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At least 19 recordsLinked to original sources

PubMed1992

Regional venous outflow, blood volume, and sympathetic nerve activity during hypercapnia and hypoxic hypercapnia.

We examined the changes in systemic blood volume and regional venous outflow from the splanchnic, coronary, and other remaining vascular beds in response to acute hypercapnia or hypoxic hypercapnia in dogs, using cardiopulmonary bypass and a reservoir. Hypercapnia (PCO2 = 105 mmHg) (1 mmHg = 133 Pa) and hypoxic hypercapnia (PO2 = 23 mmHg, PCO2 = 99 mmHg) caused marked decreases in systemic blood volume of 14 +/- 3 and 16 +/- 3 mL/kg in spleen-intact dogs, and 3 +/- 2 and 10 +/- 2 mL/kg in splenectomized dogs, respectively. Splanchnic venous outflow increased by 12% at 3.5 min hypercapnia, whereas it decreased by 60% at 3.5 min hypoxic hypercapnia. Coronary venous outflow increased by 85 and 400% at 3.5 min hypercapnia and hypoxic hypercapnia, respectively. Sympathetic efferent nerve activity revealed a significant augmentation during hypoxic hypercapnia and a relatively smaller increase (30% of the response to hypoxic hypercapnia) during hypercapnia. Carotid and aortic chemoreceptor and baroreceptor denervation attenuated significantly the response of systemic blood volume to hypercapnia and hypoxic hypercapnia. The regional venous outflow responses to hypercapnia were not altered after chemodenervation, but those to hypoxic hypercapnia were significantly attenuated after chemodenervation. These results suggest that acute hypercapnia and hypoxic hypercapnia caused a marked decrease in vascular capacitance owing primarily to an increase in sympathetic efferent nerve activity via chemoreceptor stimulation. They also indicate that blood flow to the splanchnic vascular bed during hypercapnia increased (even though the cardiac output was constant), whereas it increased to the extrasplanchnic and coronary vascular beds during hypoxic hypercapnia.

Animals↗

PubMed1990

Peripheral chemoreceptor control of fetal renin responses to hypoxia and hypercapnia.

The renin response to hypoxia in late gestation fetal sheep has been well characterized. However, the renin response to asphyxia--the combination of hypoxia and hypercapnia--has not been extensively studied. The purpose of this study was to determine 1) the interaction of hypoxia and hypercapnia in the control of renin secretion in late gestation fetal sheep and 2) the role of peripheral arterial chemoreceptors therein. Chronically catheterized fetal sheep (intact or sinoaortic denervated) were exposed to hypoxia and/or hypercapnia for 30 minutes. Hypercapnia alone had no effect on plasma renin activity or aldosterone but did result in a significant increase in angiotensin II. Hypercapnia combined with hypoxia resulted in a significant increase in renin activity, angiotensin II, and aldosterone. Sinoaortic denervation attenuated the renin and angiotensin II responses to hypercapnia plus hypoxia. The increase in renin and angiotensin II in response to hypercapnia with or without concomitant hypoxia strongly correlated with the magnitude of the decrease in arterial pH in intact fetuses only. Hypoxia alone and in concert with hypercapnia increased mean arterial pressure and decreased heart rate in intact but not sinoaortic denervated fetuses. We conclude that 1) hypercapnia more potently increases plasma renin activity than does hypoxia in late gestation fetal sheep, 2) arterial pH may be the relevant signal perceived by the peripheral arterial chemoreceptors for the control of the renin-angiotensin system during asphyxia, and 3) the cardiovascular response to hypoxia is mediated, in part, by peripheral arterial chemoreceptors.

Aldosterone↗

PubMed1975

Effects of mechanical loading and hypercapnia on inspiratory muscle EMG.

The electromyograms of the diaphragm and an external intercostal muscle were analyzed to see if the effects of hypercapnia on inspiratory muscle electrical activity could be distinguished from those of mechanical loading and to determine whether changes in inspiratory muscle electrical activity were a sueful measure of CO2 response during mechanical loading. Anesthetized dogs were studied: 1) during progressive hypercapnia without mechanical loading, 2) during flow-resistive and elastic loading at constant PCO2, and 3) during progressive hypercapnia and mechanical loading. Both mechanical loading and hypercapnia increased total inspiratory diaphragmatic and intercostal muscle electrical activity. However, inspiratory duration was increased by mechanical loads but reduced by hypercapnia. Because of these changes in inspiratory duration, the average rate of diaphragmatic electrical activity remained unaffected by mechanical loading before and after vagotomy but was increased by hypercapnia. In contrast, both hypercapnia and mechanical loading increased the average rate of intercostal muscle electrical activity. There was a greater increase in both total and average rate of intercostal muscle electrical activity during hypercapnia in the presence of mechanical loading than during unloaded breathing. However, the change in total and average rate of diaphragmatic electrical activity with PCO2 was unaffected by added mechanical loads. These results suggest that diaphragmatic but not intercostal muscle electrical activity can be used as an index of CO2 response even during mechanical loading.

Airway Resistance↗

PubMed1976

Ventilation in conscious dogs during acute and chronic hypercapnia.

Minute ventilation was measured in conscious dogs, at rest and during exercise (1 mph), over 60 min immediately following the acute inhalation of 5% carbon dioxide in air and at 2, 4, 7, and 14 days while breathing the same gas mixture in a chamber. The dogs were also studied in the immediate period of air recovery from chronic hypercapnia and 1 day later. Control studies were carried out with the dogs breathing air in the chamber under comparable conditions. A triphasic ventilation change was ovserved in dogs at rest over the 14 days of hypercapnia. After an initial marked increase in ventilation during acute hypercapnia, ventilation returned to control levels by 2 days and then appeared to be elevated above control studies from 4 to 14 days at a time when blood acid-base balance became compensated. When the same dogs were studied during exercise, ventilation was also not different from air control at 2 days of hypercapnia; however during exercise, unlike the resting studies, there was only a tendency for a secondary increase in ventilation at 7 and 14 days of hypercapnia. During the immediate recovery from chronic hypercapnia when the dogs breathed air there was no evidence of hypoventilation either at rest or exercise despite arterial alkalosis. At 24 h of recovery it appeared that dogs while at rest had a slightly reduced ventilatory response to 5% carbon dioxide relative to control studies. The findings provide suggestive evidence that other factors, in addition to acid-base balance, might contribute to the regulation of ventilation during chronic hypercapnia and the recovery from chronic hypercapnia.

Acid-Base Equilibrium↗

PubMed1991

Effects of hypoxia and hypercapnia on the force-velocity relation of rabbit myocardium.

The separate effects of hypoxia and hypercapnia on the force-velocity relation of rabbit myocardium were compared in 10 papillary or trabecular muscles superfused using control (95% O2-5% CO2), hypoxic (18% O2), and hypercapnic (20% CO2) physiological salt solutions. This level of hypoxia did not irreversibly damage the muscles and reduced peak isometric force by 53 +/- 11%. The level of hypercapnia was chosen to match the force depression (50 +/- 12%) produced by hypoxia. Multiple force-velocity points were measured by applying critically damped isotonic force steps at 90% of the time to peak isometric force and at the time to 50% peak isometric force. These points defined the force-velocity relation and maximum velocity of shortening, the extrapolated isometric force, and the maximum power of nonpotentiated and postextrasytolic potentiated contractions. Hypoxia and hypercapnia reduced maximum force and maximum power nearly equally. Maximum velocity of shortening decreased more during hypoxia (21 +/- 12%) than during hypercapnia (12 +/- 9%) (p less than 0.01). Postextrasystolic potentiation completely reversed the reduction of maximum velocity of shortening during hypercapnia but not during hypoxia. A 6% internal load could account for the reduction in maximum velocity of shortening during hypercapnia and all but 9% of the reduction in maximum velocity of shortening during hypoxia. The relative time course of the force-velocity relation was not altered by either hypoxia or hypercapnia. We conclude that hypercapnia reduces the effect of activation because increased activation (by postextrasystolic potentiation) restored the force-velocity relation and maximum velocity of shortening to control values.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1991

Effect of hypercapnia on total pulmonary resistance during wakefulness and during NREM sleep.

We investigated the effect of different levels of hypercapnia on total pulmonary resistance (RL) in 13 subjects ranging from nonsnorers with low RL to snorers with high RL and dynamic narrowing of the upper airway during inspiration. Added CO2 was adjusted to achieve a steady-state increase in PETCO2 of +2, +4, or +6 mm Hg. RL was measured at peak inspiratory flow (RLpf), at maximal resistance within breath (RLmax), and at 10 equally spaced points within inspiration in several trials. During wakefulness, hypercapnia was associated with decreased RLmax. During steady state +6 mm Hg hypercapnia, RLmax decreased by 30% (p less than 0.01). During NREM sleep, low levels of hypercapnia did not affect RL. However, +6 mm Hg hypercapnia was associated with decreased RLmax in six of eight subjects (p = 0.07), especially in subjects with high RLmax during room air breathing. The effects of hypercapnia on RLpf paralleled its effect on RLmax. We concluded that (1) the decrease in RL during awake hypercapnia suggests an increase in upper airway dimensions and stiffness, (2) the absence of increased RL during low level NREM hypercapnia (despite the increase in inspiratory flows and collapsing pressures) also suggests an increase in upper airway dimensions and stiffness, and (3) upper airway dilating muscles appear to be recruited in a coordinated fashion with inspiratory muscles in normal humans during NREM sleep. The implications of these findings in patients with obstructive sleep apnea are not clear at this point.

Airway Resistance↗

PubMed1976

The CSF HCO3 increase in hypercapnia relationshp to HCO3, glutamate, glutamine and NH3 in brain.

To study the role of carbonic anhydrase in the CSF [HCO3] increase in respiratory acidosis and its effect on brain ammonia, anesthetized rats were subjected to hypercapnia (7% CO2) for 2 hours. The animals received periodic intraventricular injections of either 'mock' CSF or 'mock' CSF and acetazolamide for 45 minutes prior and during hypercapnia when: (a) plasma [HCO3-] was allowed to increase normally and (2) plasma [HCO3] increase was prevented by i.v. HC1 infusion, CSF [HCO3] increased 8.5 mM/L after 2 hours of hypercapnia (delta PCO2 40) in the rats with intraventricular 'mock' CSF injections, and only 6 mM/L in the animals with acetazolamide injections. CSF [HCO3-] increased 7 mM/L during hypercapnia and HCl infusion with intraventricular 'mock' CSF injections, but only 2 mM/L with acetazolamide injections. Changes in total brain CO2 (increase) and brain glutamic acid (decrease) in hypercapnia were not affected by intraventricular acetazolamide and i.v. HCl. The increase of brain NH4+ and glutamine in hypercapnia was reduced in these conditions. It is concluded that there are at least two sources for the CSF [HCO3-] increase in hypercapnia; one formed in the CNS and dependent on carbonic anhydrase, and the other derived from plasma [HCO3-] increase.

Acetazolamide↗

PubMed1992

In vitro responses of caudal hypothalamic neurons to hypoxia and hypercapnia.

Results from previous studies have suggested that the hypothalamus modulates cardiorespiratory responses to hypoxia and/or hypercapnia. Many neurons in the caudal hypothalamus are stimulated by hypercapnia and hypoxia in vivo; however, it is not known if these responses are dependent upon input from other areas. Whole-cell patch and extracellular recordings from a brain slice preparation were used in the present study to determine the direct effects of hypoxia (5% CO2/95% N2 or 10% O2/5% CO2/85% N2) and hypercapnia (7% CO2/93% O2) on caudal hypothalamic neurons in vitro. Coronal sections (400-500 microns) were obtained from young Sprague-Dawley rats and placed in a recording chamber that was perfused with nutrient media equilibrated with 95% O2/5% CO2. Extracellular recordings demonstrated that hypoxia stimulated over 80% of the neurons tested; the magnitude of the response was dependent upon the degree of hypoxia. In addition, over 80% of cells that were excited by hypoxia retained this response during synaptic blockade. Hypercapnia increased the discharge frequency of 22% of the caudal hypothalamic neurons that were studied. A second set of caudal hypothalamic neurons were studied with whole-cell patch recordings; the mean resting membrane potential of these neurons was -51.8 +/- 1.0 mV with an average input resistance of 399 +/- 49 M omega. Hypoxia produced a depolarization in 76% of these neurons; a poststimulus hyperpolarization often occurred. A depolarization and/or increase in discharge rate during hypercapnia was observed in 35% of the neurons tested. Only 10% of all neurons studied were excited by both hypoxia and hypercapnia. These findings suggest that separate subpopulations of caudal hypothalamic neurons are sensitive to hypoxia and hypercapnia. Thus, this hypothalamic area may be a site of central hypoxic and hypercapnic chemoreception.

Animals↗

PubMed1992

Topical arachidonic acid restores pial arteriolar dilation to hypercapnia of postischemic newborn pig brain.

In the newborn pig, cerebral vasodilator responses to hypercapnia are lost after cerebral ischemia. We examined the effect of topical application of arachidonic acid (30 micrograms/ml, 20 min) to the postischemic piglet brain on subsequent pial arteriolar dilated in response to hypercapnia (10% CO2 ventilation) and topical isoproterenol (10(-6), 10(-7) M). After 20 min cerebral ischemia, pial arterioles did not dilate to hypercapnia but responded to isoproterenol in a fashion similar to before ischemia. Treatment with arachidonic acid after ischemia restored pial arteriolar dilation to hypercapnia. Hypercapnia caused an increase in cortical periarachnoid concentration of 6-ketoprostaglandin F1 alpha (6-keto-PGF1 alpha) before but not after ischemia. After postischemic treatment with arachidonic acid, the increase in cortical periarachnoid fluid 6-keto-PGF1 alpha during hypercapnia was restored. Therefore, topical application of arachidonic acid to cerebral vessels restores cerebral prostanoid synthesis and pial arteriolar dilation in response to hypercapnia that has been abolished by ischemia.

Administration, Topical↗

PubMed1991

Vascular responses of choroid plexus during hypercapnia in rats.

The response of blood flow to choroid plexus (CPBF) during hypercapnia is controversial. The goal of this study was to determine the effect of hypercapnia on CPBF in unanesthetized rats. Rats breathed air or a mixture of 5-8% CO2 in air, and CPBF was measured with [14C]isopropyliodoamphetamine and quantitative autoradiography. In hypercapnic rats [arterial PCO2 61.6 +/- 1.6 (SE) mmHg; n = 7] CPBF was similar to that of normocapnic control rats (525 +/- 39 ml.min-1.100 g-1; arterial PCO2 42.7 +/- 0.6 mmHg; n = 5). In contrast, blood flow to cerebral cortex increased 67% during hypercapnia. CPBF in normocapnic rats that were treated with phentolamine was similar to untreated normocapnic and hypercapnic rat CPBF. However, during hypercapnia, CPBF in phentolamine-treated rats increased 29%. Responses were similar in blood flow to choroid plexus of lateral, third, and fourth ventricles. Our findings indicate that hypercapnia has no effect on CPBF when alpha-adrenergic receptors are intact. In contrast, after blockade of alpha-adrenergic receptors, hypercapnia increases CPBF. These findings suggest that, during hypercapnia, levels of sympathetic activity or blood-borne catecholamines are increased that prevent increases in CPBF.

Amphetamines↗

PubMed1991

Hypercapnia and stimulation of the substantia innominata increase rat frontal cortical blood flow by different cholinergic mechanisms.

This study was designed to further investigate in the rat how the cerebrovascular response to excitation of the projections from the substantia innominata (SI) to the frontal cerebral cortex was mediated. Local cortical blood flow (CoBF) (by helium clearance) and tissue gas partial pressures (pO2, pCO2) (indices of energy metabolic activity) were measured in the frontal cortex in unanesthetized adult Fischer rats in response to electrical stimulation of the SI and, for comparison, in hypercapnic conditions. SI stimulation and hypercapnia increased CoBF to a similar extent (+92% and +106%, respectively). Differences between the changes in tissue gas partial pressures under hypercapnia and SI stimulation suggest that different patterns of flow-metabolism coupling prevail in the mechanisms underlying the two cerebrovascular responses. Cortical pCO2 increased under hypercapnia, but decreased during SI stimulation, indicating that a 'vascular' mechanism (i.e. independent of energy metabolism activation) is at least partly responsible for the flow increase in the latter condition. However, cortical pO2 rose more under hypercapnia than during SI stimulation, suggesting that oxygen consumption, and hence energy metabolism, was increased in the latter case. The ability of the acetylcholine esterase inhibitor physostigmine and the muscarinic receptor antagonist scopolamine to modulate the responses was quantified. In both experimental conditions, CoBF changes were potentiated by 0.15 mg/kg/h physostigmine (by factors of about 2). In contrast, 1 mg/kg scopolamine reduced by 65% the frontal CoBF response elicited by SI stimulation but was without effect on the response to hypercapnia. Thus, although a cholinergic mechanism may be implicated in both responses, activation of muscarinic receptors appears to occur when the stimulation originates from the SI but not from the hypercapnia.

Animals↗

PubMed1991

Mechanical properties of the rabbit upper airway during hypoxia and hypercapnia.

It has been suggested that the response of upper airway muscles to hypoxia may be different from the response of these muscles to hypercapnia. We therefore measured pulmonary ventilation and the mechanical properties of the isolated upper airway in 9 anesthetised rabbits during respiration of hypoxic and hypercapnic gas mixtures. Each animal was exposed to several levels of elevated inspiratory CO2 fraction, FICO2 (0.03 to 0.17) and depressed inspiratory O2 fraction, FIO2 (0.19 to 0.09). The steady-state ventilatory response, the tidal pressure in the upper airway (PTUA) and the upper airway elastance were measured under each condition. Straight lines were calculated by least squares regression relating pulmonary VT to FICO2 and FIO2 and PTUA to FICO2 and FIO2. The PTUA was estimated graphically at two levels of hypoxia and hypercapnia producing equal augmentation of VT. The ratio of PTUA during hypoxia to PTUA during hypercapnia was 1.06 +/- 0.21 (mean +/- 95% C.I.) at low VT and 1.15 +/- 0.25 at high VT. Elastance of the upper airway rose from 6.25 +/- 1.13 cmH2O/ml under control conditions to a maximum of 7.95 +/- 1.24 cmH2O/ml (P less than 0.05) during hypercapnia and to a maximum of 8.02 +/- 1.17 cmH2O/ml (P less than 0.05) during hypoxia. There was no difference between the mean (+/- 95% C.I.) change associated with hypercapnia (1.64 +/- 1.08 cmH2O/ml) and the mean change associated with hypoxia (1.77 +/- 1.26 cmH2O/ml). We concluded that hypoxia did not result in a greater change in upper airway mechanical properties than hypercapnia.

Animals↗

PubMed1976

Effects of hypercapnia on uterine and umbilical circulations in conscious pregnant sheep.

Changes in the uterine and umbilical circulations during induced hypercapnia were studied in nine unanesthetized near-term pregnant sheep. Blood flows were measured with electromagnetic flow transducers and arterial pressures with vascular catheters implanted under anesthesia 2-16 days prior to experiments. Hypercapnia was induced in the fetus alone by giving acetazolamide iv to the fetus, 100-200 mg/kg. Mean fetal arterial Pco2 increased from 49.5 to 63.4 mmHg but no significant changes in umbilical blood flow occurred. Stepwise increases in both maternal and fetal arterial Pco2 were induced by increasing maternal inspired CO2 concentration to a maximum of 12%. No dignificant changes occurred in uterine or umbilical circulations until hypercapnia was severe (maternal arterial Pco2 greater than 60 mmHg, fetal arterial Pco2 greater than 70 mmHg). With severe hypercapnia uterine vascular resistance increased significantly and uterine blood flow decreased despite an increase in maternal arterial pressure; fetal arterial pressure and umbilical blood flow increased significantly, but umbilical vascular resistance did not. We conclude that hypercapnia in conscious pregnant sheep is associated with significant changes in uterine and umbilical circulations, but only when hypercapnia is severe. Carbon dioxide is unlikely to be a factor in normal physiological regulation of the uteroplacental circulation in this species.

Acetazolamide↗

PubMed1976

Effect of meperidine on occlusion pressure responses to hypercapnia and hypoxia with and without external inspiratory resistance.

In 5 normal subjects we measured ventilation and P0.1, the pressure generated by the first 0.1 sec of inspiratory effort against a closed airway, in response to hypercapnia and hypoxia with and without added inspiratory resistance before and after oral meperidine (1.1 to 1.3 mg per kg). CO2 responses were studied in the steady state, whereas progressive hypoxia was used to elicit hypoxic responses. In general, resistance decreased ventilatory responses to hypercapnia but increased P0.1 responses to both hypoxia and hypercapnia. Meperidine depressed both ventilatory and P0.1 responses, more so in hypoxia than in hypercapnia. The combination of resistance and merperidine was additive in depressing responses to hypercapnia but in hypoxia produced little more depression than did meperidine alone. In both hypercapnia and hypoxia, meperidine decreased the augmentation of P0.1 that was associated with increased resistance. Normal subjects responded to acute increases of inspiratory resistance by increasing inspiratory motor output; this increase was distinctly blunted by meperidine.

Adult↗

PubMedDate not supplied

[Bone electrolytes in experimental chronic hypercapnia (author's transl)].

The role of the skeleton in electrolyte equilibrium, well known for various diseases, remains difficult to understand during chronic hypercapnia. An experimental study of normoxic (O2:21%) hypercapnia (CO2:8 +/- 1%) was carried out for two, four and six weeks, followed by a systematic quantitative determination, in thigh-bone samples of Na+, K+, Ca++, PO4--, N2 and CO2 in 72 rats, and of total H2O and extracellular H2O (H2Oe) in 129 rats. Considering the mean values of groups (from 16 to 42 subjects for each group), at various times of hypercapnia, bone K+ was increased during hypercapnia (+3 to 4 X 10(-3) mEq/g fresh tissue), Ca++ diminished (--12.5 to 15.4 mEq). PO4-- and Na+ temporarily decreased at two and four weeks of hypercapnia. On account of the scatter of individual results, only the variation of K+ was statistically significant (at two weeks). This increase in bone K+, accompanying a partially compensated acidaemia, is to compare with the significant hyperkaliemia observed at two and four weeks, whereas this period is characterized by a decrease in K+ in skeletal muscle, as shown in a previous work. In a group of 72 rats, the analysis of correspondances and correlations points out the bone CO2 as a very significant variable, opposite to the variable H2Oe. PO4--is positively correlated to Na+. The complexity of the results does not permit a decisive interpretation of the phenomenon. On the other hand, this study corroborates the bone calcium loss and reveals the gain in bone potassium during hypercapnia.

Animals↗

PubMed1992

Activity of abdominal muscle motoneurons during hypercapnia.

Our purpose was to examine the influence of hypercapnia on the activity of motoneurons innervating the transversus abdominis and internal oblique abdominal muscles, and of integrated phrenic and abdominal motor nerve activities. Studies were done in nine adult cats that were decerebrated, vagotomized, thoracotomized, paralyzed and ventilated mechanically. Of 42 motoneurons examined, 24 showed strong respiratory modulation (RM neurons), with the discharge confined primarily to the central expiratory period. The remaining 18 motoneurons discharged tonically, and failed to show respiratory modulation even at increased levels of central respiratory drive. Hyperoxic hypercapnia augmented the activities of the phrenic and abdominal nerves and increased the early expiratory discharge frequency of the RM neurons. The hypercapnia-induced increase in firing frequency during early expiration was accompanied by a corresponding decline in late expiration, and a virtual abolition of the inspiratory activity in the few neurons that discharged in this phase under normocapnic conditions. Finally, hypercapnia induced an increase in the number of spikes generated during each expiratory period in about half of the RM neurons, whereas the remaining cells showed a decrease. Thus, the increased peak activity of the integrated whole abdominal nerve burst with hypercapnia was brought about by a shift in the temporal pattern of motoneuron firing, or by an increase in the number of spikes generated during the expiratory period. The steep rate of rise and the pronounced early expiratory peak observed in the integrated abdominal nerve burst during hypercapnia in this preparation are consistent with the increase in motoneuron firing frequency during the early stages of the expiratory phase.

Abdominal Muscles↗

PubMed1976

The effect of hypercapnia on a blood-brain barrier mechanism in foetal and new-born sheep.

1. The effect of marked hypercapnia (arterial PCO2 100 mmHg), nonrespiratory acidosis (pH 6-95-7-15) or hypoxia (arterial PO2 10-15 mmHg) upon penetration of labelled sucrose from blood into brain and c.s.f. has been investigated in exteriorized foetal sheep and new-born lambs. 2. In hypercapnia there was a consistent increase in c.s.f./plasma sucrose ratio after 90 min I.V. sucrose to four to five times control. Brain/plasma sucrose ratios were more variable. Usually there was an increase (up to three-and-a-half-times control); sometimes there was no change or even a decrease. The effect of hypercapnia on sucrose penetration was reversible. 3. Hypercapnia reduced c.s.f. secretion rate to approximately half the control value. Hypercapnia also caused a decrease in brain extracellular space. 4. Non-respiratory acidosis did not affect sucrose penetration. Hypoxia caused a decrease in brain/plasma sucrose ratio. 5. It is concluded that hypercapnia can cuase an increase in cerebral vascular permeability to sucrose in foetal and new-born sheep. Some possible mechanisms are discussed.

Acid-Base Equilibrium↗

PubMed1977

Effects of sytemic hypoxia and hypercapnia on cutaneous and muscle vasoconstrictor neurones to the cat's hindlimb.

1. Reactions of cutaneous and muscle vasoconstrictor neurones to the hindlimb on systemic hypoxia and systemic hypercapnia were investigated in chloralose anaesthetized cats. Mainly four types of preparations were used: brain intact and decrebrate (pontomedullary) animals with and without carotid sinus (CSN) and vagal nerves (VN). 2. In brain intact animals with intact CSN and VN most cutaneous vasoconstrictor neurones were depressed and most muscle vasoconstrictor neurones were excited during systemic hypoxia and hypercapnia. The responses to hypercapnia were smaller than those to hypoxia. 3. In brain intact deafferented animals and in decerebrate animals with and without intact CSN and VN systemic hypoxia and hypercapnia induced excitation in both cutaneous and muscle vasoconstrictor neurones. The responses to hypoxia were significantly smaller in deafferented preparations when compared to those in preparations with intact CSN and VN. Furthermore in muscle vasoconstrictor neurones the size of the responses was not significantly different in decerebrate preparations from that in brain intact preparations. 4. These results indicate a distinct neuronal organization of the chemoreceptor reflexes in the vasoconstrictor systems in the brain stem. Suprapontine brain structures are most important for producing the inhibition of the cutaneous vasoconstrictor neurones during hypoxia and hypercapnia.

Animals↗