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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

A marked increase in the prostaglandin E (PGE) content in the cerebrospinal fluid (CSF) and the arterial blood of cats was observed under conditions of 3-minute hypocapnia. During 30-minute hypocapnia a restoration of the initial PGE level was seen. The PGE content in CSF increased while in the arterial blood it decreased comparatively to the control under conditions of 3-minute hypercapnia. In 30-minute hypercapnia the PGE amount in the CSF and the blood dropped in comparison with 3-minute hypercapnia being below the basal level in the blood. It is suggested that in hypocapnia PGE should limit its constrictive effect on the cerebral vessels while under conditions of hypercapnia they are to promote the realization of the cerebral vessel reaction to CO2.
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PMID:[Variations in prostaglandin E content in the arterial blood and cerebrospinal fluid under conditions of hypo- and hypercapnia]. 51 23

Changes in myocardial performance after administration of gallamine 1.5 mg kg-1 and pancuronium 0.1 mg kg-1 were investigated in hypercapnic (PaCO2 = 7.08 kPa) and hypocapnic (PaCO2 = 2.74 kPa) dogs anaesthetized with thiopentone, nitrous oxide and halothane. Administration of pancuronium during hypocapnia caused a decrease of 25% in dP/dt max (corrected for changes in preload, afterload and heart rate). This change was not seen during hypercapnia, probably because of the associated sympathetic stimulation. By contrast, gallamine was without effect on dP/dt max in both groups. The increase in heart rate and cardiac output caused by the atropine-like action of both groups. The increase in heart rate and cardiac output caused by the atropine-like action of these relaxant drugs differed in the hypercapnic and hypocapnic group of dogs, with the more pronounced response in the latter group. The duration of the chronotropic changes was the same in both groups.
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PMID:Changes in myocardial performance induced by pancuronium and gallamine in hypercapnic and hypocapnic dogs. 58 99

The influence of the prevailing PaCO2 on the water-retaining effects of sustained elevations in ADH was assessed by administering vasopressin (5 U in oil, twice daily) and a fixed water intake to dogs with eucapnia (n, 7), chronic hypercapnia (n, 6), and chronic hypocapnia (n, 8). Although water excretion initially fell to a similar extent in all three groups, cumulative water retention by day 4 of vasopressin administration was 77 mg/kg in the hypocapnic group, 46 ml/kg in the eucapnic group, and only 14 ml/kg in the hypercapnic group. These differences were reflected in a marked disparity in the degree of hyposmolality of body fluids, plasma osmolality falling by day 4 to an average value of 223, 237, and 268 mosmol/kg in the hypocapnic, eucapnic, and hypercapnic animals, respectively. In a separate group of dogs, water deprivation and water loading studies revealed that sustained hypercapnia does not affect the maximal concentrating or diluting ability of the kidney. We conclude, therefore, that the striking influence of the prevailing PaCO2 on the water-retaining effects of administered vasopressin cannot be ascribed to an altered responsiveness of the nephron per se, but that this influence reflects an alteration in the ease with which the kidney can escape from the antidiuretic effects of this substance.
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PMID:Influence of steady-state PaCO2 on escape from ADH-induced water retention in the dog. 64 65

An anaesthetic circle system without a carbon dioxide absorber is described. The efficiency of the circle, i.e., the fraction of alveolar gas in the outflow from the circle, was measured in 15 patients during halothane anaesthesia or neurolept analgesia. The fraction ranged from 0.88 to 0.95 (mean 0.91), while the ratio between the alveolar ventilation and the fresh gas inflow ranged from 0.97 to 1.71. The efficiency was not correlated to this ratio. There was no need for hyperventilation if the fresh gas inflow was 10% higher than the alveolar ventilation required to maintain normal PaCO2. The circle was used in 50 patients manually ventilated by nurse anaesthetists. Mean fresh gas inflow was 60 ml/kg. Mean PaCO2 was 5.47 kPa (41 mmHg). In a similar group of 50 other patients, in which the standard circle used in the department was employed, the mean PaCO2 was 4.80 kPa (36 mmHg). The frequency of hypercapnia was equal in the two groups, but hypocapnia was not seen when the circle without absorber was used.
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PMID:A circle system without carbon dioxide absorption. 67 46

Previous studies have demonstrated a significant pressure gradient from carotid artery to pial or middle cerebral arteries. This pressure gradient suggests that large cerebral arteries contribute to cerebral resistance. We have tested the hypothesis that large cerebral arteries contribute to regulation of cerebral blood flow during changes in blood gases and arterial pressure. Microspheres were used to measure brain blood flow in anesthetized dogs. Resistance of large cerebral arteries was estimated by determining the pressure gradient between common carotid and wedged vertebral artery catheters. Systemic hypercapnia and hypoxia dilated large cerebral arteries, and hypocapnia constricted large cerebral arteries. Resistance of large arteries was 0.6+/-0.1 (mean +/- SE) mm Hg per ml/min per 100 g during normocapnia. During hypercapnia and hypoxia, large artery resistance decreased significantly to 0.2 +/- 0.03 and 0.3 +/- 0.05, respectively. During hypocapnia large artery resistance increased significantly to 1.0 +/- 0.1. In other experiments, we found that large cerebral arteries participate in auto-regulatory responses to hemorrhagic hypotension. When arterial pressure was reduced from 110 to 58 mm Hg, autoregulation maintained cerebral blood flow constant, and resistance of large cerebral arteries decreased significantly from 1.0 +/- 0.2 to 0.6 +/- 0.1 mm Hg per ml/min per 100 g. In absolute terms, we calculated that 20-45% of the change in total cerebral resistance during these interventions was accounted for by changes in large artery resistance. These studies indicate that large cerebral arteries, as well as arterioles, participate actively in regulation of cerebral blood flow during changes in arterial blood gases and during autoregulatory responses to hemorrhagic hypotension.
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PMID:Role of large arteries in regulation of cerebral blood flow in dogs. 70 75

Experiments on anesthetized chickens were conducted to study interactions between afferent activity from the intrapulmonary and systemic CO2-sensitive chemoreceptors in the generation of respiratory amplitude (RA) and respiratory frequency (f). The thoracoabdominal cavity was opened, air sacs ruptured and each lung independently and unidirectionally ventilated. Intrapulmonary chemoreceptor activity was altered by changing the PCO2 of the ventilatory gas (PICO2) to the vascularly isolated right lung (VIL); systemic chemoreceptor activity was altered by changing the PICO2 to the denervated left gas exchange lung (GEL). Respiratory amplitude and frequency responses to changes in intrapulmonary PCO2 were determined at four levels of systemic arterial PCO2 (PaCO2). The results indicate that elevating PaCO2 shifts the pulmonary CO2-response curves for both RA and f to the left and increases the sensitivity of the RA-CO2 response curve but decreases the sensitivity of the f-CO2 response curve. We conclude that (1) interaction occurs between intrapulmonary and systemic afferent activity in the generation of RA and f, (2) the nature of the interaction is synergism with respect to RA and interference with respect to f, and (3) the interaction is greater during hypocapnia than hypercapnia.
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PMID:Intrapulmonary and systemic CO2-chemoreceptor interaction in the control of avian respiration. 70 70

We have attempted to identify the afferent endings responsible for the pulmonary-CO2 ventilatory reflex. We recorded afferent vagal impulses arising from the left lung in anesthetized dogs with separately ventilated lungs. When the left pulmonary artery was occluded, left lung PCO2 fell to 3 mm Hg and slowly-adapting pulmonary stretch receptor activity increased 46%. Firing declined to its original intensity when left lung PCO2 was raised in steps by administration of CO2, firing decreasing most between 2 and 19 mm Hg, and least between 30 and 50 mm Hg. Irritant receptor activity also increased (from 2.8 to 7.4 impulses/sec) after pulmonary arterial occlusion, the effect being reversed by administration of CO2. These procedures caused trivial changes in pulmonary and bronchial C-fiber activity. Effects on both slowly-adapting stretch receptors and irritant receptors appeared to result from a direct action of CO2 on the endings themselves, rather than from mechanical changes in the lung. Changes in slowly-adapting stretch receptor activity provide an adequate explanation for the pulmonary-CO2 ventilatory reflex, the relationship between impulse frequency and lung PCO2 suggesting that these afferents may have a role in limiting CO2 loss under conditions causing hypocapnia, but be less effective in stimulating breathing during hypercapnia.
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PMID:II. Effect of CO2 on afferent vagal endings in the canine lung. 70 75

The joint response of the respiratory and panting centres of fully-conscious unidirectionally-ventilated chickens to simultaneous combinations of hyperthermia and hypo-/hypercapnia was examined. The response was monitored by changes in the rate and amplitude of movements of the body wall and gular apparatus respectively. The response to a combination of hyperthermia plus hypercapnia bore indications of a linear summation of the individual responses of the panting centre and respiratory centre to the respective thermal and chemical stimuli. A more complex response was elicited by a combination of hyperthermia plus hypocapnia. In this case the inhibition of respiratory movements induced by the hypocapnia (hypocapnic apnea) permitted a more forceful manifestation of the component of the thermoreflex which acts via the hyoid muscles and which is responsible for the synchronous 'gular flutterin'. The rate of gular fluttering increased by up to 150% as compared to normal panting. The experimental procedure therefore provided a technique for breaking the central linkage which normally constrains the rhythm of the hyoid muscles to the more dominant rhythm of the respiratory muscles.
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PMID:Experimentally induced antagonism of chemical and thermal reflexes in the respiratory system of fully conscious chickens. 70 90

The aim of this paper has been to review and discuss the past and the recent investigations concerned with the study of cerebral transport phenomena in pathological conditions which have been divided into two main parts: (1) the effects of experimentally induced blood brain barrier (BBB) injury by (a) HgCl2 or (b) hyper-osmolar intracarotic perfusate; and (2) the effects of ischemia or of an altered oxygen saturation and pCO2 tension on glucose and/or amino acids and/or protein transport across the BBB, in the syanptosomes and cerebral capillaries. The most important observations were as follows: (1) HgCl2 or hyperosmolar perfusates produced an increased BBB permeability to protein tracers but the brain uptake of glucose analogues was found decreased following the former, and increased (except for lactamide) after the latter treatment. (2) (a) In ischemia, the noted increased vesicular transport of peroxidase, as well as the increased saturable and non-saturable passage of glucose analogues across the BBB depended on the duration of cerebral deprivation of blood supply which never resulted in degeneration of endothelial cells of the brain vessels. (b) The progressively decreased specific 2-deoxy-D-glucose uptake in the synaptosomes seen during cerebral ischemia of 30-180 minutes returned to the level of controls 1 hour after reestablishment of cerebral circulation. (c) A decrease in brain uptake of glucose analogues and amino acids (with few exceptions) was observed in severe hypoxia and hypercapnia while an increase or no change in the brain uptakes was seen in hypocapnia. (d) Preliminary investigations of the 2-DG uptake by the cerebral capillaries obtained by fractionation of the brain from animals subjected to normal or altered oxygen saturation and pCO2 tension suggested that cerebral glucose uptake may be directly related to its capillary function.
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PMID:Pathological aspects of brain transport phenomena. 78 95


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