◽  
Renal Nerves ◽  
Pressor Responses ◽  
Bilateral Carotid ◽  
Sciatic Nerve Stimulation ◽  
Stimulation Of

The effect of stimulation of skeletal muscle somatic receptor afferents on renal function and renin release was examined in anesthetized dogs (bilateral carotid occlusion and vagotomy) with controlled renal arterial pressure. Afferent sciatic nerve stimulation (20–40 V, 1 ms) at 0.6–1.5 Hz elicited cardiovascular pressor responses, renal vasoconstriction, and stimulation of renin release, whereas at 0.3–0.8 Hz cardiovascular depressor responses and inhibition of renin release without changes in renal blood flow were found. Renal denervation abolished the inhibition of renin release but not the cardiovascular depressor response to afferent sciatic nerve stimulation at 20–40 V, 1 ms, and 0.3–0.8 Hz. Peripheral somatic afferent nerves contain fibers which, when appropriately stimulated, produce either pressor or depressor cardiovascular responses. At constant renal arterial pressure, increases in renin release occur with pressor responses, whereas decreases in renin release, mediated by the renal nerves, occur with depressor responses.

Increased release of norepinephrine and dopamine from canine kidney during bilateral carotid occlusion

1987 ◽  
Vol 252 (2) ◽  
pp. F240-F245
Author(s):  
T. Bradley ◽  
P. Hjemdahl ◽  
G. F. DiBona
Keyword(s):  
Arterial Pressure ◽  
Renal Plasma Flow ◽  
Plasma Concentrations ◽  
Nerve Impulse ◽  
Artery Occlusion ◽  
Carotid Artery Occlusion ◽  
Impulse Frequency ◽  
Renal Nerve ◽  
Concentration Difference ◽  
Bilateral Carotid

The renal overflow of norepinephrine (NE) and dopamine (DA) to plasma from the innervated kidney was studied at rest and during sympathetic nervous system activation by bilateral carotid artery occlusion (BCO) in vagotomized dogs under barbiturate or barbiturate/nitrous oxide anesthesia. BCO elevated arterial pressure and the arterial plasma concentrations of NE, DA, and epinephrine (Epi). Renal vascular resistance (renal arterial pressure kept constant) increased by 15 +/- 7% (P less than 0.05) and the net renal venous outflows (renal venoarterial concentration difference X renal plasma flow) of NE and DA were enhanced (P less than 0.05). To obtain more correct estimates of the renal contribution to the renal venous catecholamine outflow, we corrected for the renal extraction of arterial catecholamines, assessed as the extractions of [3H]NE, [3H]DA, or endogenous Epi. The [3H]NE corrected renal NE overflow to plasma increased from 144 +/- 40 to 243 +/- 64 pmol X min-1 (P less than 0.05) during BCO, which, when compared with a previous study of the [3H]NE corrected renal NE overflow to plasma evoked by electrical renal nerve stimulation, "corresponds" to a 40% increase in nerve impulse frequency from approximately 0.6 Hz. If the renal catecholamine extraction was not taken into account the effect of BCO was underestimated. The renal DA overflow to plasma was about one-fifth of the NE overflow both at rest and during BCO, indicating that there was no preferential activation of noradrenergic or putative dopaminergic nerves by BCO.

Time course of recovery of arterial pressure control after carotid denervation

1990 ◽  
Vol 258 (1) ◽  
pp. H73-H79 ◽  
Author(s):  
D. S. O'Leary ◽  
A. M. Scher
Keyword(s):  
Arterial Pressure ◽  
Time Course ◽  
Pressor Response ◽  
Peripheral Resistance ◽  
Pressure Control ◽  
Artery Occlusion ◽  
Carotid Artery Occlusion ◽  
Atrial Rate ◽  
Bilateral Carotid ◽  
Pressure Changes

We examined the recovery of arterial pressure control after carotid sinus baroreceptor denervation in conscious dogs with atrioventricular block. Strength of control was assessed by measuring changes in peripheral resistance and atrial rate after step changes in cardiac output. One day after carotid denervation, arterial pressure was significantly elevated (+13.7 mmHg), and the strength of control of peripheral resistance and atrial rate were significantly decreased to 46.1 and 36.6% of control, respectively. Over 4–7 days, the strength of control of both peripheral resistance and atrial rate and the mean arterial pressure returned to the levels observed before denervation. After carotid denervation, the pressor response to bilateral carotid artery occlusion was abolished, and thus the recovery of arterial pressure control was not caused by inadequate carotid denervation or regeneration of carotid baroreceptors. The recovery of arterial pressure control after carotid denervation is probably caused by an increase in the reflex responses to pressure changes at the aortic baroreceptors and may reflect plasticity within the baroreflex pathway.

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