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Query: UMLS:C0085383 (hypocapnia)
 1,697 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of various cardiovascular reflexes and reactions on the plethysmographically recorded penile volume in rabbit was investigated. Stimulation of the aortic nerve or direct stimulation of the carotid sinus produced increase in penile volume, while carotid occlusion produced decrease. Brief volume load or protoveratrine given into the right atrium produced increase in penile volume. Asphyxia, hypercapnia, hypoxia, cyanide and lobeline produced decrease in penile volume, while hypocapnia increased it. Moderate blood taps decreased penile volume, while hypocapnia increased it. Moderate blood taps decreased penile volume. With the exception of the response to asphyxia all these reactions required intact vasomotor nerves. Clonidine increased penile volume if vasomotor nerves were intact but decreased it if the penis was decentralized. Penile volume decreased in shivering animals but increased on warming. Carotid occlusion impaired erectile responses to hypogastric and pelvic nerve stimulation. In certain experiments this effect was more pronounced in the latter case. It is concluded that the medullary neuron pool responsible for penile vasomotor tone participates in general reflex cardiovascular homeostasis and that this may have implications for normal erectile responses.
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PMID:Changes in penile volume during some cardiovascular reflexes and reactions in rabbit. 50 67

Previous workers have reported that ethyl methylene blue (EMB) diminishes cyanide-induced increases in blood lactate (CIL); the present study investigates the mechanism underlying this interaction. Accordingly, sodium cyanide (1.2 mg./Kg.) was infused into the abdominal aorta of anesthetized, spontaneously breathing dogs. Following cyanide infusion, arterial lactate concentration increased 5.4 +/- 1.1 mmol./L. and arterial PCO2 decreased 22 +/- 3 mm. Hg. A second group of dogs was pretreated with EMB (8 to 15 mg./Kg.); this dose of EMB elicited twofold increments in oxygen consumption and induced the formation in vivo of methemoglobin (0.8 +/- 0.1 gm./100 ml.). Following cyanide infusion, the increase in lactate in EMB animals was only 0.6 +/- 0.2 mmol./L.; the decrease in arterial PCO2 was limited to 5 +/- 1 mm. Hg. In order to clarify the relationship between cyanide-induced hypocapnia and CIL, cyanide was infused into a third group of dogs that were maintained isocapneic via mechanical ventilation; despite constancy of arterial PCO2, lactate increased 6.0 +/- 0.7 mmol./L. To determine the effect of EMB-induced tissue hypermetabolism on CIL, twofold increments in oxygen consumption were produced in a fourth group of dogs by pretreatment with sodium salicylate. Following cyanide infusion, salicylate-pretreated animals increased lactate 7.2 +/- 1.2 mmol./L. In order to assess the relationship between EMB-induced methemoglobinemia and the decrease in CIL, similar concentrations of methemoglobin were produced in two subsequent groups of dogs by two different techniques (i.e., by aniline pretreatment or by infusion of methemoglobinemic blood that had been prepared in vitro by addition of sodium nitrite). CIL in these animals was again markedly diminished (i.e., increments of only 0.6 +/- 0.3 mmol./L.) It is concluded that EMB diminishes CIL by a mechanism other than elimination of cyanide-induced hypocapnia or induction of tissue hypermetabolism. The results suggest that methemoglobin formation may completely account for the ability of EMB to effect a decrement in CIL.
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PMID:Interaction between ethyl methylene blue and cyanide-induced increases in blood lactate. 83 20

Previously we reported that activities of certain chemoreflex sensitive cervical preganglionic sympathetic nerves (PSN) were augmented by carotid chemoreceptor stimulation independently of phrenic nerve (PN) activity in the cat. To test the hypothesis that the PSN carotid chemoreflex could have been mediated by the expiratory neuron activity, we studied the relationship between PSN, internal intercostal expiratory nerve (IICEN) and PN activities in vagotomized, anesthetized, paralysed and artificially ventilated cats. We made the following observations. (1) Hypoxia often inhibited IICEN activity while the PN and PSN activities were stimulated. (2) during normoxia, cyanide strongly stimulated PN and PSN discharges but only moderately IICEN discharges. (3) Hyperventilation hypocapnia suppressed or eliminated PSN and PN rhythms and activities, but made some IICEN fibers fire continuously. (4) During hypocapnic apnea, cyanide stimulated PSN activity before PN and IICEN activities, although some PSN fibers were stimulated simultaneously with PN fibers. Accordingly we conclude that IICEN activity does not significantly influence chemoreflex stimulation of PSN activity and that a direct chemoreflex stimulation of IICEN is minimal in the cat. Thus, the chemoreflex PSN response is in part independent of respiratory chemoreflex pathways.
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PMID:Sympathetic peripheral chemoreflex is independent of expiratory output neurons in the cat. 263 35

To test the hypothesis that peripheral chemoreflex effect on the preganglionic cervical sympathetic nerve (PSN) activity is entirely mediated by the central respiratory drive (CRD), as expressed in the phrenic nerve (PN) activity, we studied the relationship between PN and PSN activities under controlled conditions of carotid chemosensory excitation in the anesthetized cats. The cats were vagotomized, paralyzed and artificially ventilated. Tracheal pO2 and pCO2, systemic blood pressure, activities of single or a few PSN and PN fibers and a PN bundle were simultaneously recorded. The PSN preparations, which were responsive to hypoxia and showed PN rhythm, were selected for the study. Carotid chemoreceptor excitation, produced by hypoxia (end-tidal pO2 approximately equal to 50 Torr) or by sodium cyanide injection (50-100 micrograms, i.v.), elicited 3 types of responses: (1) the PSN discharged during the silent period of PN activity, although the PSN peak activity was still coupled to the PN peak activity, (2) PSN discharged only during PN activity, and (3) during the absence of PN discharge induced by hyperventilation hypocapnia, cyanide injection stimulated the PSN without PN activity. These observations suggest a model of chemoreflex control of sympathetic nerve activity which consists of two parts: one is dependent on PN activity and the other is not. Accordingly, all PSN chemoreflex responses may not be integrated with all inspiratory chemoreflexes.
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PMID:Relationship between sympathetic and phrenic nerve responses to peripheral chemoreflex in the cat. 323 82

The purpose of this investigation was to compare the respiratory pattern of gasping with eupnea and apneusis. Decerebrate, cerebellectomized, vagotomized, paralyzed and ventilated cats were used. The ventilatory pattern, assessed by phrenic nerve activity, was reversibly altered from eupnea to apneusis or gasping by use of a cooling-for, thermode positioned inm the rostral pons or through the pontomedullary junction, respectively. Irreversible apneusis or gasping resulted from brain stem lesions or freezing at appropriate loci. Analysis of phrenic activity revealed that the rates of onset and rise of the gasp were much greater than those of the eupneic or apneustic inspiration. Moreover, in contrast to eupnea or apneusis, neither the frequency nor the intensity of gasps was altered by hypercapnia, hypocapnia, or carotid chemoreceptor stimulation by sodium cyanide. Although hypoxia caused an increase in gasping frequency, this response was transient and not dependent on carotid chemoreceptor mechanisms. These results provide no support for the concept that common mechanisms localized in medulla, underlie the neurogenesis of all automatic ventilatory patterns.
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PMID:A characterization of the respiratory pattern of gasping. 678 67

Our study was concerned with the effect of brain hypoxia on cardiorespiratory control in the sleeping dog. Eleven unanesthetized dogs were studied; seven were prepared for vascular isolation and extracorporeal perfusion of the carotid body to assess the effects of systemic [and, therefore, central nervous system (CNS)] hypoxia (arterial PO(2) = 52, 45, and 38 Torr) in the presence of a normocapnic, normoxic, and normohydric carotid body during non-rapid eye movement sleep. A lack of ventilatory response to systemic boluses of sodium cyanide during carotid body perfusion demonstrated isolation of the perfused carotid body and lack of other significant peripheral chemosensitivity. Four additional dogs were carotid body denervated and exposed to whole body hypoxia for comparison. In the sleeping dog with an intact and perfused carotid body exposed to specific CNS hypoxia, we found the following. 1) CNS hypoxia for 5-25 min resulted in modest but significant hyperventilation and hypocapnia (minute ventilation increased 29 +/- 7% at arterial PO(2) = 38 Torr); carotid body-denervated dogs showed no ventilatory response to hypoxia. 2) The hyperventilation was caused by increased breathing frequency. 3) The hyperventilatory response developed rapidly (<30 s). 4) Most dogs maintained hyperventilation for up to 25 min of hypoxic exposure. 5) There were no significant changes in blood pressure or heart rate. We conclude that specific CNS hypoxia, in the presence of an intact carotid body maintained normoxic and normocapnic, does not depress and usually stimulates breathing during non-rapid eye movement sleep. The rapidity of the response suggests a chemoreflex meditated by hypoxia-sensitive respiratory-related neurons in the CNS.
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PMID:Ventilatory responses to specific CNS hypoxia in sleeping dogs. 1079 49