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PubMed2001

Involvement of imidazoline receptors in the baroreflex effects of rilmenidine in conscious rabbits.

OBJECTIVE: It has been suggested that imidazoline receptors rather than alpha2-adrenoceptors are involved in the sympathoinhibitory action of centrally acting antihypertensive drugs such as rilmenidine. In the present study, we examined the relative importance of alpha2-adrenoceptors and imidazoline receptors in modulating the renal sympathetic and heart rate (HR) baroreflex in response to central administration of rilmenidine in conscious normotensive rabbits. METHODS: In seven conscious rabbits, chronically instrumented with a fourth ventricular (4V) catheter, aortic and vena caval cuff occluders and a renal nerve electrode, we continuously recorded renal sympathetic nerve activity (RSNA), mean arterial pressure (MAP) and HR and assessed baroreflex MAP-RSNA and MAP-HR relationships with balloon-induced ramp rises and falls in MAP. Rabbits were treated with 4V rilmenidine (22 microg/kg) followed by 4V idazoxan (30 microg/kg; a mixed alpha2-adrenoceptor and imidazoline receptor antagonist) or 4V 2-methoxy-idazoxan (1 microg/kg; an alpha2-adrenoceptor antagonist with little affinity for imidazoline receptors). RESULTS: Rilmenidine lowered blood pressure by 24% and reduced both upper and lower plateaus of the renal sympathetic baroreflex curve, such that the RSNA range (difference between plateaus) was reduced by 40% (-32 +/- 10 normalized units). Curves were shifted to the left with the fall in MAP. Idazoxan restored MAP, maximum RSNA and the RSNA baroreflex range. By contrast the alpha2-adrenoceptor antagonist 2-methoxy-idazoxan caused only a partial recovery of MAP and RSNA baroreflex upper plateau and range (-9 +/- 2 mmHg, 29 and 33% lower than control). Both antagonists partially restored the HR baroreflex. CONCLUSION: These findings suggest that in conscious rabbits, both imidazoline receptors and alpha2-adrenoceptors are involved in the central antihypertensive and baroreflex actions of rilmenidine, but that activation of imidazoline receptors is more important for its renal sympathoinhibitory action.

Adrenergic alpha-Agonists↗
PubMed2003

Central cardiovascular action of urotensin II in conscious rats.

OBJECTIVE: To examine the central cardiovascular action of urotensin II in conscious rats. METHODS: Intracerebroventricular (ICV) injections of urotensin II (1 and 10 nmol) were carried out in conscious Wistar rats. The effects of intravenous (i.v.) urotensin II (10 nmol) were also determined. RESULTS: The ICV injection of urotensin II at a dose of 1 nmol did not alter the arterial pressure or heart rate significantly, while 10 nmol urotensin II increased the arterial pressure and heart rate. The mean arterial pressure at 5 min of ICV urotensin II was 121 +/- 4 mmHg, which was significantly higher than that obtained by ICV injection of artificial cerebrospinal fluid (107 +/- 3 mmHg, P <0.05). In addition, significant increases in heart rate were observed 5-15 min after ICV urotensin II. Pre-treatment with pentolinium (5 mg/kg, i.v.) significantly attenuated the increases in mean arterial pressure (20 +/- 3 versus 8 +/- 2 mmHg, P <0.01) and heart rate (78 +/- 18 versus 7 +/- 5 beats/min, P <0.05) induced by ICV urotensin II. On the other hand, i.v. injection of urotensin II (10 nmol) elicited a depressor response associated with tachycardia; mean arterial pressure 5 min after injection was significantly lower in the urotensin II-injected rats (89 +/- 5 mmHg) than in the control rats (102 +/- 2 mmHg, P <0.05), and the heart rate was significantly higher in the former (402 +/- 11 versus 360 +/- 9 beats/min, respectively, P <0.05). CONCLUSIONS: Central urotensin II produces pressor and tachycardic responses through sympathetic activation, while peripheral urotensin II exerts a vasodilation-mediated depressor response in conscious rats.

Animals↗
PubMed2004

Restoration of baroreflex function by ketanserin is not blood pressure dependent in conscious freely moving rats.

OBJECTIVE: Since the end of the 1980s, the pathological importance of baroreflex function has attracted the attention of many investigators. In our previous studies, it was found that ketanserin lowered blood pressure (BP), decreased BP variability and enhanced baroreflex sensitivity (BRS). The present work was designed to test the hypothesis that the restoration of BRS by ketanserin is not dependent on BP level in conscious rats. DESIGN AND METHODS: Spontaneously hypertensive rats (SHR) aged 8-12 months were used. Blood pressure was recorded for 60 min and BRS was determined separately before and after intragastric administration of ketanserin, with four doses. In a second experiment, 10-week-old Sprague-Dawley rats were used for preparing a myocardial infarction (MI) model by ligating the coronary artery. MI rats were treated with ketanserin for 5 weeks, with two doses. At the end of the treatment, BP and BRS of the MI rats were studied in conscious state. In addition, the effects of ketanserin on BRS in Sprague-Dawley rats with normal BRS and the effects of prazosin and ritanserin on BRS in SHR were also observed. RESULTS: It was found that ketanserin significantly decreased BP and improved BRS in the conscious SHR. The decrease in BP was dose-dependent but the improvement of BRS was not. At the smallest dose (0.3 mg/kg), ketanserin did not lower BP but enhanced BRS. In MI rats, the treatment with ketanserin did not significantly decrease BP, but it improved BRS at both doses administered (0.6 and 10 mg/kg). Ketanserin [3 and 10 mg/kg, intragastric (i.g.)] did not affect BRS in SD rats with normal BRS. Prazosin and ritanserin did not enhance BRS in SHR when administered intravenously. Ritanserin markedly and prazosin slightly enhanced BRS in SHR following intracerebroventricular administration. CONCLUSION: The restoration of baroreflex function by ketanserin is not BP dependent and this effect is mediated by central 5-HT2A receptor.

Animals↗
PubMedDate not supplied

Acute hemodynamic effects of a new positive inotropic agent, 3,4-dihydro-6-[4-(3,4-dimethoxybenzoyl)-1-piperazinyl]-2(1H)- quinolinone (OPC-8212), in conscious and anesthetized dogs.

The acute hemodynamic effects of a new cardiotonic agent, OPC-8212 (a 1H-quinolinone derivative), were studied in six conscious and 11 anesthetized dogs using a pair of ultrasonic crystals to measure the left ventricular segment length and a micromanometer to measure the left ventricular pressure. In six anesthetized dogs subjected to aortic constriction, the ascending aortic flow (AoF) was measured before and after intervention. In the anesthetized state bolus injections of OPC-8212 increased the ejection indices dose dependently. Maximum effects were observed at 1 min, the mean velocity of the circumferential fiber shortening (mean Vcf) being augmented by 6.6% with 0.3 mg, by 39.7% with 1 mg, and by 67.2% with 3 mg. These changes were not accompanied by any significant alteration in heart rate. With aortic constriction, the left ventricular wall shortening was significantly reduced. Depressed pump function was dramatically improved with injection of 3 mg of OPC-8212, the dP/dt was elevated by 98%, the AoF by 46%, and the mean Vcf by 78%. In the conscious state the same doses induced the same type of changes in hemodynamics and dimensions, but the amplitude of the response was significantly less; increase in the mean Vcf was by 36% and that of dP/dt by 52%. Thus, OPC-8212 has a potent inotropic effect. The effect was greater in the anesthetized state, or in dogs with depressed ventricular function, than in the conscious state.

Anesthesia↗
PubMed1988

Effects of the novel calcium channel blocker, McN-5691, on cardiocirculatory dynamics and cardiac output distribution in conscious spontaneously hypertensive rat.

The purpose of this study was to characterize the cardiocirculatory effects of McN-5691 in the conscious spontaneously hypertensive rat (SHR) and in age matched Wistar-Kyoto (WKY) control rats. Animals were instrumented under halothane anesthesia for right atrial, left ventricular arterial, and venous pressure recordings. The radioactive microsphere technique was used to estimate regional blood flow and cardiac output before (control) and during intravenous (i.v.) infusion of either McN-5691 at three dosage levels (0.3, 1.0, 3.0 mg/kg), or vehicle (VH) at an infusion rate of 0.0408 ml/min. The predominant hemodynamic effect of McN-5691 (cumulative dose = 0.3-4.3 mg/kg i.v.) in conscious SHR was dose-related reduction in mean arterial pressure with normalization occurring at a cumulative dose of 1.3 mg/kg i.v. The antihypertensive effect of McN-5691 was accompanied by reductions in left ventricular peak systolic pressure (cumulative dose = 1.0-4.3 mg/kg i.v.), arterial pressure-rate product (1.3-4.3 mg/kg i.v.), and systemic vascular resistance (4.3 mg/kg i.v.). McN-5691 had no statistically significant effect on heart rate or cardiac contractility as measured by dP/dt/peak left ventricular pressure. The predominant peripheral vascular effects of McN-5691 were increases in skeletal muscle blood flow (4.3 mg/kg i.v.) and reductions in skeletal muscle (1.3-4.3 mg/kg i.v.), renal (1.3-4.3 mg/kg i.v.), gastrointestinal (4.3 mg/kg i.v.), and coronary (1.3-4.3 mg/kg i.v.) vascular resistances. Despite the fall in renal vascular resistance, renal blood flow was not changed by McN-5691. McN-5691 did not have major effects on other regions of the peripheral circulation. Thus, McN-5691 is an antihypertensive agent as defined by its ability to normalize blood pressure in the SHR, and the hemodynamic mechanism leading to this effect is reduction in peripheral vascular resistance. This antihypertensive effect is not accompanied by reflex tachycardia and is not associated with negative inotropic activity or detrimental peripheral circulatory changes in the conscious SHR.

Animals↗
PubMed1995

Coronary and systemic hemodynamic effects of the putative nitric oxide donor, FK 409, in comparison with nitroglycerin in conscious and anesthetized dogs.

We compared, the hemodynamic profile of FK 409, a new nitric oxide (NO) donor, directly with that of nitroglycerin (NTG) in chloralose-anesthetized dogs and in chronically instrumented conscious dogs. In anesthetized dogs, FK 409 and NTG (each 0.03-30 micrograms kg-1, intravenously, i.v.) both dilated large and small coronary arteries dose dependently. This coronary vasodilation was associated with dose-dependent decreases in blood pressure (BP), total peripheral resistance (TPR), and left ventricular end-diastolic pressure (LVEDP) and with increases in cardiac output (CO), heart rate (HR) and dP/dtmax. FK 409 was equipotent to NTG in dilating large coronary arteries and in reducing cardiac preload, but three times less potent as systemic and coronary arteriolar vasodilator. In general, the effects of FK 409 developed more slowly and lasted longer than those of NTG. With both drugs, dilation of large coronary arteries was sustained as compared with dilation of systemic or coronary arterioles. In conscious dogs, coronary and systemic hemodynamic effects of FK 409 and NTG (each 0.1-10 micrograms kg-1 i.v.) were qualitatively and quantitatively very similar to those observed in anesthetized dogs, except that reflex tachycardia was more pronounced in animals in the conscious state. Administered orally, FK 409 (0.3 mg kg-1) produced a marked and preferential vasodilation of large coronary arteries but had only minor effects on BP and HR. Coronary blood flow (CBF) was unchanged. FK 409 is an orally active vasodilator with a hemodynamic profile similar to that of NTG. FK 409 exhibits a slightly higher selectivity for large epicardial coronary arteries and has a longer duration of action than NTG.

Administration, Oral↗
PubMed1996

Hysteresis in atrial refractoriness in the conscious dog: influence of stimulation parameters and control by the autonomic nervous system.

This work (a) provides evidence for hysteresis in the atrial effective refractory period (AERP) in the conscious dog; (b) studies the main stimulation parameters that may affect this phenomenon; and (c) evaluates the influence of the autonomic nervous system. AERP was measured by the extrastimulus method in the conscious dog with chronic atrioventricular block (n = 6) during the increasing and decreasing phases of an S1S2 fixed protocol. AERP was longer during the increasing phase than during the decreasing phase, thus demonstrating hysteresis, calculated as the difference between the two values. Hysteresis was greater with an S1S1 basic cycle length of 300 ms than with a basic cycle length of 400 ms, 9 +/- 0.9, and 7 +/- 0.9 ms, respectively. It was also greater with trains of six basic cycles before each extrastimulus S2 than with trains of 12 basic cycles, 9 +/- 0.9 and 7 +/- 1.0 ms, respectively. Suppression of vagal tone with atropine reduced hysteresis from 8 +/- 0.6 to 4 +/- 0.6 ms, whereas suppression of cardioaccelerator tone with propranolol increased it from 9 +/- 0.9 to 14 +/- 1.2 ms. These data were confirmed by the neostigmine-induced increase in hysteresis from 8 +/- 0.8 to 11 +/- 0.8 ms and the isoproterenol-induced decrease in hysteresis from 9 +/- 0.6 to 4 +/- 0.4 ms. Overall, these results provide evidence for a hysteresis effect in the AERP in the conscious dog that is stimulation frequency-dependent and modulated by the autonomic nervous system with permanent increase by vagal tone and decrease by cardioaccelerator tone.

Adrenergic beta-Antagonists↗
PubMed1998

Renal vascular responses to angiotensin II in conscious spontaneously hypertensive and normotensive rats.

It has been postulated that exaggerated renal sensitivity to angiotensin II may be involved in the development and maintenance of hypertension in the spontaneously hypertensive rat (SHR). The purpose of this study was to compare the renal vascular responses to short-term angiotensin II infusions (50 ng/kg/min, i.v.) in conscious SHRs and Wistar-Kyoto (WKY) rats. Renal cortical blood flow was measured in conscious rats by using quantitative renal perfusion imaging by magnetic resonance, and blood pressure was measured by an indwelling carotid catheter attached to a digital blood pressure analyzer. Renal vascular responses to angiotensin II were similar in control SHRs and WKY rats. Pretreatment with captopril to block endogenous production of angiotensin II significantly augmented the renal vascular response to exogenous angiotensin II in the SHRs but not in the WKY rats. The renal vascular responses to angiotensin II were significantly greater in captopril-pretreated SHRs than in WKY rats (cortical blood flow decreased by 1.66 +/- 0.13 ml/min/g cortex in WKY rats compared with 2.15 +/- 0.14 ml/min/g cortex in SHR; cortical vascular resistance increased by 10.5 +/- 1.4 mm Hg/ml/min/g cortex in WKY rats compared with 15.6 +/- 1.7 mm Hg/ml/min/g cortex in SHRs). Responses to angiotensin II were completely blocked in both strains by pretreatment with the angiotensin II AT1-receptor antagonist losartan. Results from this study in conscious rats confirm previous findings in anesthetized rats that (a) the short-term pressor and renal vascular responses to angiotensin II are mediated by the AT1 receptor in both SHRs and WKY rats, and (b) the renal vascular responses to angiotensin II are enhanced in SHRs compared with WKY rats when endogenous production of angiotensin II is inhibited by captopril pretreatment.

Angiotensin II↗
PubMed1998

Antiischemic effect of monophosphoryl lipid A in conscious rabbits with hypercholesterolemia and atherosclerosis.

We studied whether monophosphoryl lipid A (MLA), an endotoxin derivative, protected the heart from planned ischemia in hypercholesterolemic conscious rabbits. Normal and hypercholesterolemic (8-week exposure to 1.5% cholesterol-enriched diet) conscious rabbits with right ventricular electrode and left ventricular polyethylene catheters were subjected to ventricular overdrive pacing (VOP: 500 beats/min over 10 min = control VOP). The resulting intracavitary ST-segment elevation, increase in left ventricular end-diastolic pressure (LVEDP), and a reduction of ventricular effective refractory period (VERP) were measured. Three days later the animals were given a single intravenous bolus of 10 or 30 microg/kg MLA or its solvent or both, and a second VOP (test VOP) was applied 24 h later. MLA decreased ST elevation and LVEDP increase from 2.1 +/- 0.16 to 1.27 +/- 0.25 and 0.97 +/- 0.13 mV and 14.6 +/- 1.2 to 11.1 +/- 1.0 and 12.4 +/- 1.2 mm Hg in normal animals and from 2.55 +/- 0.14 to 1.31 +/- 0.12 and 0.96 +/- 0.30 mV and from 21.0 +/- 1.6 to 11.7 +/- 1.3 and 12.4 +/- 1.3 mm Hg in atherosclerotic animals after 10- and 30-microg/kg doses, respectively (p < 0.001 for each). VOP-induced VERP reduction was also significantly alleviated by both MLA doses; nevertheless, 30-microg/kg MLA significantly prolonged resting VERP with a slight VERP reduction in response to pacing in both normal and atherosclerotic animals. We conclude that MLA produces a delayed antiischemic effect in both normal and hypercholesterolemic/atherosclerotic conscious rabbits.

Animals↗
PubMed1999

Effects of antiaggregant and antiinflammatory doses of aspirin on coronary hemodynamics and myocardial reactive hyperemia in conscious dogs.

Clinical studies have shown that low doses of aspirin (<300 mg/day) inhibit thromboxane A2 production and platelet aggregation but preserve prostacyclin synthesis. In contrast, high doses of aspirin (>1,000 mg/day) suppress the synthesis of both eicosanoids. Because the consequences of aspirin administration have never been investigated on coronary vasomotor tone in vivo, we investigated the effects of low and high doses of aspirin on systemic and coronary hemodynamics under basal conditions and after myocardial reactive hyperemia in conscious dogs. Dogs were instrumented with a Doppler flow probe and a hydraulic occluder. Coronary blood flow was measured in the conscious state at baseline and during myocardial reactive hyperemia after 10, 20, and 30 s of coronary occlusion. Thromboxane B2 serum concentrations, an index of platelet aggregation, decreased by >90% after long-term i.v. administration of aspirin, 100 mg/day for 7 days (low dose). Neither systemic and coronary hemodynamics nor reactive hyperemia were affected by the drug. After combined administration of this low dose of aspirin and of the nitric oxide synthase (NOS) inhibitor, N(omega)-nitro-L-arginine (L-NNA, 30 mg/kg/day/7 days), reactive hyperemia decreased to the same extent as when L-NNA was administered alone. After administration of a unique high-dose aspirin (1,000 mg, i.v.), myocardial reactive hyperemia was markedly reduced, and this effect was still observed after previous blockade of NOS and cyclooxygenase by L-NNA and diclofenac, respectively. Thus long-term treatment with a low antiaggregant dose of aspirin does not alter the ability of coronary vessels to dilate during myocardial reactive hyperemia in conscious dogs. In contrast, short-term administration of a high antiinflammatory dose of aspirin severely blunts myocardial reactive hyperemia through a mechanism that is independent of both cyclooxygenase and nitric oxide metabolic pathways.

6-Ketoprostaglandin F1 alpha↗
PubMed2000

Role of NPY Y1 receptors in cardiovascular control in the conscious rabbit.

Prejunctional neuropeptide Y (NPY) Y1 receptors on cardiac sympathetic neurons mediate transient inhibition of chronotropic responses in rabbit isolated right atria. The function of these receptors remains speculative. We investigated a possible functional role for these receptors in modulation of the baroreceptor-heart rate (HR) reflex in the conscious rabbit. Mean arterial pressure (MAP) responses to a range of doses of the Y1 receptor agonist [Leu31,Pro34]NPY (1-8 microg/kg, i.v.) were constructed in ganglion-blocked rabbits. After administration of the selective Y1 receptor antagonist GR231118(150 microg/kg, i.v.), two-point [Leu31,Pro34]NPY dose-pressor responses were assessed. Linear regression analysis of the relation between the shift in the [Leu31,Pro34]NPY dose-pressor response lines against time was used as an estimate of the functional half-life of GR231118. GR231118 shifted the two-point [Leu31,Pro34]NPY dose-pressor response relation by 10- to 30-fold. A single estimate of the functional half-life of a bolus dose of GR231118 was 25 +/- 2 min. This determination allowed a steady-state Y1-receptor blockade to be established by a bolus and infusion. In a separate group of rabbits, the baroreceptor-HR reflex was assessed before and 30 min after administration of GR231118 (150 microg/kg bolus, then 150 microg/ kg/h, i.v.). GR231118 caused an initial transient pressor response and bradycardia, followed by a depressor response and a more sustained tachycardia. Infusion of GR231118 had no effect on the baroreceptor-HR reflex. Prejunctional Y1 receptors appear not to mediate a tonic inhibition of cardiac sympathetic neurotransmission in the conscious rabbit during physiological manipulations in MAP. However, activation of postjunctional Y1 receptors by neuronal or circulating NPY may be important in maintenance of vascular tone in the conscious rabbit.

Animals↗
PubMed2004

Pressor responsiveness to intravenous quinpirole is blunted in malnourished, conscious rats: central vs. peripheral and spinal mechanisms.

In conscious rats, intravenous treatment with the dopamine D2-like receptor agonist quinpirole, elicited a pressor effect, which is attributed to central dopamine D2 receptor-mediated activation of sympathetic outflow associated with arginine vasopressin release. This prominent central effect is opposed to peripheral sympathoinhibitory and spinal depressor effects. The present study investigated the effects of pre- and postnatal undernutrition on the central pressor responsiveness to quinpirole. Malnourished (MalN) rats were obtained by feeding dams a multideficient diet (providing 8% protein) during pregnancy and nursing. At 90 days of age, MalN rats weighed significantly less than control (CNT) rats born to dams fed standard commercially diet (23% protein) during pregnancy and nursing. Baseline mean arterial pressure and heart rate in MalN rats were comparable to those of CNT. Intravenous treatment with quinpirole (0.3 mg/kg) in MalN conscious rats induced a pressor effect, which was significantly reduced in both magnitude and duration, when compared with CNT rats. In both groups studied, pressor response to quinpirole was fully abolished by the peripheral and central dopamine D2 receptor antagonist, metoclopramide (5 mg/kg, i.v.) whereas was significantly enhanced after pretreatment with either intravenous (0.5 mg/kg) or intrathecal (40 microg per rat at T9-T10 level) domperidone, a dopamine D2 receptor antagonist that does not cross the blood-brain barrier. However, even under peripheral and spinal dopamine D2 receptor blockade, maximum pressor effect of quinpirole remained significantly reduced in MalN when compared with CNT rats. Neither the maximum pressor nor the bradycardiac responses to intravenous phenylephrine or arginine vasopressin differed between CNT and MalN rats. This study shows that undernutrition imposed during fetal life and suckling blunted the pressor response to quinpirole in conscious rats. This blunted response appears mainly related to desensitization of brain dopamine D2 receptors rather than enhanced peripheral and/or spinal dopamine D2 receptor-mediated depressor effect or vascular hyporesponsiveness to alpha1-adrenoceptor and vasopressin receptor stimulation.

Animals↗
PubMed1993

Microcirculatory response of the pancreas to feeding, sham feeding, and truncal vagotomy in conscious dogs.

In this study, changes in the microcirculatory dynamics of the pancreas in response to normal feeding, sham feeding, and truncal vagotomy were investigated to elucidate the involvement of a neural mechanism in the physiological modulation of pancreatic blood flow in the conscious state. Continuous measurement of changes in the microcirculation of the pancreas was performed in conscious dogs by the thermoelectric method. A meat meal was given to six normal dogs, seven dogs constructed with external esophagostomy (sham feeding), and four dogs with truncal vagotomy. In response to normal feeding, pancreatic blood flow attained the peak increase of 65.2 +/- 6.2%, showing a significant and biphasic response until approximately 120 min. After sham feeding, pancreatic blood flow was significantly increased with peak values of 89.0 +/- 19.0%, but thereafter showed a rapid decrease, returning to the basal level already at 7.2 +/- 1.1 min. Although truncal vagotomy significantly and greatly reduced the peak increase of pancreatic blood flow to 28.2 +/- 5.1%, blood flow showed still a significant and sustained elevation above basal. This study provides evidence for the involvement of the neural mechanism in the physiological modulation of the microcirculation of the pancreas in the conscious state. The results strongly suggest that the cephalic phase of the increase in pancreatic blood flow is vagally mediated.

Animals↗
PubMed1995

Stimulation of endocrine, but not exocrine, pancreatic secretion during 2-deoxy-D-glucose-induced neuroglycopenia in the conscious pig.

The effects of autonomic nervous activation, initiated by 2-deoxy-D-glucose (2-DG)-induced neuroglycopenia, or endocrine and exocrine pancreatic secretion were investigated in the conscious pig. Pigs were surgically fitted with permanent pancreatic duct and duodenal reentrant cannulas, allowing long-term sampling of pancreatic juice, and a jugular vein catheter for blood sampling and infusion of 2-DG. 2-DG was administered as a 5-min intravenous infusion at three dose levels to conscious pigs. 2-DG (400 mg/kg) was found to elevate plasma glucagon and insulin levels (p < 0.01). In contrast, exocrine pancreatic secretion, measured as volume, total protein output, and output of trypsin activity was not affected by 2-DG at the dose levels of 75, 200, and 400 mg/kg. Secretin (440 pmol/kg/h), however, stimulated pancreatic exocrine output of fluid (p < 0.01), protein (p < 0.01), and trypsin (p < 0.05). It is concluded that autonomic nervous activation by 2-DG-induced neuroglycopenia, in the conscious pig under basal conditions, elevates the plasma levels of glucagon and insulin but does not affect exocrine pancreatic secretion. 2-DG-induced neuroglycopenia is, thus, a suitable model for studying autonomic neural influences on the porcine endocrine pancreas.

Animals↗
PubMed1995

Conscious sedation in the pediatric emergency department.

Anxiety-provoking and painful emergency department procedures such as laceration repair are made more tolerable to the pediatric patient and easier for the practitioner through the judicious use of pharmacologic agents for conscious sedation and analgesia. Both the American Academy of Pediatrics and the American College of Emergency Physicians have published documents that guide the physician in the use of these agents in the care of children. Most new information concerns the evaluation of new drugs for use in the pediatric emergency department, adverse effects of familiar products, and evaluation of sedative and analgesic antagonist medications that may increase a practitioner's control when conscious sedation is used. Large controlled trials of protocols and drugs are necessary to establish safe, appropriate standards for conscious sedation in the pediatric emergency department.

Administration, Oral↗
PubMed2006

Comparison between the effects on hemodynamic responses of central and peripheral infusions of hypertonic NaCl during hemorrhage in conscious and isoflurane-anesthetized sheep.

The i.v. infusion of hypertonic NaCl solutions, as in small volume hypertonic NaCl resuscitation, improves cardiovascular function in hypovolemic shock. The mechanism(s) of action of this treatment is(are) not fully elucidated. In this study, we investigate the possible importance of fully functional neurocardiovascular regulation for the effect of intracerebroventricular (i.c.v.) and i.v. administration of hypertonic NaCl on the hemodynamic responses to hemorrhage. Six groups (each n = 6) of adult ewes were subjected to hypotensive hemorrhage during treatment with i.c.v. infusion (20 microL/min) of either artificial cerebrospinal fluid (controls) or 0.5 mol/L NaCl, or i.v. infusion of 1.2 mol/L NaCl (4 mL/kg) when conscious, respectively anesthetized with isoflurane. Thirty minutes into infusion, treatment blood was withdrawn at 0.7 mL/kg per minute from a jugular vein until the mean arterial pressure dropped to a value just below 50 mmHg. In conscious animals, the amount of blood loss needed to lower the mean arterial pressure to less than 50 mmHg was increased by the i.c.v. and i.v. infusions of hypertonic NaCl (24.0 +/- 4.6 and 22.4 +/- 3.3 mL/kg, respectively), compared with controls receiving i.c.v. infusion of artificial cerebrospinal fluid (14.2 +/- 1.4 mL/kg). Isoflurane anesthesia, as such, severely compromised the cardiovascular compensatory mechanisms activated by hemorrhage and reduced the blood loss necessary to cause hypotension (10.2 +/- 2.5 mL/kg). Furthermore, anesthesia totally abolished the effect of i.c.v. hypertonic NaCl (10.4 +/- 2.2 mL/kg) and blunted the response to i.v. hypertonic NaCl (15.9 +/- 2.1 mL/kg) seen in conscious animals. The results show that an intact autonomic cardiovascular control is crucial for the effect of i.c.v. hypertonic saline and indicate that i.v. hypertonic saline exerts some of its action through the central nervous system.

Anesthetics, Inhalation↗
PubMedDate not supplied

Postmodern personhood: a matter of consciousness.

The concept of person is integral to bioethical discourse because persons are the proper subject of the moral domain. Nevertheless, the concept of person has played no role in the prevailing formulation of human death because of a purported lack of consensus concerning the essential attributes of a person. Beginning with John Locke's fundamental proposition that person is a 'forensic term', I argue that in Western society we do have a consensus on at least one necessary condition for personhood, and that is the capacity for conscious experience. When we consider the whole brain formulation of death, and the most prominent defense of it by the President's Commission for the Study of Ethical Problems in Medicine and Biomedical and Behavioral Research, we can readily identify the flaws that grow out of the failure to define human death as the permanent loss of the capacity for conscious experience. Most fundamental among these flaws is a definition of human death that reduces persons to the capacity of the brain to regulate purely physiological functioning. Such a formulation would, in theory, apply to any member of the animal kingdom. I suggest that an appropriate concept of death should capture what it is about a particular living being that is so essential to it that the permanent loss of that thing constitutes death. What is essential to being a human being is living the life of a person, which derives from the capacity for conscious experience.

Advisory Committees↗
PubMed1996

Remote controlled prolonged conscious sedation for gynaecological radiotherapy.

Conscious sedation with subanaesthetic doses of propofol is an effective technique for the management of highly anxious patients in dentistry. Prolonged administration of propofol to achieve conscious sedation in spontaneously breathing patients without an airway adjunct has not been reported previously. We describe the management of target-controlled conscious sedation with propofol for 21 h in a patient undergoing gynaecological radiotherapy.

Anesthetics, Intravenous↗