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Activation of the amygdala in rats produces cardiovascular changes that include increases in heart rate and arterial pressure as well as behavioral changes characteristic of emotional arousal. The objective of the present study was to examine the interaction of GABA and excitatory amino acid (EAA) receptors in the basolateral amygdala (BLA) in regulating cardiovascular function. Microinjection of the GABAA receptor antagonist bicuculline methiodide (BMI) or the E A A receptor agonists NMDA or AMPA into the same region of the BLA of conscious rats produced dose-related increases in heart rate and arterial pressure. Injection of the nonselective EAA receptor antagonist kynurenic acid into the BLA prevented or reversed the cardiovascular changes caused by local injection of BMI or the noncompetitive GABA antagonist picrotoxin. Conversely, local pretreatment with the glutamate reuptake inhibitor L-trans-pyrrolidine-2,4-dicarboxylic acid enhanced the effects of intra-amygdalar injection of BMI. The cardiovascular effects of BMI were also attenuated by injection of either the NMDA antagonist 3-(2-carboxypiperazin-4-yl)-propyl-1-phosphonic acid (CPP) or the AMPA receptor antagonist 1,2,3,4-tetrahydro-6-nitro-2, 3-dioxo-benzo[f]quinoxaline-7-sulfonamide (NBQX). When these two EAA receptor antagonists were combined, their ability to suppress BMI-induced tachycardic and pressor responses was additive. These findings indicate that the cardiovascular effects caused by blockade of GABAergic inhibition in the BLA of the rat are dependent on activation of local NMDA and AMPA receptors.

This study evaluated the effect of preoperative sleep on the success of conscious sedation. Seventy-six children, from 18 to 61 months of age, participated in this study. Sixty-two children received chloral hydrate (50-60 mg/kg) and hydroxyzine (15-35 mg) and 14 children received intramuscular meperidine hydrochloride (2.2 mg/kg). Parents were asked to complete a questionnaire which asked several questions about their child's activity the previous day, and their bedtime. The operator ranked the sedations on a scale of 1 to 4, with 1 being good and 4 being poor. The results were statistically evaluated using the Wilcoxon Rank sum test. The children that received a normal amount or greater amount of sleep preoperatively did not show any significantly higher degree of success (p < 0.26) with their sedation appointment. The parents' perception of their child's tiredness did demonstrate borderline (p < 0.08) significance. Children greater than 36 months of age had a significantly higher (p < 0.03) degree of successful sedations. The results of this study demonstrated that there was no clear correlation between the child's preoperative sleep and the outcome of the sedation, but that a tired child may increase the likelihood of a poor sedation. In addition, the child's age at the time of the sedation may affect the outcome of the sedation.

Objective: To propose clonazepam for use in the empiric treatment of shooting/shocking phantom limb pain., Setting: Outpatient pain clinic associated with a university hospital., Patients: Two patients with phantom limb pain after total hip disarticulation., Interventions: Treatment with clonazepam., Results and Conclusions: Clonazepam provided effective relief for > 6 months in two patients with shooting/shocking phantom limb pain. Although clonazepam therapy is not new, it appears to have been omitted from current pain texts and journals as a treatment option for phantom limb pain.

Some dental professionals may have concerns about treating patients who have seizure disorders. The authors contend that increased knowledge about seizures and how to manage them may make dental professionals more comfortable. This article reviews the various seizure types, discusses commonly used anticonvulsants and their side effects and outlines some special concerns dentists may have in providing care to these patients.

Health care professionals often inappropriately separate dental health from other health functions. Baby bottle tooth decay (BBTD) should be a concern for all professionals who work with expectant or new mothers and very young children. Research indicates that even though many mothers are aware of the etiology of the condition, they continue to allow prolonged nursing with milk or liquids other than water. Nurses can help promote good oral health for children by educating and training expectant and new mothers, children, and others who work with mothers and children in preventing BBTD.

This study evaluated the effect of preoperative sleep on the success of conscious sedation. Thirty healthy children between the ages of 18 and 61 months of age were utilized in this study. The children all received chloral hydrate (50-60 mg/kg) and hydroxyzine (15-25 mg) and nitrous oxide (30-50%). Parents were asked to complete a questionnaire which asked several questions about their child's activity the previous day, their diet, and questions that related to their bedtime. The operator ranked the sedations on a scale from 1 to 4 with 1 being good and 4 being poor. The results were then statistically evaluated using the non-parametric Mann-Whitney and Kruskal-Walls tests. The children that received a normal amount of sleep or greater amount of sleep preoperatively had a borderline (P = .06) higher degree of successful sedation. There was no correlation between the child's bedtime (early, normal, late) and the success of sedation. The parent's perception of their child's tiredness could not be correlated with the success of the sedation. The children greater than 36 months of age had a significantly (P = .02) higher degree of successful sedations. The results suggest that a well rested child may experience a more pleasant dental sedation while under chloral hydrate and hydroxyzine conscious sedation and that the child's age at the time of the sedation may affect the outcome of the sedation.

In recent years, the burgeoning disciplines of health psychology and behavioral medicine have renewed interest in the important role that environmental factors can play in the disease process. Nowhere is this concern more well-founded than in the area of cardiovascular disorders, particularly hypertension. Epidemiologists and clinicians have long suspected that stressful life events can be a sufficient trigger for the expression of hypertension in some individuals. To understand better the ways in which these variables interact in the disease process, researchers have tried, with limited success, to produce experimental hypertension in animals by exposing them to stressful environmental paradigms. Additionally, recent investigations using the borderline hypertensive rat (BHR) have demonstrated the important role genetic factors can play in mediating both the behavioral and cardiovascular responses to environmental stressors. The current paper will review these attempts and discuss recent data from experiments using a relatively new animal model that appears to be especially appropriate for the study of environmental-genetic factors in the elaboration of essential hypertension. We will also discuss potential mechanisms by which environmental stress influences arterial pressure and suggest avenues for further inquiry into the stress-disease relationship.

Significant oral health problems are associated with medical, physical, or mental disorders that occur in children. The pediatrician has the opportunity through early intervention to set the tone for a health care practice that will improve the quality of life for many disadvantaged children. When the pediatrician and pediatric dentist work hand in hand, the children can often expect a happy, healthy future.

A number of previous studies have demonstrated that some aspect of baroreflex function is altered as hypertension develops. However, no studies have determined whether a chronic stressor can alter baroreflex function in the resting state. In the present study, male borderline hypertensive rats (BHR) were divided into three groups: control, stressed daily for 5 weeks, and stressed daily for 11 weeks. At the appropriate time, 7 different dosages of angiotensin II (AII) were given intravenously as a bolus injection. Heart rate (interbeat interval, or IBI) and mean arterial pressure were tracked for 90 subsequent beats. For each group, intercorrelations between pressure and IBI were obtained. In addition, overall means of pressure and IBI for each dosage were computed for each group and plotted. Higher dosages of AII were required to produce a significant correlation between pressure and IBI in the 5-week group compared to control. In the 11-week group, only the highest dosage yielded a significant correlation between pressure and IBI. When data were expressed in terms of the highest pressure and its corresponding IBI for each group, the 5-week-stress group had a shift in set point compared to control. The 11-week group showed a shift in set point and a reduction in gain compared to control animals. The similarity between these findings and those for other models of hypertension is discussed, with special emphasis on the potential role of the central nervous system.

The borderline hypertensive rat (BHR) develops severe hypertension when chronically subjected to either a high salt diet or behavioral stress. Previous research has shown that daily exercise can attenuate the development of stress-induced hypertension in the BHR. The current study sought to determine whether exercise might also exert a similar protective effect on salt-induced hypertension. Two groups of BHR were placed on a high salt diet for 20 weeks; one of the groups also engaged in daily swim training for the entire 20 week period. A third group of BHR served as maturation controls. At the end of the experimental period, direct measurement of heart rate in conscious subjects revealed a significant resting bradycardia in the trained group on a high salt diet but no significant group differences with respect to blood pressure level. Cardiovascular responses to an episode of acute stress revealed that BHR are capable of elevating pressure in response to a novel stressor after swim training. These observations suggest that exercise may be an environmental intervention capable of increasing cardiovascular responses to acute stressors.

The effect of maternal strain on reactivity to acute stress was studied in F1 reciprocals produced by crossing the spontaneously hypertensive rat (SHR) with its normotensive progenitor, the Wistar-Kyoto (WKY). This F1 generation, known as the borderline hypertensive rat (BHR), is genetically predisposed to develop hypertension in response to chronic stress or high dietary sodium. Reciprocals, considered to be genetically equivalent aside from sex-linked traits, differ in strain of dam during intrauterine and preweanling development. At 17 weeks of age, reciprocal F1 males did not differ in open-field behavior (squares crossed, rearings, and defecation measured over 3 days in 15-min sessions) or in home-cage measurements of mean arterial pressure (MAP) and heart rate (HR). However, different patterns of cardiovascular reactivity were displayed to transfer and footshock. While WKY-mothered rats reacted with graded pressor responses, SHR-mothered rats responded maximally to transfer, showed no additional increase to footshock, and maintained peak responding after footshock was terminated. Such reactivity differences may mediate the impact of environmental variables on the genetic disposition to hypertension.

The borderline hypertensive rat (BHR) is a first-generation cross between the spontaneously hypertensive rat and the normotensive Wistar-Kyoto rat. The BHR develops frank hypertension when chronically stressed or when fed a high-sodium diet. Stress-induced hypertension can be blocked by exercise. The role of the central nervous system and kidney in hypertension development in this model is discussed.

The borderline hypertensive rat (BHR) shows large blood pressure responses to either stress or a high salt diet. Since the renal nerves have been shown to play a role in several animal models of hypertension, the current study sought to determine the effect of bilateral renal denervation on the development of stress-induced hypertension in the BHR. BHR were deprived of renal nerves under ether anesthesia after either 5 or 11 weeks of daily 2-hour stress sessions. Additional BHR received sham surgery. Unstressed BHR, age-matched to stressed groups, received denervation or sham surgery. Following a 3 week recovery period, the protocol (stress or no stress) was continued for 10 additional weeks. Tail cuff systolic blood pressures were obtained weekly. BHR stressed for 5 weeks prior to denervation failed to develop hypertension in response to continued stress. Although BHR stressed for 11 weeks prior to denervation showed a temporary reduction in pressure following denervation, blood pressure returned to the hypertensive levels of sham-operated controls after several weeks. Thus, there may be a critical period during which the renal nerves are necessary for the expression of stress-induced hypertension in the BHR. These observations are discussed in relation to the effects of renal denervation on hypertension in various animal models.

Palytoxin (PTX) inhibited phasic tension production and initiated tonic contracture in isolated paced ventricle strips at concentrations greater than 10(-10) M. PTX-induced contracture was associated with increased 45Ca2+ uptake. PTX-induced additional 45Ca2+ uptake was completely blocked by 2 mM La3+. All observed PTX effects were enhanced by elevation of [Ca2+] o from 1.9 to 6 mM and this threefold increase in [Ca2+] o resulted in a threefold increase in isotope-determined Ca2+ uptake in presence of 10(-8) M PTX. It is concluded that the observed effects of PTX could be mediated by an increase in calcium permeability of myocardial cells.

Blood pressure and heart rate responses of the spontaneously hypertensive rat (SHR) and the Wistar-Kyoto rat (WKY) to mild restraint and tone-shock pairings were compared during a pre-stress, aversive conditioning and post-stress period, after five previous days of exposure to the paradigm. Although SHR and WKY showed similar responses to the onset of the pre-stress period, SHR showed significantly larger blood pressure responses following the onset of the conditioning than WKY. Furthermore, WKY showed a significant blood pressure and heart rate reduction during the conditioning session which was absent in the SHR. During the post-stress period, the blood pressure of SHR remained significantly elevated compared to their home cage rest values, but the blood pressure of WKY returned to basal levels. It is concluded that while the SHR is more reactive than the WKY to stimulus onset, the major source of between-strain differences after 20 min relates to differences in adaptation to continued environmental stimulation. This can lead to exaggerated estimates of physiological reactivity of the SHR, and is supportive of Folkow's view that SHR are both hyperreactive and show more prolonged defense reactions.

Studies from this laboratory have shown that the first filial offspring of female spontaneously-hypertensive rats and male Wistar-Kyoto (WKY) normotensive rats develop stress-induced hypertension. The present study sought to examine the effects of intracerebroventricular administration of clonidine (8 micrograms) on cardiovascular and sympathoadrenal responses to aversive classical conditioning in these borderline hypertensive rats (BHR) and in normotensive WKY control rats. Clonidine caused significant reductions in resting arterial pressure, vascular resistance, heart rate and concentrations of epinephrine (E) in plasma for both hypertensive and normotensive rats. Central administration of normal saline to control rats of each strain did not alter basal cardiovascular or sympathoadrenal function. The presentation of a conditioned stimulus (CS) elicited a significant increase in arterial pressure and total peripheral resistance in hypertensive rats treated with saline and clonidine and in normotensive rats treated with saline. In contrast, normotensive rats treated with clonidine showed no increases in arterial pressure or vascular resistance following the onset of the conditioned stimulus. The aversive conditioning session instigated significant increases in the concentrations of norepinephrine (NE) and E in plasma in saline-treated rats. Hypertensive and normotensive rats treated with clonidine-showed a blunted increase in plasma concentrations of NE and E during this period; however, concentrations of E in hypertensive rats increased significantly from the baseline period after injection. These data suggest that an abnormality in central alpha 2-adrenoceptor-mediated inhibition of sympathoadrenal discharge and sympathetic vasomotor tone may predispose the hypertensive rat to develop stress-induced hypertension.