The stability and interrelationships of newborn sucking and heart rate

Lipsitt, Lewis P.; Reilly, Bernice M.; Butcher, Marian J.; Greenwood, Martha M.

doi:10.1002/dev.420090402

Cited by 60 publications

(24 citation statements)

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“…More generally, heart rate increases have been associated with appetitive responding for rewarding objects or events (Fowles 1980(Fowles , 1988. These effects have been reported with monetary incentives (Fowles et al 1982), responding for sucrose in neonates (Ashmead et al 1980;Lipsitt et al 1976), and the pharmacological effects of a variety of psychostimulant drugs (Pihl et al 1995;Wise 1988).One model for how this appetitive arousal model of heart rate increases is involved in alcohol reward involves the interaction of the opioid and dopamine neurotransmitter pathways. Specifically, acute alcohol administration increases beta-endorphin levels (Gianoulakis 1990), which in turn increase dopamine release (Spanagel et al 1991).…”

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confidence: 99%

Naltrexone Dampens Ethanol-Induced Cardiovascular and Hypothalamic- Pituitary-Adrenal Axis Activation

McCaul

2001

Neuropsychopharmacology

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Alcohol ingestion activates the autonomic nervous system and the hypothalamic-pituitary-adrenal axis. This study examined naltrexone effects on alcohol-induced increases in physiological responses and their association with alcohol liking. Using a within-subjects design, heavy drinking men (N ϭ 19) were maintained on each of three naltrexone doses (0, 50, and 100 mg, p.o.) over an 8-day inpatient stay. Within each naltrexone dose, subjects had three alcohol challenge sessions (none, moderate, high) The brain opioid system has been proposed to be part of the neurocircuitry involved in alcohol reward and heavy alcohol drinking (Froehlich and Wand 1997;Gianoulakis and deWaele 1994;Reid et al. 1991). Pharmacological studies indicate that opioid receptor antagonists, such as naloxone hydrochloride and naltrexone, decrease alcohol self-administration in animal models (Altshuler et al. 1980;Froehlich et al. 1990;Hubbell et al. 1986Hubbell et al. , 1991Marfaing-Jallat et al. 1983;Samson and Doyle 1985;Weiss et al. 1990). Clinical trials demonstrated that naltrexone reduces alcohol drinking and self-reported "high," alcohol craving, as well as relapse rates in recently abstinent outpatient alcohol-dependent patients (O'Malley et al. 1992;Volpicelli et al. 1992Volpicelli et al. , 1995 . These findings led to naltrexone's approval by the Food and Drug Administration as a pharmacotherapeutic agent for the treatment of alcohol dependence. Naltrexone is thought to reduce alcohol-induced high and relapse by binding to opioid receptors in discrete brain regions associated with reward and craving, and to prevent receptor activation by alcohol-induced release of endogenous opioid peptides.Alcohol induces a variety of acute physiological responses when consumed in moderate-to-high doses. It is well established that intoxicating doses of alcohol increase heart rate (Docter et al. 1966;Iwase et al. 1995 McCaul et al. 1989;Sellers et al. 1972;Turkkan et al. 1988;van de Borne et al. 1997). These heart rate increases are hypothesized to be positively associated with the reinforcing or appetitive motivational effects of alcohol (Peterson et al. 1996) . Alcohol has less predictable effects on blood pressure, with reports of blood pressure increases (Iwase et al. 1995;Sellers et al. 1972) and no effects following alcohol ingestion (Turkkan et al. 1988;van de Borne et al. 1997). Finally, alcoholinduced peripheral vasodilation and associated skin temperature increases have been consistently reported (Iwase et al. 1995;Turkkan et al. 1988) and is thought to be one explanation for the lack of a consistent rise in blood pressure after alcohol consumption.Acute administration of intoxicating doses of alcohol also activates the hypothalamic-pituitary-adrenal (HPA) axis thereby increasing ACTH and glucocorticoid levels (Inder et al. 1995;Rivier et al. 1984;Waltman et al. 1993). It remains unclear whether alcohol-induced activation of the HPA axis has any relationship to its reinforcing properties. Rodent studies show that alcohol increases pla...

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confidence: 99%

Naltrexone Dampens Ethanol-Induced Cardiovascular and Hypothalamic- Pituitary-Adrenal Axis Activation

McCaul

2001

Neuropsychopharmacology

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“…The reproducibility of these tests is reported elsewhere. 11,13 In the salt taste test, 3 solutions were used to assess neonatal salt taste responsiveness: water, 0.1 molar (mol/L) NaCl, and 0.3 mol/L NaCl. After a 1-minute baseline period, the nipple was inserted and taste stimuli were presented in the following order (as seen in Table 1): 2 water trials (trials 1 and 2); 2 NaCl trials (trials 3 and 4); 2 water trials (trials 5 and 6); 2 NaCl trials (trials 7 and 8); and 2 final water trials (trials 9 and 10).…”

Section: Methodsmentioning

confidence: 99%

“…After a 20-minute wait, 270 neonates also were given a sucrose taste test with water, 5% and 15% solutions in this order 11,12 but with a contingent-reinforcement procedure in which the infant's sucking behavior triggered the pump. Because babies actually receive the water or sucrose solutions during these tests (obviously not possible for 0.3 mol/L NaCl), this procedure results in more vigorous sucking (Table 1).…”

Section: Methodsmentioning

confidence: 99%

“…Sucrose taste responses were analyzed by using difference scores (MSB for sucrose minus MSB for water) in sucking responsiveness between two sucrose solutions and water; newborns typically produce more sucks for sucrose than for water. 11,14 Neonatal blood pressure was measured 2 to 4 days after birth in the hospital, along with length, weight, and several skinfold thicknesses. Blood pressure was recorded at a separate session from the taste testing and was measured with a Physiometrics ultrasonic device, with the use of appropriately sized upper arm cuffs.…”

Section: Methodsmentioning

confidence: 99%

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Neonatal Blood Pressure and Salt Taste Responsiveness

et al. 2002

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Abstract-To test the association between neonatal blood pressure (BP) and salt taste response, 283 healthy hospitalized neonates were administered small drops (0.06 mL) of water and 0.1 molar (mol/L) and 0.3 mol/L NaCl solutions by means of cannulas through a nipple with a pressure transducer to record sucking responses. Neonatal and 1-month BPs were recorded by ultrasound. Mean number of sucks per burst was scored as "aversive" if the 0.3 mol/L salt minus water difference score was ՅϪ10 mean sucks per burst, "preferential" if this difference was Ͼ0, and "neutral" otherwise.Babies with "preferential" responses had higher diastolic BPs than those with neutral (1.9 mm Hg) or aversive responses (3.1 mm Hg) (P trendϭ0.05). After adjustment for age, gender, birth weight, and activity for babies with at least one grandparent receiving antihypertensive medication, mean adjusted systolic pressure was 6.7 mm Hg higher (Pϭ0.003) (P trendϭ0.003) and mean adjusted diastolic pressure was 5.0 mm Hg higher (Pϭ0.010) (P trendϭ0. T he underlying cause of essential hypertension is unclear, but it is likely that the many factors leading to the common outcome of persistent elevation of blood pressure are represented by different subtypes within a given population. One important subtype is sodium or salt-sensitive hypertension, 1,2 which may have strong genetic or familial components. 3 If an appropriate measure of sodium/salt sensitivity were available early in life as a risk factor for hypertension, it might be possible to detect susceptible individuals and intervene in a timely way.Numerous studies have demonstrated that infant blood pressures aggregate in families and are predictive of later blood pressures. 4 -9 Since the processes responsible for essential hypertension operate before clinical detection, it is reasonable to search for predictors of essential hypertension in infants.This report concerns the relation of neonatal salt taste responsiveness and infant blood pressure. It is possible that early life exposure to NaCl could have developmental effects on salt taste preference and subsequently on blood pressure.We present the details of a study of the association between neonatal blood pressure and salt taste responsiveness in a sample of infants and in subgroups categorized by family history of hypertension.

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“…In cardiovascular psychophysiology this idea is reflected by the hypothesis that cardiovascular responses are a direct function of reward value: the more valuable a reward, the higher the cardiovascular response (e.g., Belanger & Feldman, 1962;Brenner, Beauchaine, & Sylvers, 2005;Elliot, 1969;Fowles, 1983;Lipsitt, Reilly, Butcher, & Greenwood, 1976;Tranel, 1983;Smith, Allred, Morrison, & Carlson, 1989;Smith, Nealey, Kircher, & Limon, 1997;Smith, Ruiz, & Uchino, 2000).…”

Section: Manipulation Checks and Cardiac Reactivitymentioning

confidence: 99%

Pay attention to your manipulation checks! Reward impact on cardiac reactivity is moderated by task context

Richter

2010

Biological Psychology

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Two experiments assessed the moderating impact of task context on the relationship between reward and cardiovascular response. Randomly assigned to the cells of a 2 (task context: reward vs. demand) x 2 (reward value: low vs. high) between-persons design, participants performed either a memory task with an unclear performance standard (Experiment 1) or a visual scanning task with an unfixed performance standard (Experiment 2). Before performing the task-where participants could earn either a low or a high reward-participants responded to questions about either task reward or task demand. In accordance with the theoretical predictions derived from Wright's (1996) integrative model, reactivity of pre-ejection period increased with reward value if participants had rated aspects of task reward before performing the task. If they had rated task demand, pre-ejection period did not differ as a function of reward. MANIPULATION CHECKS AND CARDIAC REACTIVITY 4Pay Attention to Your Manipulation Checks! Reward Impact on Cardiac Reactivity is Moderated by Task Context.Common sense suggests that the more you desire something the harder you will work to get it. In cardiovascular psychophysiology this idea is reflected by the hypothesis that cardiovascular responses are a direct function of reward value: the more valuable a reward, the higher the cardiovascular response (e.g., Belanger & Feldman, 1962;Brenner, Beauchaine, & Sylvers, 2005;Elliot, 1969;Fowles, 1983;Lipsitt, Reilly, Butcher, & Greenwood, 1976;Tranel, 1983;Smith, Allred, Morrison, & Carlson, 1989;Smith, Nealey, Kircher, & Limon, 1997;Smith, Ruiz, & Uchino, 2000).Drawing on an analysis by Wright (1996), , 2009

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The stability and interrelationships of newborn sucking and heart rate

Cited by 60 publications

References 3 publications

Naltrexone Dampens Ethanol-Induced Cardiovascular and Hypothalamic- Pituitary-Adrenal Axis Activation

Naltrexone Dampens Ethanol-Induced Cardiovascular and Hypothalamic- Pituitary-Adrenal Axis Activation

Neonatal Blood Pressure and Salt Taste Responsiveness

Pay attention to your manipulation checks! Reward impact on cardiac reactivity is moderated by task context

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