Ventilatory response to alterations of H+ ion concentration in small areas of the ventral medullary surface

Schlaefke, M. E.; See, Wolf R.; Loeschcke, H. H.

doi:10.1016/0034-5687(70)90083-6

Cited by 190 publications

(60 citation statements)

References 12 publications

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“…may be responsible for much of the progressive increase in VT and only some of the increase in f. The most likely receptor is the central chemoreceptor because when stimulated directly by acidity in the cat it causes increases in VT with a negligible effect onf (Schlaefke, See & Loeschcke, 1970) or when stimulated indirectly by hypercapnia in IX-sectioned rats it causes a proportionately greater increase in VT than inf (Cragg, Drysdale & Singh, 1981).…”

Section: Discussionmentioning

confidence: 99%

Ventilation in intact and glossopharyngeal nerve sectioned anaesthetized rats exposed to oxygen at high pressure.

Cragg¹,

Drysdale²,

Hamilton³

1986

The Journal of Physiology

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were smallest at 4 and greatest at 8 atm absolute. In IX-sectioned rats the rates of rise of VT at 4, 6 and 8 atm absolute and off at 4 atm absolute were similar to those of intact rats. At 6 atm absolute and even more so at 8 atm absolute, however, f decreased. Hence the slope of FE in IX-sectioned compared with intact rats was similar at 4 atm absolute but smaller at 6 and 8 atm absolute. In fact at 8 atm absolute F'E remained constant in IX-sectioned rats.3. Since the slope of VE versus time in intact rats was steeper the greater the pressure and since the removal of carotid bodies in IX-sectioned rats reduced the G'E slope at 6 and 8 atm absolute, the stimulus to the hyperventilation induced by o.h.p. cannot be an accumulation of CO2 in the brain resulting from the lack Of 02 desaturation of haemoglobin. This theory would predict that PE should be identical at all pressures above 3-5 atm absolute.4. The findings in the IX-sectioned rats indicate a major contribution of the carotid bodies to the f increase in o.h.p. They may be stimulated by a histotoxic hypoxia induced by early 02 poisoning. Since the VT increase on exposure to o.h.p.was both large and fairly similar in intact and IX-sectioned rats, it is suggested that a large part ofthe VT increase was caused by stimulation ofthe central chemoreceptors by lactic acidosis induced by an o.h.p.-induced histotoxic hypoxia of the brain.

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Section: Discussionmentioning

confidence: 99%

Ventilation in intact and glossopharyngeal nerve sectioned anaesthetized rats exposed to oxygen at high pressure.

Cragg¹,

Drysdale²,

Hamilton³

1986

The Journal of Physiology

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“…to the ewe) were administered daily. The lateral ventricle catheter was flushed each day with 0.3 ml sterile artificial cerebrospinal fluid (CSF) (31) in order to maintain catheter patency. Fetal arterial blood samples were taken each day for blood gas and pH analysis (Radiometer ABL 330) as well as measurement of blood glucose and lactate (YSI 2300; Yellow Springs Instruments).…”

Section: Methodsmentioning

confidence: 99%

Insulin-like growth factor-1 is a potent neuronal rescue agent after hypoxic-ischemic injury in fetal lambs.

Johnston

Mallard²,

Williams³

et al. 1996

J. Clin. Invest.

181

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This study was designed to determine the potential of IGF-1 as a neuronal rescue agent after cerebral ischemia. Unanesthetized late gestation fetal sheep were subjected to 30-min cerebral ischemia by inflation of carotid artery occluder cuffs. 2 h later either 0.1 g rhIGF-1, 1 g rhIGF-1, 10 g rhIGF-1, or vehicle was infused into a lateral cerebral ventricle over 1 h. Histologic outcome was assessed 5 d later. Overall neuronal loss was reduced with 0.1 g ( P Ͻ 0.05) and 1 g ( P Ͻ 0.002) rhIGF-1, but treatment with 10 g was not effective. With 1 g rhIGF-1 neuronal loss scores were significantly lower in brain regions examined including cortex, hippocampus, and striatum, whereas with 0.1 g rhIGF-1 the parietal cortex and thalamus were not improved and the improvement seen in other regions was less than with 1 g rhIGF-1. Treatment with 1 g rhIGF-1 also delayed the onset of seizures and reduced their incidence. Moreover, the secondary phase of cytotoxic edema was reduced and delayed in onset. We conclude that low dose rhIGF-1 therapy promotes neuronal rescue after cerebral hypoxic-ischemic injury in utero, but the effect is dose dependent. Importantly, rhIGF-1 is effective and nontoxic when administered 2 h after the hypoxic ischemic insult.

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“…Enhancement of respiration associated with an increase in H+ or PCO, of the cerebrospinal fluid originally demonstrated by Leusen (1954a, b) is now known to be mediated by central chemoreceptors located in the ventral surface of the medulla (Loescheke, Koepchen & Gertz, 1958;Mitchell, Loescheke, Severinghaus, Richardson & Massion, 1963; Schlaefke, See & Loeschcke, 1970; Trouth, Patrickson, Holloway & Wright, 1982;Loeschcke, 1982). Perfusion with acidic solutions with constant Pc0.…”

Section: Introductionmentioning

confidence: 97%

Differential effects of carbon dioxide and pH on central chemoreceptors in the rat in vitro.

Harada¹,

Kuno²,

Wang³

1985

The Journal of Physiology

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Ventilatory response to alterations of H+ ion concentration in small areas of the ventral medullary surface

Cited by 190 publications

References 12 publications

Ventilation in intact and glossopharyngeal nerve sectioned anaesthetized rats exposed to oxygen at high pressure.

Ventilation in intact and glossopharyngeal nerve sectioned anaesthetized rats exposed to oxygen at high pressure.

Insulin-like growth factor-1 is a potent neuronal rescue agent after hypoxic-ischemic injury in fetal lambs.

Differential effects of carbon dioxide and pH on central chemoreceptors in the rat in vitro.

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