The diving reflex in infants: a preliminary report.
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Age Factors↗
Biomedical subjects
J A McCubbin
Publications and source records attributed to J A McCubbin.
Classically conditioned hyperglycemia in the obese mouse.
The obese (C57BL/6J ob/ob) mouse is a commonly used animal model of non-insulin-dependent diabetes mellitus. It has recently been demonstrated that this mouse is not consistently hyperglycemic, however, unless it is subjected to environmental stress. In the present study, hyperglycemia in obese mice was induced by classical conditioning. Obese diabetic mice and lean control animals were exposed to shaking stress. All animals developed hyperglycemia in response to shaking. To demonstrate classical conditioning, some obese and lean animals were exposed to a metronome prior to and during the shaking. Other animals were exposed to the metronome and shaking in a noncontingent fashion and one group of animals was exposed to the metronome without any exposure to shaking. All animals received seven exposures to one of the three above conditions over a 3-day period. On the 4th day all animals were exposed to the metronome alone, following which blood samples were drawn. Classical conditioning of stress hyperglycemia was demonstrated in obese, but not in lean, mice.
Animals↗
Alprazolam reduces stress hyperglycemia in ob/ob mice.
We have shown that the C57BL/6J ob/ob (obese) mouse, a commonly used model of type II diabetes mellitus, is not in fact consistently hyperglycemic except when exposed to environmental stress. In an attempt to modify stress hyperglycemia in this animal, we administered either a 5 mg/kg dose of the benzodiazepine alprazolam or vehicle (propylene glycol) intraperitoneally to both obese mice and their lean littermates prior to a rest and a stress period. Alprazolam modified the hyperglycemic effect of stress only in the obese mice. Alprazolam significantly reduced plasma corticosterone in obese animals at rest and following stress. In addition, alprazolam significantly increased plasma insulin in all animals at rest and following stress. These data suggest a possible role for benzodiazepines in the modification of stress hyperglycemia in type II diabetes mellitus.
Alprazolam↗
Opioid dysfunction and risk for hypertension: naloxone and blood pressure responses during different types of stress.
Opioidergic inhibition of sympathetic nervous system responses may be deficient in persons at risk for essential hypertension (McCubbin et al: Hypertension 7:808, 1985). The opiate antagonist naloxone increases blood pressure responses during psychological stress in young adults with low causal blood pressure, but has no pressor effect in subjects with high casual blood pressure. The purpose of the present study was to determine the role of altered baroreflex function in the abnormal pressor effect of naloxone in persons at risk for hypertension development. We tested this by comparison of the effects of naloxone on responses to psychological stress with responses to orthostatic stress in persons with high and low casual blood pressure. The results suggest that abnormal opioidergic control of systolic blood pressure responses to psychological stress is not likely a result of altered baroreflex function. Persons at risk for hypertension show evidence of an opioid peptide lesion that can probably be localized either at the adrenal medullae or at levels of central autonomic control that are parallel with or rostral to baroreflex circuits.
Adolescent↗
Naltrexone potentiates glycemic responses during stress and epinephrine challenge in genetically obese mice.
The genetically obese mouse (C57BL/6J ob/ob) is a commonly used animal model of non-insulin-dependent diabetes mellitus. These mice show exaggerated glycemic responses during behavioral stress and adrenergic stimulation, but the precise glucoregulatory mechanisms are not well characterized. The ob/ob mice have multiple endocrine abnormalities, including elevated pituitary and circulating beta-endorphin levels; and a relationship between hyperglycemia and altered opioid function has been suspected. We now report that opiate antagonism with naltrexone potentiates hyperglycemic responses during stress and epinephrine challenge in obese mice. This effect of opioid blockade suggests that endogenous opioids inhibit stress- and epinephrine-induced hyperglycemia in the genetically obese mouse.
Animals↗
Gender effects on blood pressures obtained during an on-campus screening.
In a blood pressure screening of 167 male and female college students, we varied the gender of the screener to evaluate gender effects on blood pressure. Four repeated determinations of resting systolic and diastolic blood pressure were obtained with an automated oscillometric device in a quiet semi-darkened room. Analysis of systolic blood pressure indicated a significant interaction between screener gender, subject gender, and repeated determinations. Screener/subject gender concordance produced relatively stable systolic blood pressures across four repeated determinations. Gender discordance resulted in larger changes in systolic pressures across the four determinations. This pattern was not obtained with diastolic pressures. Measures of recent stress and somatic anxiety interacted with gender effects on blood pressure. These gender effects on systolic blood pressure may explain, in part, higher reported incidence of "white coat hypertension" in females.
Adolescent↗
Opioidergic inhibition of circulatory and endocrine stress responses in cynomolgus monkeys: a preliminary study.
Twenty-five female cynomolgus monkeys (Macaca fascicularis) were exposed to psychological stress (threat of capture) after blockade of endogenous opioids with naloxone and after saline control injections. Heart rates were monitored continuously and blood samples were obtained for determination of plasma levels of cortisol and beta-endorphin-like immunoreactivity. Results indicate that the stress manipulation resulted in increased heart rates as well as plasma cortisol levels in monkeys pretreated with saline. Blockade of opioid receptors with naloxone potentiated the stress-induced rise in plasma cortisol and stimulated release of beta-endorphin-like immunoreactivity. The drug effect on heart rate reactivity was significantly correlated with the drug effects on both cortisol and beta-endorphin. When saline-treated monkeys were divided into high and low heart rate reactivity groups, the effects of naloxone on heart rate, cortisol, and beta-endorphin-like immunoreactivity responsiveness were significantly greater in low heart rate reactors. These data suggest that monkeys with low heart rate responses to stress have an effective opioidergic inhibition of circulatory and pituitary-adrenocortical reactivity. Monkeys showing excessive heart rate reactivity during psychological stress have a less active opioidergic inhibitory mechanism. The potential pathophysiological consequences of impaired opioidergic inhibition are discussed in light of the relationship between exaggerated stress reactivity and atherosclerotic lesion formation.
Animals↗
Endogenous opioids inhibit ambulatory blood pressure during naturally occurring stress.
OBJECTIVE: Laboratory experiments suggest that endogenous opioids inhibit blood pressure responses during psychological stress. Moreover, there seem to be considerable individual differences in the efficacy of opioid blood pressure inhibition, and these differences may be involved in the expression of risk for cardiovascular disease. To further evaluate the possible role of opioid mechanisms in cardiovascular control, the present study sought to document the effects of the long-lasting oral opioid antagonist naltrexone (ReVia, DuPont, Wilmington, DE) on ambulatory blood pressure responses during naturally occurring stress. METHOD: Thirty male volunteers participated in a laboratory stress study using naltrexone followed by ambulatory blood pressure under placebo and during the subsequent 24-hour period. Within-subject analyses were performed on ambulatory blood pressures under placebo and naltrexone conditions. RESULTS: Laboratory results indicate no significant group effects of naltrexone on blood pressure levels or reactivity. Ambulatory results indicate that during periods of low self-reported stress, no effect of opioid blockade was apparent. In contrast, during periods of high stress, opioid blockade increased ambulatory blood pressure. CONCLUSIONS: These findings suggest that naltrexone-sensitive opioid mechanisms inhibit ambulatory blood pressure responses during naturally occurring stress.
Adolescent↗
Endogenous opiate peptides, stress reactivity, and risk for hypertension.
Endogenous opiate peptides can regulate neuroendocrine and circulatory responses to behavioral stress and may be important in the pathogenic effects of sympathoadrenal reactivity. We tested this hypothesis by examining the effect of the opiate antagonist naloxone on blood pressure responses to behavioral stress in young adults with high, medium, or low casual blood pressures. Naloxone increased mean arterial pressure responses to stress in subjects with low casual pressure, but had no significant effect on responses in subjects with high casual pressure. These results suggest opioidergic inhibition of sympathetic nervous system responses may be deficient in persons at risk for essential hypertension.
Adolescent↗