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Biomedical subjects

C A Richard

Publications and source records attributed to C A Richard.

At least 19 recordsLinked to original sources

Cerebellar fastigial nuclei activity during blood pressure challenges.

The cerebellar fastigial nuclei (FN) assist in regulating compensatory responses to large blood pressure changes and show structural injury and functional impairment to cardiovascular challenges in syndromes with sleep-disordered breathing. The patterned time course of FN responses to elevation or lowering of blood pressure and location of responsive regions within the nuclei are unclear. We evaluated FN neural activity in six anesthetized rats using optical imaging procedures during elevation and lowering of arterial pressure by phenylephrine and nitroprusside, respectively. Hypertension diminished optical correlates of FN neural activity, while measures of activity increased to hypotension, with peak neural responses occurring 5-10 s later than peak blood pressure changes. Blood pressure responses were followed by heart rate changes, and peak respiratory rates developed even later, in close temporal proximity to FN activity patterns. Although overall topographical response trends were similar, regional patterns of altered neural activity appeared to both hypertension and hypotension. The extent of neural change was greater during recovery from hypertension than for hypotension at high-dose levels. Blood pressure levels saturated with increasing phenylephrine doses, while FN activity continued to decline. No saturation appeared in heart or respiratory rate trends. The findings suggest that the FN compensate for large blood pressure changes by sympathoexcitatory and inhibitory processes, which accompany late-developing somatic or respiratory adjustments.

Animals↗

Physiological range of human chorionic gonadotropin for support of early human pregnancy.

OBJECTIVE: To determine the physiological range of hCG in early pregnancy. DESIGN: Retrospective study of patient charts. SETTING: Magee-Women's Hospital IVF clinic, Monroeville, Pennsylvania. PATIENT(S): Sixty patients with successful, singleton birth outcomes. INTERVENTION(S): Serum hCG measurements on days 12-16 post-oocyte retrieval (OR). MAIN OUTCOME MEASURE(S): Lowest values, highest values, mean values, quartile mean values, and 48-hour doubling times for days 12-16 post-OR. RESULT(S): The average production of hCG in successful pregnancies is roughly 4-fold greater than the lowest amount observed in successful pregnancies, suggesting that a considerable excess of hCG is normally produced. Additionally, the average doubling time is almost 2-fold greater than the slowest doubling rate. CONCLUSION(S): The data from this study provide a set of values for the minimum and maximum threshold of hCG for days 12-16 post-OR that may be physiologically required, although not entirely predictive, for a successful IVF pregnancy outcome.

Chorionic Gonadotropin↗

Changes in ventral medullary light reflectance during hypercapnia in awake and sleeping cats.

Activity within rostral and intermediate ventral medullary surface areas, measured as 660 nm scattered light changes, was examined in six cats, (five experimental, one control site) following 5% CO(2) challenges during waking, quiet sleep, and rapid eye movement (REM) sleep states. Activity declined to hypercapnia in all states, with a smaller decline in quiet sleep compared to waking, and intermediate values in REM sleep. The decline occurred more rapidly, with a shorter latency, during wakefulness, but with a much slower return to baseline than during quiet sleep. During REM sleep, the latency to nadir and recovery were greater than in other states. Regional patterns of activation emerged which differed in extent of activation between states.

Animals↗

IgG-coated erythrocytes augment LPS-stimulated TNF-alpha secretion, TNF-alpha mRNA levels, and TNF-alpha mRNA stability in macrophages.

Previous studies have shown that IgG-coated erythrocytes (EIgG) augment the LPS-stimulated increase in serum TNF-alpha levels in animals and the LPS-stimulated secretion of TNF-alpha by isolated macrophages. The present study evaluated the mechanism for the effect of EIgG on LPS-stimulated TNF-alpha secretion in the murine macrophage cell line, RAW 264.7. Incubation of the macrophages with EIgG or IgG-coated glass beads caused a dose-dependent augmentation of LPS-stimulated TNF-alpha secretion. The addition of EIgG increased the rate of LPS-stimulated TNF-alpha protein secretion between 2 and 4 hr after LPS. Accordingly, EIgG increased the levels of TNF-alpha mRNA at 2 and 3 hr after LPS. The increase in the LPS-stimulated TNF-alpha mRNA levels caused by EIgG was associated with an increase in TNF-alpha mRNA stability. Thus, the augmentation of LPS-stimulated TNF-alpha secretion by EIgG was associated with an increase in TNF-alpha mRNA levels which at least partly resulted from an increase in the stability of TNF-alpha mRNA.

Animals↗

Sleep states alter ventral medullary surface responses to blood pressure challenges.

Ventral medullary surface (VMS) activity declines during rapid eye movement (REM) sleep, suggesting a potential for reduced VMS responsiveness to blood pressure challenges during that state. We measured VMS neural activity, assessed as changes in reflected 660-nm wavelength light, during pressor and depressor challenges within sleep/waking states in five adult, unrestrained, unanesthetized cats and in two control cats. Phenylephrine elevated blood pressure and elicited an initial VMS activity decline and a subsequent rise in VMS activity in all states, although the initial decline during quiet sleep occurred only in rostral placements. Phasic REM periods elicited a momentary recovery from the evoked activity rise, and arousals diminished the overall elevation in activity. A sodium nitroprusside depressor challenge increased VMS activity more in REM sleep than in quiet sleep, with the increase being even less in waking. Enhanced responses to depressor challenges during REM sleep suggest a loss of dampening of evoked activity during that state; state-related differential baroreflex sensitivity may result from sleep-waking changes in VMS responses to blood pressure challenges.

Adrenergic alpha-Agonists↗

State influences on ventral medullary surface and physiological responses to sodium cyanide challenges.

Intravenous sodium cyanide (NaCN) administration lowers ventral medullary surface (VMS) activity in anesthetized cats. Sleep states modify spontaneous and blood pressure-evoked VMS activity and may alter VMS responses to chemoreceptor input. We studied VMS activation during peripheral chemoreceptor stimulation by intravenous NaCN using optical procedures in six cats instrumented for recording sleep physiology during sham saline and control site trials. Images of scattered 660-nm light were collected at 50 frames/s with an optical device after 80-100 microg total bolus intravenous NaCN delivery during waking and sleep states. Cyanide elicited an initial ventilatory decline, followed by large inspiratory efforts and an increase in respiratory rate, except in rapid eye movement sleep, in which an initial breathing increase occurred. NaCN evoked a pronounced decrease in VMS activity in all states; control sites and sham injections showed little effect. The activity decline was faster in rapid eye movement sleep, and the activity nadir occurred later in waking. Sleep states alter the time course but not the extent of decline in VMS activity.

Animals↗

Physiological and ventral medullary surface activity during hypovolemia.

The objective was to determine ventral medullary surface responses to blood loss sufficient to induce shock. We examined changes in scattered light from rostral and intermediate areas of the ventral medullary surface in four intact, drug-free cats during acute hypovolemia. Scattered light images, collected during 660 and 560 nm illumination to measure cellular activity and hemodynamic aspects, respectively, were digitized at 50 frames/s during baseline, and during withdrawal of 20-30% blood volume. Hypovolemia elicited a profound hypotension and eventual bradycardia. In all cats, a modest increase in ventral medullary surface reflectance (activity decline) accompanied initial blood loss; as hypovolemia continued, and blood pressure declined, reflectance switched to a decline (activity increase), with the lowest reflectance occurring at maximal blood loss. Hypovolemia elicited multiple transient physiologic behaviors, including tachycardia, tachypnea, intermittent isolated and sustained bursts of enhanced inspiratory efforts, and extensor activation of the somatic musculature. The phasic physiological behaviors during hypovolemia were accompanied by partial recovery of medullary surface reflectance and blood pressure towards baseline values; however, reflectance continued to decrease as blood pressure progressively fell after these recovery efforts. Patterns of reflectance were not uniform over areas examined; isolated regions of enhanced or diminished reflectance appeared upon the overall images. Optical signals indicating hemodynamic changes followed the neural activity patterns, but not precisely. Regions within the ventral surface are responsive to hypovolemia, and to transient behaviors associated with momentary restoration of blood pressure; these ventral surface areas may assume essential roles in the systemic response to hypovolemic-induced shock.

Animals↗

Increased infant axillary temperatures in non-REM sleep during mother-infant bed-sharing.

This study addressed the effect of mother-infant bed-sharing on infant body temperature and possible mediating mechanisms. Axillary temperatures were recorded for the entire night in 26 infants on both a bed-sharing night and a solitary sleeping night, accompanied by polysomnography and video-taping to allow assignment of sleep stages and behavioral analysis. All infants were approximately 3 months old, healthy, Latino and breast-feeding; 16 of the infants bed-shared since birth while the others routinely slept alone. Bed-sharing was associated with a significantly increased mean axillary temperature compared to solitary sleeping in both routine bed sharers and routine solitary sleepers. This increase was expressed only in non-REM sleep, with no differences during REM sleep or waking. The increase in temperature during bed-sharing may be related to an increased frequency of transient, movement-associated arousals during bed-sharing.

Adult↗

IgG-coated erythrocytes augment the lipopolysaccharidestimulated increase in serum tumor necrosis factor-alpha.

Previous studies have shown that the injection of IgG-coated erythrocytes (EIgG) caused an increase in the mortality rate due to bacterial lipopolysaccharide (LPS). This observation led to the present evaluation of the effect of EIgG on the LPS-stimulated increase in serum tumor necrosis factor-alpha (TNF-alpha) levels and TNF-alpha secretion by macrophages. The prior injection of EIgG augmented the increase in LPS-stimulated serum TNF-alpha levels ninefold at 1 h after LPS. Serum TNF-alpha levels were augmented when LPS was injected 2 or 6 h after EIgG but not at 0.5 or 12 h after EIgG. Complement activation caused by EIgG may contribute to the priming for TNF-alpha, because activation of complement with cobra venom factor caused a threefold augmentation of the LPS-stimulated serum TNF-alpha levels. Isolated macrophages that had ingested EIgG or were adherent to immobilized IgG showed augmented TNF-alpha secretion in response to LPS. Thus clearance of immune complexes from the blood can augment the LPS-stimulated increase in serum TNF-alpha levels that is due, in part, to complement activation and signaling via FcgammaR.

Animals↗

Optical imaging of the ventral medullary surface across sleep-wake states.

We hypothesized that spontaneous activity declines over widespread areas of the cat ventral medullary surface (VMS) during rapid eye movement (REM) sleep. We assessed neural and hemodynamic activity, measured as changes in reflected 660- and 560-nm wavelength light, from the VMS during sleep and waking states in five adult, unrestrained cats and in two control cats. Relative to quiet sleep, overall activity declined, and variability, assessed by standard deviation, increased by 25% during REM sleep. Variability in activity during waking also increased by 45% over quiet sleep, but mean activity was unchanged. REM sleep onset was preceded by a reduction in the hemodynamic signal from 5 to 60 s before neural activity decline. The activity decline during REM sleep, previously noted in the goat rostral VMS, extends to intermediate VMS areas of the cat and differs from most neural sites, such as the cortex, hippocampus, and thalamus, which increase activity during REM sleep. The activity decline during REM sleep has the potential to modify VMS responsiveness to baroreceptor and chemoreceptor challenges during the REM state.

Animals↗

Apnea and periodic breathing in bed-sharing and solitary sleeping infants.

Mother-infant bed sharing, compared with the solitary sleeping condition, has recently been associated with several physiological and behavioral effects. Because the physiological effects of bed sharing may also include respiratory changes, we compared the incidence of central and obstructive apneas and periodic breathing in bed-sharing and solitary sleeping infants. Twenty routinely bed-sharing mother-infant pairs and fifteen routinely solitary sleeping pairs slept for 3 nights in a sleep laboratory. After an initial adaptation night, each pair spent 1 night bed sharing and 1 night in solitary sleep in random order. Apnea and periodic breathing were scored from polysomnographic recordings. The frequency of central apnea was significantly increased on the bed-sharing night, compared with the solitary night, regardless of routine sleeping arrangement. There were significantly fewer obstructive apneas on the bed-sharing night than on the solitary night, but only in routinely solitary sleeping infants. In both groups, there was a significantly higher frequency of periodic breathing events on the bed-sharing night than on the solitary night. These findings demonstrate that the bed-sharing environment can have a significant impact on respiratory control in the infant. Evidence is also presented to suggest that routine bed sharing may result in subtle neurophysiological and/or developmental differences in infants.

Female↗

Bedsharing promotes breastfeeding.

OBJECTIVE: Because breastfeeding is thought to be protective against sudden infant death syndrome (SIDS), environmental or child care factors that promote breastfeeding might reduce infant vulnerability to SIDS. The effect of mother-infant bedsharing on nocturnal breastfeeding behavior was studied in 20 routinely bedsharing and 15 routinely solitary sleeping Latino mother-infant pairs when the infants were 3 to 4 months old. METHODOLOGY: All pairs were healthy and exclusively breastfeeding at night. The videotape portion of all-night laboratory polysomnographic studies was used for the analyses. For each pair, an adaptation night was followed by one night each of bedsharing and solitary sleeping. RESULTS: The most important finding is that when tested in their usual sleeping conditions, routinely bedsharing infants breastfed approximately three times longer during the night than infants who routinely slept separately: this reflected a two-fold increase in the number of breastfeeding episodes and 39% longer episodes. Breastfeeding was also facilitated on the bedsharing night relative to the solitary night within the routinely bedsharing group: the number and total duration of breastfeeding episodes were significantly larger on the bedsharing night. CONCLUSIONS: We suggest that, by increasing breastfeeding, bedsharing might be protective against SIDS, at least in some contexts. Furthermore, maternal reproductive physiology could be impacted because nursing frequency affects ovulation. This is the first study to directly measure nocturnal breastfeeding behavior in any cultural group.

Adult↗

Diethyldithiocarbamate ameliorates the effect of lipopolysaccharide on both increased nitrite production by vascular smooth muscle cells and decreased contractile response of aortic rings.

The depression of vasoconstrictor responsiveness caused by bacterial lipopolysaccharide (LPS) is mediated, in part, by the induction of nitric oxide synthase (NOS) and the resultant increase in nitric oxide production by vascular smooth muscle. The present study evaluated the ability of the antioxidant, diethyldithiocarbamate (DDTC), to attenuate the LPS-stimulated induction of NOS in cultured vascular smooth muscle cells (VSMC) and the depression of in vitro vascular reactivity caused by LPS administration to rats. The LPS-stimulated increase in nitrite production by cultured VSMC was inhibited 85% by DDTC (100 microM). When VSMC were stimulated with a combination of LPS, interferon-gamma (INF) and tumor necrosis factor (TNF) nitrite production was 5-fold greater than with LPS alone. DDTC inhibited 49% of the increase caused by LPS plus INF and TNF. Aortic rings taken from animals injected with LPS showed a depression of maximum force in response to phenylephrine which was reversed by inhibition of NOS activity. Pretreatment of animals with DDTC attenuated this depression of vascular reactivity. The DDTC treatment did not reduce the increase in serum TNF levels caused by LPS. These results suggest that DDTC can attenuate the LPS-stimulated induction of NOS in vascular smooth muscle and may thereby ameliorate the impairment of vascular reactivity.

Amino Acid Oxidoreductases↗

The antioxidant, U74389, ameliorates the depression of vascular reactivity caused by lipopolysaccharide.

There is growing evidence that an oxidant stress contributes to the deleterious effects of bacterial lipopolysaccharide (LPS). The present study evaluated the ability of the antioxidant, U74389, to prevent the depression of vascular reactivity caused by LPS. Aortic rings taken from rats given LPS showed a depression of maximum force in response to phenylephrine that was reversed by an inhibitor of nitric oxide synthase. Pretreatment of animals with U74389 attenuated this depression of vascular reactivity. U74389 did not limit the increase in serum tumor necrosis factor levels caused by LPS. These results show that U74389 can ameliorate the depression of vascular reactivity caused by LPS possibly by interfering with the induction of nitric oxide synthase.

Animals↗

Respiratory patterning following cerebral ventricular administration of cocaine.

Intravenous (IV) cocaine in the conscious cat causes extreme tachypnea and reduction in breath-to-breath variability. In this study, we examined respiratory patterning following administration of cocaine into the cerebral ventricles. Intraventricular cocaine elicited a tachypnea that was nearly identical to that for IV cocaine. At the high dose, peak respiratory rate increased by 380%. Breath-to-breath variability was dramatically reduced by cocaine, especially in the early stages of the intoxication; during these stages, the tachypnea was occasionally interrupted by prolonged inspiratory efforts. Procaine was administered as a control for the anesthetic effects of cocaine and caused an initial tachypnea that was similar to that for cocaine. For both cocaine and procaine, the mean ratios of inspiratory to expiratory durations were unaffected, indicating that the tachypnea was accomplished by approximately equal reductions in inspiratory and expiratory durations. We conclude that the tachypnea following cocaine administration results principally from central rather than peripheral mechanisms. In addition, the data suggest that anesthetic actions mediate the principal respiratory effects of cocaine.

Animals↗