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6-Hydroxykaempferol 3-β-rutinoside


  • Brand : BIOFRON

  • Catalogue Number : BD-P0473

  • Specification : 98.0%(HPLC)

  • CAS number : 205527-00-0

  • Formula : C27H30O16

  • Molecular Weight : 610.52

  • PUBCHEM ID : 10371537

  • Volume : 10mg

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provides coniferyl ferulate(CAS#:205527-00-0) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate

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Arousal and cardio-respiratory responses to respiratory stimuli during sleep are important protective mechanisms that rapidly become depressed in the active sleep state when episodes of hypoxia or asphyxia are repeated: whether responses to repeated hypercapnia are similarly depressed is not known. This study aimed to determine if arousal and cardio-respiratory responses also become depressed with repeated episodes of hypercapnia during sleep and whether responses differ in active sleep and quiet sleep. Eight newborn lambs were instrumented to record sleep state and cardio-respiratory variables. Lambs were subjected to two successive 12 h sleep recordings, assigned as either sequential control and test days, or test and control days performed between 12.00 and 00.00 h. The control day was a baseline study in which the lambs breathed air to determine spontaneous arousal probability. During the test day, lambs were exposed to a 60 s episode of normoxic hypercapnia (Fractional inspired An external file that holds a picture, illustration, etc.
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Object name is tjp0582-0369-mu2.jpg in N2) during every quiet sleep and active sleep epoch. The probability of lambs arousing during the hypercapnic exposure exceeded the probability of spontaneous arousal during quiet sleep (58%versus 21%, χ2= 54.0, P < 0.001) and active sleep (39%versus 20%, χ2= 10.0, P < 0.01), though the response was less in active sleep. Exposure to hypercapnia also resulted in a significant increase in ventilation in quiet sleep (150 ± 22%) and active sleep (97 ± 23%, P < 0.05), though the increase was smaller in active sleep (P < 0.05). Small (< 5%) blood pressure increases and heart rate decreases were evident during hypercapnia in quiet sleep, but not in active sleep. Arousal and cardio-respiratory responses persisted with repetition of the hypercapnic exposure. In summary, although arousal and cardio-respiratory responses to hypercapnia are less in active sleep compared with quiet sleep, these protective responses are not diminished with repeated exposure to hypercapnia.


The effects of repeated exposure to hypercapnia on arousal and cardiorespiratory responses during sleep in lambs


Renea V Johnston, Daniel A Grant, Malcolm H Wilkinson, and Adrian M Walker

Publish date

2007 Jul 1




A putative endogenous excitatory drive to the respiratory system in rapid eye movement (REM) sleep may explain many characteristics of breathing in that state, e.g. its irregularity and variable ventilatory responses to chemical stimuli. This drive is hypothetical, and determinations of its existence and character are complicated by control of the respiratory system by the oscillator and its feedback mechanisms. In the present study, endogenous drive was studied during apnoea caused by mechanical hyperventilation. We reasoned that if there was a REM-dependent drive to the respiratory system, then respiratory activity should emerge out of the background apnoea as a manifestation of the drive.

Diaphragmatic muscle or medullary respiratory neuronal activity was studied in five intact, unanaesthetized adult cats who were either mechanically hyperventilated or breathed spontaneously in more than 100 REM sleep periods.

Diaphragmatic activity emerged out of a background apnoea caused by mechanical hyperventilation an average of 34 s after the onset of REM sleep. Emergent activity occurred in 60 % of 10 s epochs in REM sleep and the amount of activity per unit time averaged approximately 40 % of eupnoeic activity. The activity occurred in episodes and was poorly related to pontogeniculo-occipital waves. At low CO2 levels, this activity was non-rhythmic. At higher CO2 levels (less than 0.5 % below eupnoeic end-tidal percentage CO2 levels in non-REM (NREM) sleep), activity became rhythmic.

Medullary respiratory neurons were recorded in one of the five animals. Nineteen of twenty-seven medullary respiratory neurons were excited in REM sleep during apnoea. Excited neurons included inspiratory, expiratory and phase-spanning neurons. Excitation began about 43 s after the onset of REM sleep. Activity increased from an average of 6 impulses s−1 in NREM sleep to 15.5 impulses s−1 in REM sleep. Neuronal activity was non-rhythmic at low CO2 levels and became rhythmic when levels were less than 0.5 % below eupnoeic end-tidal levels in NREM sleep. The level of CO2 at which rhythmic neuronal activity developed corresponded to eupnoeic end-tidal CO2 levels in REM sleep.

These results demonstrate an endogenous excitatory drive to the respiratory system in REM sleep and account for rapid and irregular breathing and the lower set-point to CO2 in that state.


Endogenous excitatory drive to the respiratory system in rapid eye movement sleep in cats


John Orem, Andrew T Lovering, Witali Dunin-Barkowski, and Edward H Vidruk*

Publish date

2000 Sep 1




Arousal from sleep is an important protective response to hypoxia that becomes rapidly depressed in active sleep (AS) when hypoxia is repeated. This study questioned whether there might also be selective depression of cardio-respiratory responses to hypoxia during AS.

Nine newborn lambs (7-22 days of age) were studied over three successive nights. The first and third nights were baseline studies (inspired oxygen fraction, Fi,O2= 0.21). During the second night, during every epoch of sleep, lambs were exposed to 60 s episodes of isocapnic hypoxia (Fi,O2= 0.10).

During quiet sleep (QS), the probability of arousal in hypoxia exceeded the probability of spontaneous arousal (P < 0.001) throughout repeated exposures to hypoxia. Similarly, there were persisting increases in ventilation (135 ± 25 %), blood pressure (3 ± 1 %) and heart rate (3 ± 1 %). By contrast, rapid depression of all responses occurred during repetitive hypoxia in AS. Thus, the probability of arousal in hypoxia exceeded the probability of spontaneous arousal during the first 10 hypoxia exposures (P < 0.001) but not thereafter. Similarly, during the first 10 exposures to hypoxia, the changes in ventilation (88 ± 15 %) and blood pressure (5 ± 1 %) were greater than subsequent responses (P < 0.05). We conclude that, when repeated, hypoxia rapidly becomes ineffective in stimulating protective arousal, ventilatory and blood pressure responses in AS, but not in QS. Selective depression of responses during AS may render the newborn particularly vulnerable to hypoxia in this state.


Repetitive hypoxia rapidly depresses cardio-respiratory responses during active sleep but not quiet sleep in the newborn lamb


Renea V Johnston, Daniel A Grant, Malcolm H Wilkinson, and Adrian M Walker

Publish date

1999 Sep 1;