Systemic Hypercapnia Research Articles

Extended latency of the cortical component of the somatosensory-evoked potential accompanying moderate increases in cerebral blood flow during systemic hypoxia in cats

In 24 adult cats, the somatosensory-evoked potential (SEP) and cerebral blood flow (CBF) were measured under paralyzed, anesthetized conditions during exposure to two different ventilatory regimens. Group I cats (ventilated from 20 to 2% oxygen) responded ith a significant increase in white matter blood flow from 25.0 ± 7.8 to 43.8 ±10.5 ml/100 g/min recorded at 7% O 2. Gray matter blood flows in these animals increased but not to significant levels above the control blood flow measured at 20%. No significant changes in blood flow were observed in group II animals ventilated over the range of 25–30% oxygen as gray matter rose slightly (but not significantly) with hypoxia and white matter flows remained at levels of 25–30 ml/100g/min. The latency of the cortical component of the SEP was related to the degree of hypoxia. For both groups, significan textension in the latency to the occurrence of the cortical component of the SEP (normalized to the % of control SEP) occurred in each case ( P < 0.05). An inverse, linear relationship existed between the latency to the appearance of cortical component (ms) and the percentage oxygen concentration of the ventilatory mixture. No significant changes in thalamocortical conduction times were found, which indicates that hypoxia may have generalized effects on the synaptic pathways supporting the conduction of the SEP. The variation in blood flow and the latency of the cortical component observed between groups I and II may reflect the oxygen concentration used at the beginning of the experiment (25 vs 20%) and the gradations between them vs 3 and 2%. No systemic hypercapnia nor acidiosis was found within the mid-range oxygen concentrations which could account for the variations in flow and the evoked response. The results show that the SEP may be a reliable indicator of hypoxia as blood flows increase during transient cerebral hyperfusion probably resulting from vasodilation.

Chemical control of tracheal vascular resistance in dogs.

With anesthetized dogs we have measured upper tracheal vascular resistance on both sides of the trachea simultaneously by perfusing the cranial tracheal arteries and measuring inflow pressures at constant flows. The ratio of pressure to flow gave vascular resistance (Rtv). Lung airflow, blood pressure (BP), heart rate, and pressure in a cervical tracheal balloon (Ptr) were also measured. In paralyzed dogs, systemic hypoxia due to artificial ventilation with 10% O2-90% N2 increased Rtv by +8.1 +/- 1.0% (SE), Ptr by +76 +/- 22.8%, and BP by +18.9 +/- 24%. After bilateral cervical vagosympathectomy the increases in Rtv and BP were present (+8.8 +/- 0.9 and +22.3 +/- 0.3%, respectively). After carotid body denervation Rtv, Ptr, and BP increased (+6.4 +/- 1.3, +58.6 +/- 31.6, and +14.6 +/- 3.3%, respectively). After vagotomy Rtv and BP increased (+14.1 +/- 1.7 and +22.4 +/- 10.1%, respectively). Tracheal perfusion with hypoxic blood caused a small vasodilation (-2.2 +/- 1.1%). Systemic hypercapnia due to artificial ventilation with 8% CO2-92% air increased Rtv by +16.7 +/- 3.8%, Ptr by +67 +/- 2.0%, and BP by +12.9 +/- 9.9%. Tracheal perfusion with hypercapnic blood caused a small vasodilation (-2.5 +/- 1.2%). Stimulation of the carotid body chemoreceptors with KCN caused a small increase in Rtv (+1.2 +/- 0.5%) and increases in Ptr (+49.8 +/- 13.6%) and BP (+11.1 +/- 2.1%). Systemic hypoxia and hypercapnia caused tracheal vasoconstriction mainly by an action on the central nervous system.

Hypocapnia and hypercapnia in the dog: effects on myocardial blood-flow and haemodynamics during beta- and combined alpha- and beta-adrenoceptor blockade.

We have recently demonstrated an increase in myocardial blood-flow (MBF) during systemic hypercapnia independent of myocardial oxygen consumption. During hypocapnia no significant decrease of MBF was observed; however, a significant increase of myocardial oxygen extraction resulted. The present study was undertaken to examine whether these effects were caused by changes in the sympathoadrenal activity. During beta-adrenoceptor blockade and combined alpha- and beta-blockade the effects of hypocapnia and hypercapnia on MBF and haemodynamics were examined. Closed-chest dogs were anaesthetized with pentobarbital and hypocapnia was induced by hyperventilation. Carbon dioxide was added to the inspiratory gas to create normocapnia and hypercapnia. Hypocapnia did not result in any changes of MBF, coronary vascular resistance or myocardial oxygen extraction, neither during beta-adrenoceptor blockade nor during combined alpha- and beta-blockade. Hypercapnia did not increase MBF, neither during beta-blockade nor during combined alpha- and beta-blockade. However, both myocardial oxygen consumption and mechanical performance of the heart were reduced during hypercapnia. Thus, a relative myocardial overperfusion, indicated by decreased coronary vascular resistance and myocardial oxygen extraction, was observed during hypercapnia. In conclusion, the unaltered MBF during hypocapnia and the coronary overperfusion during hypercapnia were not related to changes in the sympathoadrenal activity.

The pattern of sympathetic neurone activity during expiration in the cat.

The properties of sympathetic preganglionic neurone activity during expiration were studied in pentobarbitone-anaesthetized (n = 26) and in non-anaesthetized, mid-collicular decerebrate (n = 5), paralysed, artificially ventilated cats in which the electrical activity of the phrenic nerve and of the cervical sympathetic trunk was recorded. In control conditions (end-tidal PCO2 between 35 and 40 mmHg, zero end-expiratory pressure) sympathetic activity during expiration was either steady at a low level (n = 11) or showed a modest progressive increase from a low level in early expiration (n = 17). Very infrequently (n = 3), it showed a transient increase during the second half of expiration. Artificial ventilation with positive end-expiratory pressures in the range from 2.1 +/- 0.4 (mean +/- S.D.) to 6.7 +/- 0.6 cmH2O caused, in cats with intact vagus nerves, an increase in sympathetic neurone activity during the second half of expiration. Within this range of pressures, the magnitude of the increase was related to the magnitude of the positive end-expiratory pressure. This effect reversed at higher positive end-expiratory pressures. Pressures in excess of 10.2 +/- 1.8 cmH2O caused inhibition of sympathetic activity. The sympatho-excitatory effect of positive end-expiratory pressure disappeared after bilateral cervical vagotomy. With intact vagus nerves, it also disappeared at levels of systemic hypocapnia (end-tidal PCO2 less than or equal to 15 mmHg) which abolished phrenic nerve activity. In hypocapnia, artificial ventilation with peak tracheal pressures greater than 7.2 +/- 1.1 cmH2O caused inhibition of sympathetic activity, while ventilation with lower end-expiratory pressures had no effect on sympathetic activity. It may be concluded that the sympatho-excitatory effect of positive end-expiratory pressure is mediated by vagal afferents and requires a certain level of brain-stem respiratory neurone activity. Sympatho-excitation during expiration was also observed, in normocapnic conditions, during short-duration static lung inflation with tracheal pressures in the range from 2.5 +/- 0.3 to 7.0 +/- 0.8 cmH2O as well as during artificial ventilation with zero end-expiratory pressure when lung inflation occurred in expiration. These responses were abolished by bilateral cervical vagotomy and during systemic hypocapnia. Sympatho-excitation during expiration was also observed when systemic hypercapnia was produced in vagotomized cats by artificial ventilation with gas mixtures containing 5 or 10% CO2.(ABSTRACT TRUNCATED AT 400 WORDS)

Modulation of the centrally-evoked visceral alerting/defence response by changes in CSF pH at the ventral surface of the medulla oblongata and by systemic hypercapnia.

In the present study on nine cats, repeated tests were made of the effects of superfusion of the ventral surface of the medulla oblongata with acid or alkaline CSF. Only two animals showed slight hyperventilation, tachycardia, mesenteric vasoconstriction and variable changes in hindlimb vascular conductance when the ventral surface was superfused with acid CSF; alkaline CSF produced opposite effects. These changes are qualitatively similar to, but much smaller than, published results which support the idea that the central chemoreceptor areas for CO2 are near the surface of the ventral medulla. But, in accord with those who have disputed this idea, the remaining 7 animals showed no response to superfusion with acid or alkaline CSF. Yet, all 9 animals showed marked hyperventilation in response to inhalation of 5% or 8% CO2. These findings accord with the view that chemosensitive structures on the ventral medulla represent part, but not all of the central chemosensitive mechanism for CO2. Inhalation of CO2 also induced bradycardia, mesenteric vasodilatation and either vasodilatation or vasoconstriction in hindlimb, attributable to a predominance of the direct myocardial depressant and local vasodilator effects of CO2, over the increase in sympathetic activity produced by central hypercapnia. But, despite the different effects of acid CSF and inhaled CO2 on baselines, they produced comparable effects on the visceral altering/defence response evoked by electrical stimulation in the ventral amygdalo-hypothalamic pathway viz, the magnitude of the characteristic hindlimb dilatation was reduced while that of the mesenteric constriction was increased.(ABSTRACT TRUNCATED AT 250 WORDS)

Neural effects of systemic hypoxia and hypercapnia on hindlimb vascular resistance in acute spinal cats.

The effects of systemic hypoxia and hypercapnia on the neurogenic component of hindlimb vascular resistance were studied in 10 unanesthetized acute Cl spinal cats. Hindlimb perfusion pressure (PP) was measured under conditions of constant flow of normoxic and normocapnic blood from a donor cat. Ventilation with 5% CO2 and 10% CO2 in O2 caused increases in PP of 15 +/- 2 (mean +/- SE) mm Hg and 27 +/- 3 mm Hg from a control level of 106 +/- 6 mm Hg during ventilation with 100% O2. Changing the inspired gas mixture from 95% O2 plus 5% CO2 to 12.5%, 10%, 7.5%, or 5% O2 plus 5% CO2 in N2 caused increases in PP of 1.5 +/- 1, 14 +/- 2, 38 +/- 6, and 69 +/- 15 mm Hg respectively from a control level of 121 +/- 9 mm Hg. These vasoconstrictor effects were abolished by ganglionic blockade with hexamethonium (10 mg/kg iv). We conclude that in the acute Cl spinal cat a large part of the population of sympathetic preganglionic neurons in the lumbar spinal cord, controlling vascular smooth muscle of the hindlimb, is excited by systemic hypoxia or hypercapnia over a considerable range of PaO2 and PaCO2 values.

Effects of systemic hypercapnia on one lung hypoxic pulmonary vasoconstriction in the dog

Effects of systemic hypercapnia on one lung hypoxic pulmonary vasoconstriction in the dog

Vascular capacitance responses to severe systemic hypercapnia and hypoxia in dogs.

The magnitude of vascular capacitance change induced by hypercapnia, hypoxia, or hypoxic hypercapnia was estimated during the administration of experimental gas mixtures to anesthetized dogs for 25 min. Mean circulatory filling pressure (Pcf) was determined by fibrillating the heart and equilibrating arterial and venous pressures with a pump. We assumed that the total blood volume remained constant and that the magnitude of change in peripheral venous volume equaled the sum of the changes in blood volume in the cardiopulmonary and arterial beds. We further assumed that active (reflex) peripheral venoconstriction occurred if the cardiopulmonary and arterial bed blood volumes, as well as the Pcf, increased. Within 3 min, severe hypercapnia and hypoxic hypercapnia induced a 5.2 and 7.3 ml/kg reduction in systemic vascular capacity, and, by 19 min of experimental gas presentation, increased Pcf by 5.5 and 7.0 mmHg, respectively. Severe hypoxia had less effect (0.7 ml/ kg and 2.5 mmHg, respectively) at 19 min. Severe hypercapnia also increased the central venous, systemic arterial, and pulmonary arterial pressures and decreased heart rate. Hypoxic hypercapnia additionally increased cardiac output. We conclude that severe systemic hypercapnia, whether alone or in combination with hypoxia, causes a significant active reduction in vascular capacitance, but severe hypoxia is less effective.

Vasoactive drugs produce selective changes in flow to experimental brain tumors.

Most vasoactive drugs do not readily penetrate the blood-brain barrier and do not affect cerebral blood flow. We tested the hypothesis that vasoactive drugs may alter blood flow to brain tumors in which the blood-brain barrier is abnormal. Blood flow was measured with microspheres in dogs with brain tumors induced by avian sarcoma virus. Intravenously administered adenosine increased blood flow to tumor more than twofold but did not alter flow to normal brain. Intravenously administered norepinephrine decreased blood flow to tumor but not to normal brain. Thus, vasoactive drugs, which have little effect on blood flow to normal cerebrum, produce large changes in blood flow to brain tumors. We also examined responses to systemic hypercapnia. Hypercapnia increased blood flow to normal cerebrum more than twofold but failed to increase flow to tumors. Impaired vasodilator responses to hypercapnia in brain tumors, which cannot be explained primarily by an abnormality of the blood-brain barrier, probably reflect another fundamental difference between vessels in normal brain and brain tumors. The finding that vasoactive drugs have selective effects on blood flow to brain tumors has important implications for delivery of lipid-soluble chemotherapeutic drugs to the tumors.

Splenic, renal, and cardiac nerves have unequal dependence upon tonic supraspinal inputs

Stimulation of visceral receptors can lead to unequal reflex responses in splenic, renal and cardiac sympathetic nerves. Activity of splenic nerves is often more excited or less inhibited than that of cardiac or renal nerves. This study was undertaken to determine potential differences in resting discharge among these 3 nerves. Dependence upon supraspinal drive was evaluated by comparing the relative decrease in activity of these nerves in chloralose-anesthetized cats 30 min to 2 h following high cervical spinal cord transection. After this transection, discharge rates of cardiac and renal nerves were significantly depressed to less than 50% of initial values. In contrast, splenic nerve activity was not significantly affected. To determine if this sustained splenic nerve activity resulted from greater responsiveness to potential external sources of excitation, splenic, renal and cardiac neural responses to factors known to affect sympathetic discharge in spinal animals were compared. Neither increased arterial pressure, decreased arterial pressure, systemic hypercapnia and acidosis, nor thoracolumbar dorsal rhizotomy revealed specific inputs responsible for the preferential maintenance of splenic nerve activity in spinal cats. It was concluded that ongoing activity of splenic nerves is less dependent upon supraspinal sources of excitation than is activity of renal or cardiac nerves. The cause of this difference among these 3 components of sympathetic outflow remains to be determined.

2-Deoxyglucose uptake in the central nervous system during systemic hypercapnia in the peripherally chemodenervated rat

Changes in 2-deoxyglucose (2-DG) uptake in the central nervous system during systemic hypercapnia were determined by the [ 3H]2-DG autoradiographic method in peripherally chemodenervated rats. Autoradiographs were made from serial transverse sections of the brain and analyzed by a computer-based interactive image processing system for areas having increases or decreases in metabolic activity compared with control animals. The most pronounced change shown by autoradiographs of the hypercapnic animals was a generalized decrease in the metabolism of the gray matter throughout the central nervous system with respect to the normocapnic controls. However, several central structures showed evidence of either no change or an increased metabolism in the hypercapnic animals. In the brain stem these areas were localized to the ventrolateral region of the nucleus of the solitary tract rostral to the obex, around the region of the nucleus retroambiguus, in a region of the ventrolateral medullary reticular formation extending rostrally from the obex to the level of the intramedullary rootlets of the facial nerve, in the region of the ventral nucleus raphe pallidus, and in the region of the lateral parabrachial nucleus. In the diencephalon these regions included the supraoptic nucleus and the dorsal hypothalamic area, extending into the caudal portion of the paraventricular nucleus. The thoracolumbar cord showed activation of the lateral aspects of the dorsal horns, the region of lamina X and the region of the intermediolateral nucleus. These data may be interpreted as a functional map of the central structures activated in hypercapnia in the peripheral chemodenervated rat. It appears likely that these structures are involved in mediating the cardiorespiratory responses associated with the activation of central chemoreceptors by the increased carbon dioxide concentrations.

Responses of sympathetic preganglionic neurons to systemic hypercapnia in the acute spinal cat

The relation between end-tidal (ET) pCO 2 and firing rate of sympathetic preganglionic neurons (SPN) of the cervical sympathetic trunk was studied during hyperoxic hypercapnia in acute C1 or C4 spinal cats. The cats were under barbiturate anesthesia or anemically decerebrate. The firing rate of the majority of the tonically active strands (18/22) increased in hypercapnia and showed a continuous relation to ET pCO 2 within the range studied. The firing rate of the remaining 4 strands was unaffected. The maximum increase in firing rate of the responsive strands was 3.7 times the control value on average (range 2.5–14.0). Recruitment of units which were silent in control conditions also occurred. These data demonstrate the existence of a spinal mechanism responsible for excitation of SPN during systemic hypercapnia.

Is the central inspiratory activity responsible for pCO2-dependent drive of the sympathetic discharge?

Out of 27 cats anesthetized with chloralose-urethane mixture, paralyzed, vagotomized and artificially ventilated, phrenic nerve response to systemic hypercapnia (7-8 vol.% CO2/O2 mixture) was accompanied by an increase in blood pressure and sympathetic discharge in 19 cats. Out of these 19 cats, 12 were totally debuffered and in the remaining 7 cats one carotid sinus nerve was left intact. Single unit activity in the sympathetic cervical nerve and spontaneous mass activity in the cervical, splanchnic, renal sympathetic and phrenic nerves were recorded. Evoked response in the phrenic nerve was produced by electrical stimulation of the descending bulbospinal inspiratory pathways in the midplane area of the medulla or in the ventrolateral cervical spinal cord. Starting from the control mean end-tidal CO2 concentration of 4.7 vol.% (+/- 1.0 S.D.) a progressing hypocapnia was induced by hyperventilation up to the end-tidal CO2 concentration of 1.3-3.2 vol.% (mean 2.4 vol.% +/- 0.5 S.D.) significantly below paCO2 apneic threshold. In chemo- and baroreceptor denervated cats with a pressor and excitatory sympathetic response to hypercapnia, a hypocapnia resulted in a fall of the arterial blood pressure (mean 16.9 mm Hg +/- 7.5 S.D., 2.2 kpa +/- S.D.). With the increasing paCO2 over the period of hypocapnic apnea a pressor and excitatory sympathetic response preceded, in all experiments, the onset of the phrenic nerve rhythmic activity. The difference between paCO2 threshold for the pressor and sympathetic response (35.7 mm Hg +/- 3.6 S.D., 4.7 kpa +/- 0.5 S.D.) and paCO2 threshold for the reappearance of the phrenic nerve rhythmic activity (43.6 mm Hg +/- 2.6 S.D., 5.8 kpa +/- 0.3 S.D.) was highly significant. If apneic hypocapnia was combined with the continuous stimulation of the afferent fibers of the superior laryngeal nerve the CO2 threshold for phrenic rhythmic activity was significantly increased whereas CO2 threshold for the pressor and sympathetic excitatory response remained unchanged. CO2 administration during hypocapnia apnea caused a progressing reduction of the magnitude of the evoked phrenic nerve response. From these findings it is concluded that the central excitatory effect of CO2 on the sympathetic activity may be accomplished in the absence of the rhythmic respiratory activity and independently of the subthreshold tonic inspiratory activity. Pressor and sympathetic excitatory response to CO2 observed during hypocapnic apnea is presumably caused by a neuronal pool different from that responsible for the central inspiratory activity. It is suggested that this CO2 sensitive neuronal mechanism might be involved in the central generation of sympathetic tone.

Regulation of blood flow to respiratory muscles during hypoxia and hypercapnia.

AbstractThe effect of systemic hypoxia or hypercapnia on regional blood flow was measured in respiratory muscles, limb muscles, and kidneys of rabbits by using radioactive microspheres. Blood flow to both the diaphragm and the intercostal muscles was increased in a direct relationship with the severity of the hypoxia or hypercapnia in spontaneously breathing animals. Blood flow to the kidneys decreased while blood flow to limb muscle remained unchanged. During mechanical ventilation, following paralysis with Flaxedil, blood flow to the respiratory muscles was about 10% of that seen during quiet breathing and was unchanged by hypoxia or hypercapnia. Renal flow decreased as in the nonparalyzed animals while flow to limb muscle remained unchanged during the hypoxic and hypercapnic episodes. It is concluded that the major factor involved in regulating blood flow to the respiratory muscles is their level of activity.

Role of large arteries in regulation of cerebral blood flow in dogs.

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.

Functional discrimination of postganglionic neurones to the cat's hindpaw with respect to the skin potentials recorded from the hairless skin.

1. Functional characteristics of postganglionic neurones innervating the hairless skin of the cats hindpaw have been analyzed with respect to the skin potentials recorded from the surface of the hair-less skin in chloralose anaesthetized, immobilized, and artificially ventilated animals. 2. Postganglionic neurones of which the activity was closely correlated with the fast transient negative atropine-sensitive skin potentials were called SM (sudomotor) neurones. Other, spontaneously active, postganglionic neurones whose activity was not correlated with these potentials were called VC (vasoconstrictor) neurones. 3. The SM neurones have low resting activity of 0.2±0.1 imp/s (mean±S.D.) or are silent; their axons conduct with 0.77±0.11 m/s. These neurones are activated by vibrational stimuli (tapping on the experimental frame), by noxious cutaneous stimuli, by systemic hypoxia and systemic hypercapnia. Their activity shows respiratory modulation, but no cardiac modulation. 4. The VC neurones have resting activity of 1.1±0.4 imp/s; their axons conduct with 0.52±0.11 m/s. These neurones are inhibited by noxious cutaneous stimuli, by systemic hypoxia and by systemic hypercapnia. Vibrational stimuli inhibit part of these neurones or are without effect. The activity in the VC neurones shows respiratory and cardiac modulations. These functional properties of the VC neurones to the hairless skin are largely identical to those innervating the hairy skin which were investigated recently in our laboratory. 5. The activity of the VC neurones is correlated with slow transient skin potentials which are atropine resistant. Decrease of the activity in these neurones is accompanied by slow transient skin potentials with positive polarity.

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.

Vascular response to short-term systemic hypoxia, hypercapnia, and asphyxia in the cat.

Acute systemic hypoxia, hypercapnia, or asphyxia was produced in ketamine-anesthetized, paralyzed cats by ventilating them for 2-4 min with appropriate gas mixtures. A sustained rise in arterial pressure occurred in all cases. Vascular responses to hypoxia (7% O2, 10% 02, or 14% O2) included muscle constriction, cutaneous (hindpaw) dilatation (no change with 14% O2), renal constriction (unchanged flow), and unchanged intestinal resistance. Asphyxia (hypoxia + 10% CO2) produced a similar pattern, except that intestinal dilatation occurred. Hypercapnia (10% CO2 + 21% O2) produced muscle constriction, renal constriction (unchanged flow), intestinal dilatation, and no change in cutaneous resistance. Intestinal dilatation seemed in all cases a response to elevated CO2 only. Hypercapnia augmented the effects of hypoxia in skin and skeletal muscle. The variation of responses in different vascular beds suggests a patterning of sympathetic discharge, and varying responsivity to local and humoral factors.

Effects of local and systemic hypercapnia on the discharge of stretch receptors in the airways of the dog

We have investigated the effects of local and systemic administration of 8 % CO 2 on the afferent discharge from slowly adapting stretch receptors located in a functionally isolated, in situ segment of trachea and extrapulmonary bronchi in dogs. Stretch receptors situated in the trachea were not affected by hypercapnia. Discharge from bronchial stretch receptors was diminished by local CO 2 administration, especially at low airway transmural pressures. Systemic hypercapnia was generally ineffective. The results indicate that stretch receptors in extrapulmonary bronchi are more accessible to CO 2 airway lumen than to perfusion with hypercapnic blood.

Effect of stimulation of carotid chemoreceptors on total and regional cerebral blood flow.

This study was performed to determine whether stimulation of the carotid chemoreceptors increases total or regional cerebral blood flow and whether activation of arterial chemoreceptors contributes to cerebral vasodilation during systemic hypoxemia. In anesthetized and ventilated dogs, carotid chemoreceptors were stimulated with nicotine or hypoxic and hypercapnic blood. To measure total and regional cerebral blood flow, we used labeled 15-mu microspheres. Stimulation of chemoreceptors did not increase cerebral blood flow or produce significant redistribution of cerebral blood flow, even though the chemoreflex was intact in these animals (as manifested by vasoconstriction in muscle, kidney, and small bowel) and the cerebral vessels dilated in response to systemic hypercapnia. In other studies in anesthetized, ventilated dogs and rhesus monkeys, cerebral vasodilator responses to systemic hypoxemia were observed before and after denervation of carotid and aortic chemoreceptors. Systemic hypoxemia produced large and equivalent increases in cerebral blood flow before and after chemodenervation. We conclude that stimulation of carotid chemoreceptors does not produce cerebral vasodilation and that chemoreceptors do not contribute significantly to cerebral vasodilation during systemic hypoxemia.