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Query: UMLS:C0020440 (hypercapnia)
 7,939 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hypercapnia causes vasodilatation of retinal arterioles. Prostaglandin E1, injected close to retinal arterioles from the vitreal side cause vasodilatation apparently similar to that caused by hypercapnia. An inhibitor of prostaglandin synthase (indomethacin) was injected into the ocular circulation. There was a reversible inhibition of the retinal vasodilatation normally induced by hypercapnia. Indomethacin injected close to retinal arterioles from the vitreal side causes reversible vasoconstriction and inhibits the vasodilatory effect of hypercapnia. It is concluded that prostaglandin E1 satisfies three criteria for a candidate for a mediator of hypercapnia-induced arteriolar dilatation.
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PMID:[The role of prostaglandins in the regulation of retinal blood flow]. 225 Sep 34

In unanaesthetized fetal lambs at 125-135 days gestation in utero central acidosis caused by perfusion of the cerebral ventricular system with a solution containing less than 1 mM-HCO3- (cerebrospinal fluid (c.s.f.) pH 6.98) or intravenous infusion of ammonium chloride (c.s.f. pH 7.1) produced an increase in the depth and frequency of episodic breathing but no change in electrocortical activity, heart rate or arterial pressure. Administration of prostaglandin synthetase inhibitors, sodium meclofenamate (0.8-10 mg/kg I.V. or 0.6-2.6 mg/kg intracerebrally) or acetylsalicylic acid (6.7 mg/kg I.V.) caused prolonged episodes of fetal breathing during low and high voltage electrocortical activity, with a large increase in breath amplitude. Blood gas values, heart rate, blood pressure, electrocortical activity and eye movements were not altered. In fetuses whose brain stems had been sectioned in the upper pons or the inferior colliculus, sodium meclofenamate induced prolonged deep breathing. Intravenous prostaglandin E2 abolished the continuous breathing induced by meclofenamate, but not breathing movements enhanced by hypercapnia or hypoxia. It is concluded that the central chemoreceptors respond to acidosis in near-term lamb fetuses qualitatively as in adult animals. Secondly, the results suggest that prostaglandin E2 and the inhibitors of prostaglandin synthesis also act centrally in the lower pons or medulla to modulate fetal breathing.
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PMID:Central stimulation of breathing movements in fetal lambs by prostaglandin synthetase inhibitors. 392 89

A critical review of the literature of retrolental fibroplasia indicates that the cause of this disease is not yet known. Oxygen is certainly a critical factor but it is still not possible to make precise recommendations as to the amount or the duration of therapy that is safe. We have overemphasized the role of oxygen in the past, and as a result of this the false impression has been created that RLF is a disease that can be prevented. This gross oversimplification of a complex disease with multiple causes has resulted in many unjustified malpractice claims. A study of the present epidemic indicates that excessive oxygen administration probably plays a minor role, in contrast to the first epidemic in which prolonged oxygen administration was clearly a major factor. A reasonable working hypothesis is that the developing retina is highly sensitive to any disturbance in its oxygen supply, either hyperoxemic or hypoxemic. The retinal circulation is subject to the same wide fluctuations as the cerebral circulation in newborn infants. The very low-birth-weight, sick premature infant suffers from a number of conditions, many of which can seriously disturb the retinal circulation, resulting in hypoperfusion and ischemia. These factors (immaturity, hyperoxia, hypoxia, blood transfusions, intraventricular hemorrhage, apnea, infection, hypercarbia, hypocarbia, patent ductus arteriosus, prostaglandin synthetase inhibitors, vitamin E deficiency, lactic acidosis, prenatal complications, genetic factors) may all be present in an infant. They may interact to produce various degrees of retinal damage. Nearly all of these factors cannot be prevented or controlled by our present methods of care. Unfortunately, this means that RLF is an extremely difficult disease to prevent, treat, or investigate. A disease of this complexity with multiple causes will require very large numbers of infants in any controlled study of a therapy. Retrolental fibroplasia should not be considered an avoidable iatrogenic disease in very low-birth-weight infants. Its cause in these infants is not known.
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PMID:A reexamination of the role of oxygen in retrolental fibroplasia. 641 99

Breathing movements in the sheep fetus have been observed from a gestational age of about 40 days. From 95 to 115 days fetal breathing movements are almost continuous, interrupted by apnoea rarely exceeding 2 min. From 115 days until term (about 147 days) breathing and movements of the trunk and limbs are episodic. Breathing normally occurs only during rapid-eye-movement sleep as identified by low-voltage cortical electrical activity. Active movements of the neck muscles occur predominantly in high-voltage electrocortical activity. Hypercapnia or acid cerebrospinal fluid perfusion cause an increase in the regularity and depth of breathing when present, and recruit intercostal and laryngeal abductor activity. Isocapnic hypoxia, however, in contrast to the hyperventilation seen postnatally, causes arrest of fetal breathing movements. This effect is due to a central inhibition. Section of the brain stem, from the caudal hypothalamus rostrally, causes dissociation of fetal breathing movements and electrocortical activity into independent rhythms. Section of the brain stem caudally, in the upper pons or at the inferior colliculus, also causes a dissociation of electrocortical activity from breathing movements, which become almost continuous. Isocapnic hypoxia causes an increase in the rate and depth of breathing movements. It is concluded that the arrest of breathing in intact fetal lambs is not due to a direct effect on the respiratory centre in the medulla. The lumbar polysynaptic flexor reflex response becomes episodic after 115 days gestation but, in contrast to fetal breathing movements, is enhanced during high-voltage electrocortical activity. Isocapnic hypoxia arrests movements of the fetal limbs and trunk and inhibits the lumbar flexor reflex. This inhibition of the reflex is prevented by section of the spinal cord at T12, but persists after section of the brain stem in the upper pons. It is attributed to an action on the medulla, independent of the systemic arterial chemoreceptors. Small doses of pentobarbitone (5 mg/kg) cause arrest of fetal breathing movements by a suprapontine mechanism, abolished by brain stem transection, and inhibition of the lumbar flexor reflex by an action on the spinal cord, persisting after transection at T12. Inhibitors of prostaglandin synthetase (indomethacin, meclofenamate or aspirin) induce continuous fetal breathing movements, while prostaglandin E2 arrests fetal breathing. The site of action is on the medulla, as shown by section of the brain stem and of afferents from the systemic arterial chemoreceptors.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:The central control of fetal breathing and skeletal muscle movements. 642 29