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PubMed1980

Adrenal medullary responses to stimulation of the splanchnic nerve in the conscious calf.

1. Right adrenal medullary and various cardiovascular responses to stimulation of the peripheral end of the right splanchnic nerve have been investigated in conscious calves, 2--5 weeks after birth. 2. The output of both adrenaline and noradrenaline was linearly related to stimulus frequency over the range 2.0--10.0 Hz, 2 1/2 min after stimulation was initiated. Peak outputs of both amines were obtained in response to stimulation at 15.0 Hz. 3. The output of adrenaline invariably exceeded that of noradrenaline, roughly in the proportion 3:2. At all frequencies tested between 7.0 and 40.0 Hz this difference was statistically significant (P less than 0.1). 4. Continuous stimulation at either 4.0 or 10.0 Hz produced a small but significant rise in the output of dopamine-beta-monooxygenase (DBH) activity from the right adrenal gland. Mean maximal outputs were obtained after 10 min; the levels were closely similar at both 4.0 and 10.0 Hz and could not be related to stimulus frequency or to the output of either adrenaline or noradrenaline. 5. The results are discussed in relation to perfusion studies in vitro and experiments in anaesthetized animals. It is concluded that the levels of DBH in adrenal effluent plasma is an unreliable index of catecholamine exocytosis in the conscious calf.

Adrenal Medulla↗
PubMed1982

Adrenal catecholamine output in response to stimulation of the splanchnic nerve in bursts in the conscious calf.

1. Different patterns of stimulation have been applied to the peripheral end of the right splanchnic nerve, below behavioural threshold, in conscious 2-5 week-old calves. 2. The effects of continuous stimulation at 4 Hz for 10 min were compared with those of stimulation at 40 Hz in 1 s bursts at 10 s intervals for the same period. Delivering the same total number of impulses in the form of bursts in this way increased the output of both adrenaline and noradrenaline and this increase was statistically significant in the case of adrenaline (P less than 0.02) but not noradrenaline. 3. The effects of stimulation in 1 s bursts at 10 s intervals for 2-3 min were investigated over the frequency range 10-150 Hz and compared with the effects of continuous stimulation over the range 1-15 Hz obtained previously in conscious calves of the same age (Edwards, Furness and Halle, 1980). The output of adrenaline but not noradrenaline was found to significantly greater in response to stimulation in bursts at frequencies of up to 40 Hz than when the equivalent number of impulses were delivered at a constant rate (P less than 0.02). 4. It is concluded that the release of catecholamines from the adrenal gland is maximal at relatively high frequencies (40-100 Hz) when the impulses are delivered in bursts.

Adrenal Medulla↗
PubMed1983

Glomerular filtration rate and salt and water reabsorption during pregnancy in the conscious rat.

1. Glomerular filtration rate (g.f.r.) and salt and water reabsorption were measured in age-matched conscious virgin rats and rats at different stages of pregnancy that were infused with saline at 40 and 200 microliters min-1. 2. G.f.r. and salt and water reabsorption were significantly higher at all stages of pregnancy irrespective of the the rate of infusion. 3. The similarity in both time course and magnitude, of changes in renal function between conscious and anaesthetized rats at the two infusion rates suggests that the detection of differences in the anaesthetized rat during pregnancy is not dependent on either the anaesthetic/surgery employed or the rate of expansion of the extracellular fluid volume. 4. During the induction of the diuresis in 20-day pregnant rats infused at 40 microliters min-1 urine flow was higher and osmolality lower than in virgin rats and rats at earlier stages of pregnancy, suggesting that late-pregnant rats have an altered ability for elaborating concentrated or dilute urine.

Absorption↗
PubMed2004

Control of muscle glucose uptake: test of the rate-limiting step paradigm in conscious, unrestrained mice.

The aim of this study was to test whether in fact glucose transport is rate-limiting in control of muscle glucose uptake (MGU) under physiological hyperinsulinaemic conditions in the conscious, unrestrained mouse. C57Bl/6J mice overexpressing GLUT4 (GLUT4(Tg)), hexokinase II (HK(Tg)), or both (GLUT4(Tg) + HK(Tg)), were compared to wild-type (WT) littermates. Catheters were implanted into a carotid artery and jugular vein for sampling and infusions at 4 month of age. After a 5-day recovery period, conscious mice underwent one of two protocols (n = 8-14/group) after a 5-h fast. Saline or insulin (4 mU kg(-1) min(-1)) was infused for 120 min. All mice received a bolus of 2-deoxy[(3)H]glucose (2-(3)HDG) at 95 min. Glucose was clamped at approximately 165 mg dl(-1) during insulin infusion and insulin levels reached approximately 80 microU ml(-1). The rate of disappearance of 2-(3)HDG from the blood provided an index of whole body glucose clearance. Gastrocnemius, superficial vastus lateralis and soleus muscles were excised at 120 min to determine 2-(3)HDG-6-phosphate levels and calculate an index of MGU (R(g)). Results show that whole body and tissue-specific indices of glucose utilization were: (1) augmented by GLUT4 overexpression, but not HKII overexpression, in the basal state; (2) enhanced by HKII overexpression in the presence of physiological hyperinsulinaemia; and (3) largely unaffected by GLUT4 overexpression during insulin clamps whether alone or combined with HKII overexpression. Therefore, while glucose transport is the primary barrier to MGU under basal conditions, glucose phosphorylation becomes a more important barrier during physiological hyperinsulinaemia in all muscles. The control of MGU is distributed rather than confined to a single rate-limiting step such as glucose transport as glucose transport and phosphorylation can both become barriers to skeletal muscle glucose influx.

Adaptation, Physiological↗
PubMed2005

Chronic exposure to cocaine binging predisposes to an accelerated course of dilated cardiomyopathy in conscious dogs following rapid ventricular pacing.

Despite extensive study, the extent to which cocaine use predisposes to cardiac injury remains unknown. We hypothesized that chronic cocaine binging would increase susceptibility to a subsequent cardiac insult, even in the absence of demonstrable effects on baseline hemodynamics. We studied progression of dilated cardiomyopathy (DCM) induced by rapid ventricular pacing (240 beats per minute) in five conscious, chronically instrumented dogs, after exposure to repetitive cocaine binging (COC) in the form of four consecutive 1 mg/kg i.v. boluses daily for 8 days, to simulate human cocaine abuse. We compared the results with nine control dogs (CON) undergoing the exact pacing protocol, without prior cocaine exposure. Baseline hemodynamics were not significantly altered by chronic cocaine exposure. Following 2 weeks of pacing, COC dogs exhibited accelerated progression to DCM, depressed plasma nitric oxide levels (CON, 17 +/- 2 microM; COC, 10 +/- 2 microM, p < 0.05), and a significantly greater increase in plasma epinephrine (CON, 33 +/- 6 pg/ml; COC, 104 +/- 24 pg/ml). After only 2 weeks of pacing, COC dogs demonstrated progressive DCM of a magnitude comparable with end-stage pacing-induced DCM. Chronic cocaine binging increases susceptibility to a subsequent myocardial insult and accelerates progression of DCM in conscious dogs following rapid pacing. These data suggest that although chronic cocaine use alone may not affect myocardial function, it predisposes to greater susceptibility to a superimposed insult.

Animals↗
PubMed2006

Tonic nociceptinergic inputs to neurons in the hypothalamic paraventricular nucleus contribute to sympathetic vasomotor tone and water and electrolyte homeostasis in conscious rats.

Central administration of nociceptin/orphanin FQ (N/OFQ) produces bradycardia, hypotension, diuresis, and antinatriuresis in rats. Because N/OFQ peptide (NOP) receptors exist in the paraventricular nucleus (PVN) of the hypothalamus, we hypothesized that N/OFQ acts in the PVN to alter cardiovascular and renal function. To test this premise, N/OFQ (10 and 100 pmol) or artificial cerebrospinal fluid (vehicle) was microinjected into the right PVN of conscious, chronically instrumented rats infused i.v. with isotonic saline. After injection, N/OFQ, but not vehicle, dose-dependently decreased renal sympathetic nerve activity (RSNA) and increased urine flow rate. At 100 pmol, N/OFQ also decreased urinary sodium and potassium excretion and increased free water clearance. In separate groups, the diuretic response to N/OFQ injection into the PVN was blunted in chronic bilaterally renal denervated rats and abolished in intact rats continuously infused i.v. with [Arg(8)]vasopressin (60 fmol/kg/min). Finally, in other studies bilateral microinjection of the NOP receptor antagonist [Nphe(1),Arg(14),Lys(15)]N/OFQ-NH(2) (UFP-101; 300 pmol) into the PVN increased heart rate and RSNA and decreased urine flow rate without altering electrolyte excretion. Pretreatment of separate rats with UFP-101 (300 pmol, PVN) blocked the N/OFQ-evoked (100 pmol) cardiovascular, renal sympathetic nerve, and renal excretory responses. Together, these findings demonstrate that in conscious rats activation of NOP receptors in the PVN by N/OFQ produces bradycardia, renal sympathoinhibition, and water diuresis. Moreover, UFP-101 blocks a tonically active inhibitory influence of endogenous N/OFQ on central sympathetic outflow and vasopressin pathways which arise from the PVN to affect heart rate and urine output.

Animals↗
PubMed2006

Central adenosine signaling plays a key role in centrally mediated hypotension in conscious aortic barodenervated rats.

We tested the hypothesis that clonidine-evoked hypotension is dependent on central adenosinergic pathways. Five groups of male, conscious, aortic baroreceptor-denervated (ABD) rats received clonidine (10 microg/kg i.v.) 30 min after i.v. 1) saline, 2) theophylline (10 mg/kg), or 3) 8-(p-sulfophenyl)theophylline (8-SPT) (2.5 mg/kg) or 1 h after i.p. 4) dipyridamole (5 mg/kg) or 5) an equal volume of sesame oil. Blockade of central (theophylline) but not peripheral (8-SPT) adenosine receptors abolished clonidine hypotension. In contrast, dipyridamole substantially enhanced the bradycardic response to clonidine. In additional groups, intracisternal (i.c.) dipyridamole (150 microg) and 8-SPT (10 microg) enhanced and abolished, respectively, clonidine (0.6 microg i.c.)-evoked hypotension. Because clonidine is a mixed I1/alpha2 agonist, we also investigated whether adenosine signaling is linked to the I1 or the alpha2A receptor by administering the selective I1 (rilmenidine, 25 microg) or alpha2A [alpha-methylnorepinephrine (alpha-MNE), 4 microg] agonist 30 min after central adenosine receptor blockade (8-SPT; 10 microg i.c.) or artificial cerebrospinal fluid. The hypotensive response elicited by rilmenidine or alpha-MNE was abolished in 8-SPT-pretreated rats. To delineate the role of the adenosine A2A receptor in clonidine-evoked hypotension, i.c. clonidine (0.6 microg) was administered 30 min after central adenosine receptor A2A blockade [5-amino-7-(2-phenylethyl)-2-(2-furyl)-pyrazolo[4,3-epsilon]-1,2,4-triazolo[1,5-c]-pyrimidine (SCH58261); 150 microg i.c.]. The latter virtually abolished the hypotensive and bradycardic responses elicited by clonidine. In conclusion, central adenosine A2A signaling plays a key role in clonidine-evoked hypotension in conscious aortic barodenervated rats.

Adenosine A2 Receptor Agonists↗
PubMed1986

Circulating atrial natriuretic peptides in conscious rats: regulation of release by multiple factors.

Cardiocytes in the atria contain a prohormone that gives rise to atrial natriuretic peptides (ANP's), which have intrinsic hemodynamic regulatory activity. The distribution of ANP's in the brain suggests the involvement of these peptides in central cardiovascular regulation. In conscious rats with chronic indwelling catheters, volume loading with isotonic saline or glucose increased the amount of circulating immunoreactive ANP's by a factor of 4 to 5, as determined by radioimmunoassay. Hyperosmotic challenge with a hypertonic NaCl solution or anesthesia with halothane caused similar increases in plasma ANP's. Results obtained with the denervated-heart preparation indicate that neuronal influences are important in the release of ANP's induced by volume loading. As judged from reversed-phase high-performance liquid chromatography of extracted plasma and radioimmunoassay of collected fractions, the circulating physiologically important ANP's in the conscious rodent appear to be alpha-rANP(5-28) (atriopeptin III) and either alpha-rANP(3-28) [ANF(8-33)] or alpha-rANP(1-28) (ANF).

Anesthesia↗
PubMed2001

Measuring plasma paracetamol concentrations in all patients with drug overdose or altered consciousness: does it change outcome?

OBJECTIVE: To assess whether measuring plasma paracetamol concentrations in all patients with drug overdose or collapse (altered consciousness) changes outcome. METHOD: A retrospective survey was performed of all patients attending the Accident and Emergency Department at Guy's Hospital, London over a 12 month period who had plasma paracetamol concentrations measured (it is hospital policy that patients presenting after any drug overdose, or with a collapse/altered consciousness have a plasma paracetamol concentration). RESULTS: A total of 440 patients were identified who had plasma paracetamol concentrations measured, of whom 411 were eligible for the study. Altogether 115 patients presented after a collapse and paracetamol was detected in four of these. A total of 296 patients presented after a drug overdose-136 denied overdose with a paracetamol containing product and paracetamol was not detected in any of these 136 cases. Of the remaining 160 patients who gave a positive history for overdose with paracetamol, 122 presented within 24 hours and 94 had detectable paracetamol values with 16 cases above the treatment line, 12 presented more than 24 hours after ingestion, and 26 presented with a staggered overdose. One patient died as a result of paracetamol overdose. CONCLUSIONS: This is the first study in the United Kingdom to evaluate the clinical value of routine paracetamol levels in patients presenting to the emergency department after any overdose or a collapse. Taking blood samples for plasma paracetamol estimation in patients who deny taking paracetamol is of little clinical value. However, there is the potential for missing significant paracetamol poisoning in patients presenting with collapse and so screening with a plasma paracetamol concentration is clinically justified in these patients. Such an approach can only be justified in a country in which paracetamol poisoning is prevalent, such as the United Kingdom.

Acetaminophen↗
PubMed2006

Prognosis of status epilepticus: role of aetiology, age, and consciousness impairment at presentation.

BACKGROUND: Identification of outcome-predictive factors could lower risk of under- or over-treatment in status epilepticus (SE). Older age and acute symptomatic aetiology have been shown to predict mortality, but other variables are controversial and level of consciousness has received relatively little attention. The objective of this study was to assess variables predictive of mortality, particularly those available at presentation. METHODS: The discharge database (1997-2004) of two university hospitals was screened for adult patients with EEG confirmed SE, excluding cerebral anoxia. Outcome at discharge (mortality, return to baseline clinical conditions) was analysed in relation to demographics, clinical features, and aetiology. Aetiologies were also classified based on whether or not they were potentially fatal independently of SE. RESULTS: Mortality was 15.6% among 96 patients with a first SE episode, 10 of whom also experienced recurrent SE during the study period. Eleven other patients had only recurrent SE. Mortality was 4.8% among these 21 patients with recurrent SE. Return to baseline condition was more frequent after recurrent than incident SE (p=0.02). For the first SE episode, death was associated with potentially fatal aetiology (p=0.01), age>or=65 (p=0.02), and stupor or coma at presentation (p=0.04), but not with gender, history of epilepsy, SE type, or time to treatment>or=1 h. CONCLUSIONS: At initial evaluation, older age and marked impairment of consciousness are predictive of death. Surviving a first SE episode could lower the mortality and morbidity of subsequent episodes, suggesting that underlying aetiology, rather than SE per se, is the major determinant of outcome.

Acute Disease↗
PubMed1997

Painful generalised clonic and tonic-clonic seizures with retained consciousness.

Two patients in whom consciousness and memory were retained during bilateral clonic or tonic-clonic seizures are reported on, and three patients reported on previously are reviewed. Ictal semiology differed from myoclonic and supplementary motor seizures, which are other seizure types characterised by bilateral motor movements and retained awareness. In the two new patients ictal pain was a prominent feature. It is proposed that propagation of seizure activity may be confined to the sensorimotor areas bilaterally while sparing the neural structures involved in maintaining consciousness and in processing language and memory. This unusual type of seizure may be misdiagnosed as a pseudoseizure. Detailed description of the ictal events and further laboratory evaluation including video-EEG monitoring may be necessary to make the distinction.

Adolescent↗
PubMed1985

Influence of hypoxemia and respiratory acidosis on the plasma kinetics and tissue distribution of digoxin in the conscious dog.

The aim of the present study was to investigate the influence of hypoxemia combined with respiratory acidosis on the kinetics of digoxin in conscious dogs. One group of three beagles was exposed to air and 7 days later to 10% O2, 10% CO2, and 80% N2. In a second group of three dogs, the order of exposure to the two atmospheric conditions was reversed. The dogs received 25 micrograms/kg digoxin and blood and urine samples were collected over the next 29 h. At the conclusion of the second treatment, the dogs were sacrificed to determine digoxin concentrations in the left ventricle, liver, renal cortex, and skeletal muscle. Digoxin total body clearance increased from 6.2 +/- 0.9 in control to 9.0 +/- 1.0 mL X min-1 X kg-1 in hypoxemic and hypercapnic dogs (p less than 0.05). The digoxin apparent volume of distribution at steady state (Vss) was increased in the dogs with hypoxemia and hypercapnia (11.63 +/- 1.11 vs. 8.62 +/- 0.41 L/kg in the controls, p less than 0.05). As a consequence the digoxin plasma half-life remained unchanged (18.6 +/- 1.5 h in hypoxemic and hypercapnic dogs versus 20.1 +/- 2.8 h in the controls). In dogs with hypoxemia and hypercapnia, the ratio of tissue to plasma digoxin concentrations tended to increase in the liver, in the renal cortex, and in the left ventricle and remained unchanged in the left hind leg muscle. In vitro studies showed that the digoxin total binding to erythrocyte membranes was slightly increased in the dogs with hypoxemia and hypercapnia, resulting from an increase in the apparent intrinsic association constant for digoxin (p less than 0.003). It is concluded that hypoxemia combined with respiratory acidosis changes digoxin disposition in the conscious dog and is the cause of a digoxin redistribution into the tissues.

Acidosis, Respiratory↗
PubMed2004

Concept formation: 'object' attributes dynamically inhibited from conscious awareness.

We advance a dominant neural strategy for facilitating conceptual thought. Concepts are groupings of "object" attributes. Once the brain learns such critical groupings, the "object" attributes are inhibited from conscious awareness. We see the whole, not the parts. The details are inhibited when the concept network is activated, ie. the inhibition is dynamic and can be switched on and off. Autism is suggested to be the state of retarded concept formation. Our model predicts the possibility of accessing nonconscious information by artificially disinhibiting (turning off) the inhibiting networks associated with concept formation, using transcranial magnetic brain stimulation (TMS). For example, this opens the door for the restoration of perfect pitch, for recalling detail, for acquiring accent-free second languages beyond puberty, and even for enhancing creativity. The model further shows how unusual autistic savant skills as well as certain psychopathologies can be due respectively to privileged or inadvertent access to information that is normally inhibited from conscious awareness.

Adult↗
PubMed2005

Characterization of 5-HT7-receptor-mediated gastric relaxation in conscious dogs.

We aimed to evaluate the gastric relaxant capacity of the 5-HT(1/7)-receptor agonist 5-carboxamidotryptamine (5-CT) in conscious dogs and to clarify the mechanism of action by use of selective antagonists, vagotomy, and in vitro experiments. A barostat enabled us to monitor the intragastric volume in response to different treatments (intravenously administered) before and after supradiaphragmatic vagotomy [results presented as the maximum volume change after treatment (mean; n = 5-11)]. In vitro experiments were performed with isolated muscle strips cut from four different stomach regions of the vagotomized dogs [results were fitted to the operational model of agonism to determine the efficacy parameter tau (n = 5)]. 5-CT (0.5-10 microg/kg) caused a dose-dependent gastric relaxation (29-267 ml) that was completely blocked by the selective 5-HT(7)-receptor antagonist SB-269970 (50 microg/kg). After vagotomy, the relaxation to 10 microg/kg 5-CT was significantly less pronounced (73 vs. 267 ml; P < 0.05) but still blocked by SB-269970, whereas the response to the nitric oxide donor nitroprusside was similar to that before vagotomy (178 vs. 218 ml). In vitro, 5-CT concentration dependently inhibited the PGF(2alpha)-contracted muscle strips before and after vagotomy. Although before and after vagotomy the response in every region was mediated by 5-HT(7) receptors (apparent affinity dissociation constant: SB-269970, 8.2-8.6 vs. 8.3-8.6, respectively), the response after vagotomy was less efficacious (log tau: 1.9 to 0.5 vs. 1.4 to -0.1). The results indicate that the 5-CT-induced proximal stomach relaxation in conscious dogs before and after vagotomy is mediated via 5-HT(7) receptors. The decreased efficacy of 5-CT in vitro after vagotomy is probably related to vagotomy-induced changes in receptor density or coupling efficiency and provides a possible explanation for the decreased in vivo response to 5-CT after vagotomy.

Animals↗
PubMed1984

Relation between intestinal motility and mesenteric blood flow in the conscious dog.

Blood flow in a mesenteric artery and electrical activity of the corresponding segment of jejunum or ileum were simultaneously measured in eight conscious dogs. Each was fitted chronically with an electromagnetic flow probe and transparietal electrodes. In some dogs an intestinal cannula was placed cephalad to the segment investigated. Continuous 24-h records were obtained in each dog receiving a daily meal. Jejunal blood flow increased after the meal, decreased progressively during the postprandial period (7-12 h), and then exhibited cyclic variations associated with the occurrence of migrating myoelectric complexes (MMCs) during the next 6-10 h. The ileal blood flow increased, then remained high and nearly constant during the postprandial disorganization of the MMC pattern, and exhibited cyclic variations associated with all MMCs even when the dog was fasted for 48 h. Cyclic variations in blood flow were abolished when the intestinal content was drained through the cannula. It is concluded that in the conscious dog the blood flow profile in a mesenteric artery is associated with the motor profile of the segment. This association is due to the presence of digestive matter, probably nutrients in the jejunum and bile in the ileum.

Animals↗
PubMed2001

Acute cold exposure induces vagally mediated Fos expression in gastric myenteric neurons in conscious rats.

Acute cold exposure-induced activation of gastric myenteric neurons in conscious rats was examined on longitudinal muscle-myenteric plexus whole mount preparations. Few Fos-immunoreactive (IR) cells (<1/ganglion) were observed in 24-h fasted rats semirestrained at room temperature. Cold exposure (4 degrees C) for 1-3 h induced a time-related increase of Fos-IR cells in corpus and antral myenteric ganglia with a maximal plateau response (17 +/- 3 and 18 +/- 3 cells/ganglion, respectively) occurring at 2 h. Gastric vagotomy partly prevented, whereas bilateral cervical vagotomy completely abolished, Fos expression in the myenteric cells induced by cold exposure (2 h). Hexamethonium (20 mg/kg) also prevented 3-h cold exposure-induced myenteric Fos expression by 76-80%, whereas atropine or bretylium had no effect. Double labeling revealed that cold (3 h)-induced Fos-IR myenteric cells were mainly neurons, including a substantial number of choline acetyltransferase-containing neurons and most NADPH-diaphorase-positive neurons. These results indicate that acute cold exposure activates cholinergic as well as nitrergic neurons in the gastric myenteric ganglia through vagal nicotinic pathways in conscious rats.

Animals↗
PubMed2006

Baroreflex responses to electrical stimulation of aortic depressor nerve in conscious SHR.

Baroreflex responses to changes in arterial pressure are impaired in spontaneously hypertensive rats (SHR). Mean arterial pressure (MAP), heart rate (HR), and regional vascular resistances were measured before and during electrical stimulation (5-90 Hz) of the left aortic depressor nerve (ADN) in conscious SHR and normotensive control rats (NCR). The protocol was repeated after beta-adrenergic-receptor blockade with atenolol. SHR exhibited higher basal MAP (150 +/- 5 vs. 103 +/- 2 mmHg) and HR (393 +/- 9 vs. 360 +/- 5 beats/min). The frequency-dependent hypotensive response to ADN stimulation was preserved or enhanced in SHR. The greater absolute fall in MAP at higher frequencies (-68 +/- 5 vs. -38 +/- 3 mmHg at 90-Hz stimulation) in SHR was associated with a preferential decrease in hindquarter (-43 +/- 5%) vs. mesenteric (-27 +/- 3%) resistance. In contrast, ADN stimulation decreased hindquarter and mesenteric resistances equivalently in NCR (-33 +/- 7% and -30 +/- 7%). Reflex bradycardia was also preserved in SHR, although its mechanism differed. Atenolol attenuated the bradycardia in SHR (-88 +/- 14 vs. -129 +/- 18 beats/min at 90-Hz stimulation) but did not alter the bradycardia in NCR (-116 +/- 16 vs. -133 +/- 13 beats/min). The residual bradycardia under atenolol (parasympathetic component) was reduced in SHR. MAP and HR responses to ADN stimulation were also preserved or enhanced in SHR vs. NCR after deafferentation of carotid sinuses and contralateral right ADN. The results demonstrate distinct differences in central baroreflex control in conscious SHR vs. NCR. Inhibition of cardiac sympathetic tone maintains reflex bradycardia during ADN stimulation in SHR despite impaired parasympathetic activation, and depressor responses to ADN stimulation are equivalent or even greater in SHR due to augmented hindquarter vasodilation.

Animals↗
PubMed2004

Sodium channel enhancer restores baroreflex sensitivity in conscious dogs with heart failure.

We compared the cardiac inotropic, lusitropic, and chronotropic responses to the Na(+) channel enhancer LY-368052 in conscious dogs before and after development of congestive heart failure (CHF). We also examined the effect of LY-368052 on baroreflex sensitivity and the efferent neural mechanisms of the bradycardic response in heart failure. Dogs were chronically instrumented, and heart failure was induced by right ventricular pacing at 240 beats/min for 3-4 wk. LY-368052 dose-dependently increased left ventricular contractile performance before and after the development of CHF to a similar extent. The inotropic effect of LY-368052 in heart failure was not altered by either ganglionic or beta-adrenergic receptor blockade. LY-368052 improved cardiac relaxation and induced bradycardia in dogs with heart failure but not in normal dogs. The negative chronotropic effect of LY-368052 was eliminated by ganglionic blockade but not beta-adrenergic blockade, suggesting that the bradycardia was mediated by the autonomic nervous system via enhanced parasympathetic tone. Baroreflex sensitivity was assessed as the pulse interval-mean arterial pressure slope in response to temporary pharmacological (nitroglycerin or phenylephrine) and mechanical (brief occlusion of inferior vena cava) alterations of arterial pressure in conscious dogs before and after development of heart failure. Baroreflex sensitivity was significantly depressed in heart failure and restored completely by acute treatment with LY-368052. Thus the Na(+) channel enhancer LY-368052 maintains its beta-receptor-independent inotropic effect in chronic CHF and specifically improves ventricular relaxation and depressed baroreflex function.

Adrenergic beta-Antagonists↗