Biomedical subjects

C E Wood

Publications and source records attributed to C E Wood.

At least 19 recordsLinked to original sources

PubMed1992

Reflex control of fetal arterial pressure and hormonal responses to slow hemorrhage.

Late-gestation fetal sheep respond to slow hemorrhage with increases in plasma concentrations of adrenocorticotropic hormone (ACTH), hydrocortisone, arginine vasopressin (AVP), and plasma renin activity (PRA) that correlate to the acidemia and hypercapnia also produced by hemorrhage. This study was designed to investigate the role of peripheral chemoreceptors in the mediation of these responses. Chronically catheterized fetal sheep were left intact or were subjected to bilateral section of cervical vagosympathetic trunks and carotid sinus nerves. At least 5 days after surgical preparation (between 121 and 138 days of gestation) fetuses were bled at a rate of 11 ml/10 min for 2 h. Denervated fetuses were studied with or without simultaneous infusion of phenylephrine. Denervation exaggerated the decrease in mean arterial pressure and arterial pH and the increase in arterial PCO2 during hemorrhage. Infusion of phenylephrine in the denervated fetuses prevented the decrease in blood pressure and reduced the magnitudes of changes in blood gases. Fetal plasma ACTH, hydrocortisone, and PRA responses to the hemorrhage were exaggerated in the denervated fetuses (not infused with phenylephrine) compared with the intact fetuses. Phenylephrine infusion attenuated the ACTH response and inhibited the AVP response but did not alter the PRA response. We conclude that the sectioned fibers are important for the maintenance of blood pressure and blood gases during hemorrhage and that the PRA, AVP, and ACTH responses to slow hemorrhage are not mediated by peripheral chemoreceptors.

Animals↗

PubMed1992

Prostaglandin E2 releases ovine fetal ACTH from a site not perfused by the carotid vasculature.

Placental prostaglandin E2 (PGE2) is thought to influence the ovine fetal adrenocortical system to control the timing of parturition. We investigated whether physiological infusions of PGE2 increase fetal immunoreactive adrenocorticotropin (iACTH) at the fetal brain or pituitary or at a site not perfused by the carotid vasculature. PGE2 was infused into the carotid artery (ica) at 0 (n = 5), 10 (n = 5), or 100 ng/min (n = 4) or into the vena cava (ivc) at 10 (n = 5) or 100 ng/min (n = 5) for 30 min in fetuses between 119 and 130 days gestation. Blood gases, vasopressin, cortisol, and arterial and central venous pressure were unchanged. Heart rate increased only in the 100 ng/min ica group. iACTH increased only in the 100 ng/min ivc group from 59 +/- 26 to 180 +/- 73 pg/ml. We conclude that PGE2 infused to create physiological plasma concentrations similar to those at the end of gestation stimulates iACTH from a site other than the fetal brain or pituitary.

Adrenocorticotropic Hormone↗

PubMed1992

Effect of age and blood pressure on the heart rate, vasopressin, and renin response to hypoxia in fetal sheep.

The purpose of these studies was to determine whether attenuating the increase in arterial and central venous pressure (CVP) during acute hypoxia can augment the renin and arginine vasopressin (AVP) responses to isocapnic hypoxia in chronically instrumented sheep fetuses. Young (122 +/- 2 days; n = 7) and old (133 +/- 1 days, n = 7) fetuses were exposed to hypoxemia (arterial PO2 = approximately 12-13 Torr) without and with attenuation of the increase in mean arterial pressure (MAP) and CVP with the simultaneous infusion of sodium nitroprusside (NP). NP did not attenuate the bradycardia induced by hypoxia. Plasma renin activity did not increase with hypoxia even when the potentially inhibitory effect of increased MAP and CVP was attenuated with NP. The AVP response to hypoxia was greater in the old fetuses. Furthermore, NP did augment the AVP response to hypoxia in the young but not old fetuses. We conclude that increases in MAP and CVP (i.e., baroreceptor input) do not influence the decrease in heart rate and lack of renin responses to acute hypoxia in the sheep fetus and that increased MAP and CVP seems to restrain the AVP response to hypoxia in younger sheep fetuses.

Animals↗

PubMed1992

Abnormal neuroendocrine responses during exercise in heart transplant recipients.

BACKGROUND: Osmotic and neural factors stimulate neuroendocrine activity during exercise. In contrast to excitatory mechanisms, afferent information from cardiac mechanoreceptors inhibits integrative centers in the hypothalamus and medula oblongata, which serves to buffer neuroendocrine activity. Orthotopic cardiac transplantation results in the loss of afferent information from cardiac mechanoreceptors. Thus, transplantation possibly results in exaggerated neuroendocrine responses when patients are physically active. METHODS AND RESULTS: We measured the neuroendocrine response to moderate and strenuous exercise performed at the same relative intensity in 11 heart transplant recipients (50 +/- 14 years old) 18 +/- 12 months after transplantation and 11 control subjects matched with respect to sex, age, and body size. Plasma levels of norepinephrine, vasopressin, renin activity, atrial natriuretic peptide, angiotensin II, and aldosterone were measured at rest, during a maximal graded exercise test, and during submaximal exercise at 40% and 70% of peak power output on a cycle ergometer (W). Plasma renin activity and atrial natriuretic peptide were elevated at rest in heart transplant recipients (p < or = 0.05). Heart rate (%HRmax reserve), rating of perceived exertion, and reductions in plasma volume (% delta from rest) at the conclusion of the three exercise conditions did not differ between heart transplant recipients and control (p > or = 0.05). Relative changes in neuroendocrine hormones were similar (p > or = 0.05) in heart transplant recipients and control during exercise at 40% of peak power output. Relative changes in plasma norepinephrine, vasopressin, atrial natriuretic peptide, and plasma renin activity were greater (p < or = 0.05) in heart transplant recipients during exercise at 70% of peak power output and the graded exercise test. CONCLUSIONS: We interpret these data as a possible indication of ablation of cardiac mechanoreceptor afferents and unopposed neuroendocrine stimulation in heart transplant recipients. Furthermore, chronic neuroendocrine hyperactivity is likely in ambulatory heart transplant recipients. Although cyclosporine nephrotoxicity is implicated in the development of hypertension, our data suggest that chronic neuroendocrine hyperactivity, which alters renal volume regulation, also contributes to the incidence and severity of hypertension in heart transplant recipients.

Afferent Pathways↗

PubMed1991

Influence of reproductive state on pituitary-adrenal activity in the ewe.

Plasma corticosteroid concentrations are altered in pregnancy, during the reproductive cycle and by ovariectomy in many species. This study was designed to examine basal ACTH and cortisol in ewes of four different reproductive statuses: ovariectomized, nonpregnant cycling, nonpregnant noncycling, and pregnant. Blood samples were drawn every 4 hr for 48 hr from ewes during quiet, undisturbed conditions and analyzed for plasma ACTH, cortisol and progesterone concentrations. There were no significant changes in ACTH, cortisol or progesterone over time. Mean progesterone concentrations were significantly greater in the pregnant ewes than in all other ewes, and were greater in cycling ewes than noncycling or ovariectomized ewes. Mean ACTH was significantly greater in pregnant ewes than noncycling ewes, and mean cortisol was significantly greater in cycling ewes than in nonpregnant cycling or noncycling ewes. Ovariectomized ewes also had significantly greater mean cortisol concentrations than cycling ewes. The results demonstrate that there is an increase in basal ACTH and cortisol in ovine pregnancy.

Adrenocorticotropic Hormone↗

PubMed1991

Intravenous acid infusion stimulates ACTH secretion in sheep.

Both respiratory and metabolic acidemia stimulate the secretion of adrenocorticotropic hormone (ACTH), vasopressin, and renin. The present study was designed to test the blood pressure, heart rate, and endocrine responses of conscious sheep to low-rate infusions of H+. We infused HCl and lactic acid at a rate of 500 mueq/min into the inferior vena cava of seven chronically catheterized adult sheep. Control experiments in six sheep consisted of infusion of HCl at a rate of 100 mueq/min. Only the 500 mueq/min infusion of HCl stimulated reflex responses. This infusion increased mean arterial blood pressure and plasma ACTH concentration but transiently decreased blood pH only after the onset of the reflex responses. Heart rate appeared to increase initially but then decreased. Overall, the apparent changes in heart rate were not statistically significant. None of the infusions significantly altered plasma renin activity or vasopressin concentration. We speculate that heart rate, plasma renin activity, and vasopressin may have been partially inhibited by the increase in blood pressure. However, the lack of effect of lactic acid suggests that the HCl stimulated reflex ACTH and blood pressure responses via a mechanism not related to the concentration of the acid in the infusate or to the total amount of acid infused. It is possible that HCl, but not lactic acid, stimulated release of a humoral agent that stimulated ACTH secretion directly or reflexly. The results do not appear consistent with the stimulation of a venous chemoreceptor sensitive to H+.

Adrenocorticotropic Hormone↗

PubMed1991

Does intracarotid PGE2 increase plasma ACTH concentration in conscious adult ewes?

The hypothesis that prostaglandin E2 (PGE2) is a circulating mediator of adrenocorticotropic hormone (ACTH) secretion in sheep was tested in conscious adult ewes using 30-min carotid artery infusions of 0, 5, 10, 100, and 500 ng.kg-1. min-1 PGE2 in saline. ACTH, cortisol, and aldosterone were significantly increased during the 500 ng.kg-1.min-1 infusion (166 +/- 61 to 233 +/- 38 pg/ml, 27 +/- 5 to 45 +/- 2 ng/ml, and 52 +/- 11 to 85 +/- 25 pg/ml, respectively). PGE2 infusions of 100 ng.kg-1.min-1 increased ACTH from 104 +/- 31 to 168 +/- 31 pg/ml and cortisol from 18 +/- 5 to 42 +/- 2 ng/ml. PGE2 infusions did not increase arginine vasopressin, plasma renin activity, or hematocrit. Heart rate and mean arterial pressure were minimally but significantly increased during the 500 ng.kg-1.min-1 infusion, from 84.9 +/- 2.8 to 99.3 +/- 5.4 beats/min and 95.5 +/- 1.8 to 101.0 +/- 3.4 mmHg, respectively. In a second study to test whether lower infusion rates of PGE2 increase plasma ACTH in sheep with lower resting hormone concentrations, sheep were infused and sampled through a tether system, preventing any disturbances due to human contact the day of an experiment. For all infusion rates ACTH baselines were less than or equal to 55 +/- 17 pg/ml, and cortisol baselines were less than or equal to 6 +/- 3 ng/ml.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenocorticotropic Hormone↗

PubMed1991

Cortisol inhibits ACTH secretion in late-gestation fetal sheep.

In sheep, parturition is initiated by an increase in fetal adrenal secretion of cortisol. In term fetuses, adrenocorticotropic hormone (ACTH) secretion is increased despite increasing plasma concentrations of cortisol. The present study was performed to investigate whether fetal ACTH secretion is under negative-feedback control by cortisol. Ten chronically catheterized fetal sheep (140 days gestation) were used in this study. Five were infused with hydrocortisone sodium succinate (10 micrograms/min) and five with 0.9% physiological saline for 5 h. Fetal and maternal blood samples were drawn at 1-h intervals. Infusion of hydrocortisone sodium succinate significantly increased fetal plasma cortisol concentration from 38.2 +/- 8.4 ng/ml to mean levels between 74.6 +/- 11.6 and 88.5 +/- 4.7 ng/ml. Fetal plasma ACTH concentration was significantly decreased from 129 +/- 36 to 31 +/- 5 pg/ml after 5 h of infusion. Infusion of saline did not alter fetal plasma cortisol or ACTH concentration. Neither of the infusions significantly altered maternal plasma concentrations of ACTH or cortisol, or fetal or maternal blood gases, or plasma concentrations of sodium or potassium. With one exception, all fetuses were born alive at 145 +/- 1 and 144 +/- 1 days gestation in the saline- and hydrocortisone sodium succinate-infused groups, respectively. The results of this study demonstrate that at 140 days gestation fetal ACTH secretion is under negative-feedback control by cortisol.

Adrenocorticotropic Hormone↗

PubMed1991

Does the ovine placenta secrete ACTH under normoxic or hypoxic conditions?

In the sheep, maternal plasma cortisol is increased in late pregnancy, and fetal plasma cortisol and adrenocorticotropic hormone (ACTH) rise precipitously in late gestation. In many species, the placenta contains ACTH. These experiments were designed to test whether the ovine placenta contains ACTH and whether there is net secretion of ACTH by the uteroplacental unit into either the maternal or fetal circulation. Pregnant ewes and their fetuses were prepared with maternal and fetal arterial and uterine and umbilical venous catheters. Arterial and venous samples were taken from both sides of the placenta before and during hypoxia induced by the ewe breathing 9-11% O2, and arteriovenous (a-v) differences in ACTH, PO2, PCO2, and progesterone were analyzed. A positive a-v difference in PO2 (48.2 +/- 3.4 mmHg) and negative a-v differences in PCO2 and progesterone (-3.5 +/- 0.7 mmHg and -25 +/- 5 ng/ml, respectively) were found across the placenta in the ewe, and a positive a-v difference in PCO2 (4.8 +/- 0.9 mmHg) and negative a-v differences in PO2 and progesterone (-8.1 +/- 1.5 mmHg and -13 +/- 3 ng/ml, respectively) were found across the placenta in the fetus, indicating that the umbilical and uterine venous catheters were properly placed. Hypoxia decreased fetal and maternal arterial PO2 from 22.8 +/- 1.3 to 13.8 +/- 0.7 and from 98.8 +/- 3.3 to 37.0 +/- 2.6 mmHg, respectively, and increased fetal and maternal arterial ACTH immunoreactivity from 95 +/- 60 to 2,676 +/- 795 and from 149 +/- 21 to 275 +/- 88 pg/ml, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenocorticotropic Hormone↗

PubMed1991

Arginine vasopressin responses to hypoxia and hypercapnia in late-gestation fetal sheep.

The purpose of this study was to determine the interaction of hypoxia and hypercapnia in the control of arginine vasopressin (AVP) secretion in fetal sheep and to determine the role of the peripheral arterial chemoreceptors in that response. We measured the plasma AVP response to hypercapnia and/or hypoxia in catheterized intact or sinoaortic-denervated fetal sheep between 123 and 144 days of gestation. Ewes were exposed to the following inspired gases: two successive 30-min periods of normocapnic normoxia, 30 min of normocapnic normoxia followed by 30 min of normocapnic hypoxia, two successive 30-min periods of hypercapnic normoxia, or 30 min of hypercapnic normoxia followed by 30 min of hypercapnic hypoxia (i.e., asphyxia). Hypercapnia per se had no significant effect on fetal plasma AVP. Normocapnic hypoxia per se resulted in a significant increase in fetal plasma AVP. Although hypercapnia resulted in a significant acidemia, the decrease in arterial pH was more marked under hypoxic conditions. Hypercapnia/acidemia augmented the AVP response to hypoxia. Fetal sinoaortic denervation did not significantly attenuate any of the AVP responses. We conclude that hypercapnia augments the fetal AVP response to hypoxia and that the AVP response to neither normocapnic nor hypercapnic hypoxia is dependent on afferent information carried in the carotid sinus or aortic nerves.

Animals↗

PubMed1991

Effect of ovariectomy on vasopressin, ACTH, and renin activity responses to hypotension.

The gonadal axis is thought to modulate adrenocorticotropic hormone (ACTH), arginine vasopressin (AVP), and plasma renin activity (PRA) responses to stimuli in several species. These experiments were designed to compare the responses to hypotension in chronically ovariectomized ewes and intact ewes. The ewes were infused with nitroprusside at rates of 5, 10, or 15 micrograms.kg-1.min-1 or infused with vehicle for 10 min. The response to 15 micrograms.kg-1.min-1 was also tested with or without treatment with 10 mg of dexamethasone 2 h before nitroprusside. Blood samples were collected before and at 5, 10, 15, 20, and 30 min after the start of the infusion for measurement of plasma ACTH, AVP, and PRA. In both groups of animals there were significant responses to hypotension. There was a significant effect of ovariectomy on ACTH, AVP, and PRA responses. ACTH and PRA responses were lower in the ovariectomized ewes; AVP responses were increased in the ovariectomized ewes. Administration of dexamethasone inhibited ACTH responses and did not inhibit PRA responses in both groups of ewes. Administration of dexamethasone did not inhibit the AVP response in the intact ewes but did reduce the response in the ovariectomized ewes.

Adrenocorticotropic Hormone↗

PubMed1991

Corticotropin-releasing factor in the ovine fetus and pregnant ewe: role of placenta.

In the sheep, maternal plasma adrenocorticotropic hormone and cortisol are increased in late pregnancy, and fetal plasma cortisol and adrenocorticotropic hormone rise precipitously in late gestation. To test whether the ovine placenta secretes corticotropin-releasing factor (CRF) into either the maternal or fetal circulation, pregnant ewes and their fetuses were prepared with femoral arterial catheters and uterine and umbilical venous catheters. Samples were taken from all sites before and during hypoxia. There was no difference in CRF concentration across the placenta in the mothers or the fetuses under resting or hypoxemic conditions, but maternal and fetal arterial plasma CRF concentrations increased between 128 and 145 days. In a second study, maternal and fetal femoral venous plasma CRF concentrations were measured 1-19 days before spontaneous parturition. The mean concentration increased 8.6 +/- 0.6 pg/ml 11-19 days before parturition to 13.0 +/- 1.0 and 13.2 +/- 1.4 pg/ml in fetuses 4-8 and 1-3 days before parturition, respectively. Maternal plasma concentrations did not significantly increase in the days closer to parturition. These studies demonstrate that there are low but measurable CRF concentrations in fetal and maternal sheep plasma but that these are not the result of tonic placental secretion of CRF.

Animals↗

PubMed1991

Role of the sympathetic nervous system in cold-induced hypertension in rats.

Hypertension develops in rats exposed chronically to cold [6 +/- 2 degrees C (SE)] and includes both an elevation of mean arterial pressure and cardiac hypertrophy. Previous studies suggest that cold-exposed animals, at least initially, have a large sustained increase in the activity of their sympathetic nervous system, suggesting a failure of the baroreceptor system to provide sufficient negative feedback to the central nervous system. The present study was designed to investigate whether alterations in the activity of the sympathetic nervous system, including the baroreceptor reflex, occur during exposure to cold and whether they contribute to cold-induced hypertension. Twenty male rats were prepared with indwelling catheters in the femoral artery and vein. Ten of the rats were exposed to cold (6 +/- 2 degrees C) chronically, while the remaining 10 were kept at 26 +/- 2 degrees C. Withdrawal of arterial blood samples (less than 5 ml/kg), measurement of direct arterial pressures, and measurement of baroreflex function were carried out at 0800 h at intervals throughout the experiment. Norepinephrine and epinephrine concentrations in plasma were also determined at intervals throughout the experiment. Systolic, diastolic, and mean blood pressures of cold-exposed rats were increased to levels significantly above those of controls. The sensitivity of the baroreflex (delta heart period/delta mean arterial pressure) was decreased in the cold-treated group. The concentration of norepinephrine in plasma increased after 24 h of exposure to cold and remained elevated throughout the experiment, whereas the concentration of epinephrine in plasma increased initially but returned to control levels after 19 days of exposure to cold.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1991

Do plasma ACTH and cortisol concentrations in the late-gestation fetal sheep vary diurnally?

This study tested the hypothesis that fetal plasma ACTH and cortisol concentrations vary diurnally, and the mean concentration and the amplitude of the rhythm vary as a function of fetal gestational age. Nine chronically-catheterized fetal sheep were studied between 120 and 142 days' gestation. All of the fetuses were born spontaneously and alive. The pregnant ewes were maintained in a room with a regular light cycle (on at 07.30, off at 17.30). Food and water were available ad libitum. Blood samples were drawn at 4-h intervals throughout a 24-h period. There were no significant daily variations in fetal plasma ACTH, cortisol, or progesterone concentrations, except in the last 3 days of fetal life. In these fetuses ACTH and cortisol concentrations were increased in the afternoon and evening. We conclude that there is no diurnal rhythm in ovine fetal hypothalamo-pituitary-adrenal axis activity, and that the increased plasma concentrations of ACTH and cortisol in the afternoon and evening hours of the last few days of fetal life might be a response to increased uterine contraction activity.

Adrenocorticotropic Hormone↗

PubMed1991

Induction of parturition by cortisol: effects on negative feedback sensitivity and plasma CRF.

In fetal sheep, plasma concentrations of both adrenocorticotropic hormone (ACTH) and cortisol increase at the end of gestation. The increase in fetal plasma cortisol concentration induces placental 17 alpha-hydroxylase and 17, 20 lyase activities and therefore stimulates the placenta to secrete relatively more estrogen and relatively less progesterone. The resultant increase in the estrogen-to-progesterone ratio is thought to increase uterine contractility and initiate labour. We had previously demonstrated that the efficacy of cortisol-induced suppression of ACTH secretion at the end of gestation was reduced. We hypothesized that cortisol-induced stimulation of placental steroidogenesis promoted the secretion of a steroid hormone which reduced negative feedback efficacy, and therefore allowed both ACTH and cortisol secretion to increase simultaneously. Others had proposed that cortisol stimulates the placental secretion of corticotrophin releasing factor, which might also stimulate fetal ACTH secretion. This study was designed to test the hypotheses that cortisol reduces its own feedback efficacy or stimulates CRF secretion. Five pregnant ewes with twin pregnancies were studied after chronic catheterization. One fetus was subjected to infusion of hydrocortisone sodium succinate (10 micrograms/min, iv) and the other to infusion of saline. After 5 and 53 h of infusion, each fetus was subjected to a period of hypotension produced by infusion of sodium nitroprusside. The infusion of hydrocortisone sodium succinate decreased plasma progesterone concentrations in the fetal circulation into which the steroid was infused, and in the maternal circulation. Fetal plasma CRF concentrations were increased on the third day of infusion, the day in which the fetuses went into labour.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenocorticotropic Hormone↗

PubMed1990

Progesterone-cortisol interaction in control of renin activity but not aldosterone.

In addition to its effect of inhibiting adrenocorticotropic hormone (ACTH) secretion, cortisol (hydrocortisone) inhibits the renin-angiotensin system in both fetal and adult sheep. We have found that progesterone attenuates the inhibition of ACTH by cortisol. These studies test whether progesterone interacts with cortisol in control of the renin-angiotensin-aldosterone system. Conscious adult ewes were infused with vehicle, cortisol (4 micrograms.kg-1.min-1), progesterone (0.5 microgram.kg-1.min-1), or cortisol with progesterone for 60 min. Beginning 120 min after the start of the infusion, renin secretion was stimulated by infusing sodium nitroprusside (10 micrograms.kg-1.min-1 iv). Cortisol infusion decreased plasma K+ concentration and reduced the plasma renin activity (PRA) and aldosterone responses to nitroprusside. Progesterone alone had no effect on PRA, aldosterone, or K+. Progesterone reduced the inhibition of PRA, but not aldosterone or K+, by cortisol. The data also indicate that the suppression of renin, as well as the suppression of ACTH, involves receptors or intracellular mechanisms with which progesterone interacts, whereas the inhibition of aldosterone involves a mechanism that progesterone does not affect.

Aldosterone↗

PubMed1990

Peripheral chemoreceptor control of fetal renin responses to hypoxia and hypercapnia.

The renin response to hypoxia in late gestation fetal sheep has been well characterized. However, the renin response to asphyxia--the combination of hypoxia and hypercapnia--has not been extensively studied. The purpose of this study was to determine 1) the interaction of hypoxia and hypercapnia in the control of renin secretion in late gestation fetal sheep and 2) the role of peripheral arterial chemoreceptors therein. Chronically catheterized fetal sheep (intact or sinoaortic denervated) were exposed to hypoxia and/or hypercapnia for 30 minutes. Hypercapnia alone had no effect on plasma renin activity or aldosterone but did result in a significant increase in angiotensin II. Hypercapnia combined with hypoxia resulted in a significant increase in renin activity, angiotensin II, and aldosterone. Sinoaortic denervation attenuated the renin and angiotensin II responses to hypercapnia plus hypoxia. The increase in renin and angiotensin II in response to hypercapnia with or without concomitant hypoxia strongly correlated with the magnitude of the decrease in arterial pH in intact fetuses only. Hypoxia alone and in concert with hypercapnia increased mean arterial pressure and decreased heart rate in intact but not sinoaortic denervated fetuses. We conclude that 1) hypercapnia more potently increases plasma renin activity than does hypoxia in late gestation fetal sheep, 2) arterial pH may be the relevant signal perceived by the peripheral arterial chemoreceptors for the control of the renin-angiotensin system during asphyxia, and 3) the cardiovascular response to hypoxia is mediated, in part, by peripheral arterial chemoreceptors.

Aldosterone↗

PubMed1990

Effect of self-monitoring on maintenance and generalization of conversational skills of persons with mental retardation.

The effect of self-monitoring on the generalization and maintenance of conversational skills of adults with mental retardation was examined. Target behaviors were asking nondirected questions, answering directed questions, and asking directed questions. Although training alone did not result in generalization of these skills to the assessment setting, the addition of self-monitoring did. Results were maintained over 6 months and generalized to the untrained behavior of answering nondirected questions. The importance of the effect was supported by social comparison and subjective evaluation data. Results indicate that self-monitoring may be effective in increasing generalization and maintenance of conversational skills.

Adult↗