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Biomedical subjects

A Mokashi

Publications and source records attributed to A Mokashi.

At least 91 records · Page 5Linked to original sources
PubMed1987

Carotid body chemosensory function in prolonged normobaric hyperoxia in the cat.

The effects of normobaric hyperoxia on carotid body chemosensory function in the cat were studied. The hypothesis was that carotid body chemosensory function would be affected by chronic exposure to 100% O2 at sea level. It was based on the assumptions that carotid body tissue is exposed to high PO2 because of its high blood flow and that its O2 chemosensing mechanism is sensitive to O2 radical-induced reactions. Twelve cats were exposed to 100% O2 for 60-67 h, and 10 control cats were maintained in room air at sea level. They were anesthetized with pentobarbital sodium (Nembutal), and chemosensory afferents from a cut carotid sinus nerve were isolated and identified. The responses of single or a few clearly identifiable chemoreceptor afferents to isocapnic hypoxia and hypercapnia during hyperoxia and to the bolus injections of cyanide, nicotine, and dopamine were studied. We found that chronic hyperoxia severely blunted or eliminated the O2-sensitive response of the carotid chemoreceptors while augmenting the hypercapnic response. The response to cyanide but not to nicotine and dopamine were attenuated. Thus the hypoxic and hypercapnic responses that normally interact were separable. The lack of the cyanide response was consistent with the lack of the hypoxic response, suggesting a possible shared mechanism of carotid chemoreceptor response. Qualitatively normal responses to dopamine and nicotine indicated that the respective receptors were relatively intact after chronic exposure to hyperoxia and that the sensory nerves themselves were not affected by the prolonged O2 exposure.

Animals↗
PubMed1987

Time-dependent effect of hypoxia on carotid body chemosensory function.

The time-dependent effects of hypoxia on the discharge rate carotid chemoreceptors were measured in anesthetized cats. Hypoxic exposure of two different durations were used: a short-term exposure (2-3 h) was used to measure the response of the same carotid chemoreceptors; and a long-term exposure (28 days at inspired PO2 of 70 Torr) to study carotid chemoreceptor properties in one group of cats relative to those of a control group. In the chronically hypoxic and control groups, determinations were made of the 1) steady-state responses to four levels of arterial PO2 (PaO2) at constant levels of arterial PCO2; 2) steady-state responses to acute hypercapnia during hyperoxia; and 3) maximal discharge rates during anoxia. We found that the acute responses of carotid chemoreceptor afferents to a given level of hypoxia (PaO2 = 30-40 Torr) did not significantly change within 2-3 h. After long-term exposure the carotid chemoreceptor responses to hypoxia significantly increased, with no significant changes in the hypercapnic response and in the maximal discharge rate during anoxia. We conclude that isocapnic hypoxia may not elicit a sufficient cellular response within 2-3 h in the cat carotid body to sensitize the O2 responsive mechanism, but hypoxia of longer duration will sensitize such a mechanism, thereby augmenting the chemosensory activity.

Acid-Base Equilibrium↗
PubMed1986

Adrenergic mechanisms in oxygen chemoreception in the cat aortic body.

Sixteen cats were studied to test the hypothesis that oxygen chemoreception in the cat aortic body is dependent on the beta-adrenergic mechanism. The chemoreceptor activity was measured from a few aortic chemoreceptor afferents in each cat, anesthetized with alpha-chloralose (60 mg X kg-1). Three types of experiments were conducted. Aortic chemoreceptor responses to steady-state hypoxia (PaO2 range, 100-30 Torr) were measured (a) before and during intravenous infusion of the beta-receptor agonist, isoproterenol (0.5 micrograms X kg-1) in nine spontaneously breathing cats, and (b) before and after intravenous injection of the beta-receptor antagonist, propranolol (1 mg X kg-1) in seven cats which were paralyzed and artificially ventilated. In the third category (c) the stimulatory effect of hypotension on aortic chemoreceptor activity was measured in six of the seven cats in group (b) before and after propranolol injection. Isoproterenol infusion only moderately stimulated aortic chemoreceptor activity. This stimulation was blocked by propranolol. However, propranolol did not attenuate aortic chemoreceptor responses to hypoxia or to hypotension. We conclude that the beta-receptor adrenergic mechanism does not mediate oxygen chemoreception in the cat aortic body.

Animals↗
PubMed1986

Influence of ganglioglomerular nerve on carotid chemoreceptor activity in the cat.

The dependence of the carotid chemoreceptor responses to blood-borne stimuli on the ganglioglomerular nerve (GGN) activity was investigated in cats which were anesthetized, paralyzed and artificially ventilated. The activity of a few carotid chemoreceptor afferents from a slip or from the cut left carotid sinus nerve (CSN) and the activity of a few GGN fibers were recorded. The responses of the same chemoreceptor afferents to steady-state hypoxia at a constant paCO2 and to steady-state hypercapnia during hyperoxia were compared before and after the transection of the ipsilateral ganglioglomerular nerve (IGGN). Similarly the effects of IGGN transection on the responses of the same chemoreceptor afferents to graded doses of intravenous injections of sodium cyanide (20-60 micrograms) and nicotine (20-60 micrograms) at constant blood gas levels were studied. On the average, IGGN transection during normoxia only slightly changed the carotid chemoreceptor activity. Also, it did not significantly change the hypoxic and hypercapnic responses, and those to sodium cyanide and nicotine injections. Thus, the mean carotid chemoreceptor responses to physiological and pharmacological stimuli were largely independent of the GGN. However, certain GGN fibers were strongly stimulated by hypoxia and hypercapnia. Clearly, the total GGN traffic to the carotid body was not sufficiently strong to exert a significant control over the mean carotid chemoreceptor activity.

Animals↗
PubMed1986

Responses of ganglioglomerular nerve activity to respiratory stimuli in the cat.

We studied the responses of the ganglioglomerular nerve (GGN) efferents to brief periods of hypoxia and hypercapnia and to several levels of steady-state arterial PO2 and PCO2 and to intravascular injection of cyanide in thirteen anesthetized cats. The cats breathed spontaneously. A branch of the GGN which was cut close to the carotid body was divided into several filaments, and the activity of each filament was tested until clean and identifiable action potentials were obtained. The GGN efferent activity, breath-by-breath inspiratory volume, tracheal PO2 and PCO2 and arterial blood pressure were recorded simultaneously. We found that the GGN contained spontaneously active fibers which showed a range of responses to the respiratory stimuli. Fifty-eight percent of the filaments with dominant cardiovascular rhythm showed the least response to blood gas stimuli. Forty-two percent showed clear responses to hypoxia and hypercapnia. These responses developed slowly with the onset of the stimulus but decreased promptly with the withdrawal of the stimulus. These GGN efferents were also promptly stimulated by sodium cyanide. The steady-state response curve to hypoxia was hyperbolic and to hypercapnia it was linear. Some of these fibers showed stronger respiratory rhythms than others. The responses of these GGN efferents were associated with the respiratory responses to hypoxia and hypercapnia. For the same respiratory drive, however, the steady-state hypoxic stimulus elicited a greater GGN response than did hypercapnia.

Adrenergic Fibers↗
PubMed1985

Peripheral chemoreceptors in respiratory oscillations.

The hypothesis that instability of cardiorespiratory control may depend on the response and sensitivity of carotid body chemoreceptors to arterial blood gases was studied in anesthetized cats under three different experimental conditions. 1) Following administration of the peripheral dopamine receptor blocker [domperidone (0.6-0.8 mg X kg-1, iv)], carotid chemoreceptor activity and its sensitivity to CO2 during hypoxia increased, leading to cardiorespiratory oscillations at low arterial PO2 in four of eight cats. Inhalation of 100% O2 promptly decreased chemoreceptor activity and eliminated the oscillations. Inhalation of CO2 stimulated the chemoreceptor activity and ventilation but did not eliminate the oscillations. Bilateral section of carotid sinus nerves abolished the cardiorespiratory oscillations. The implication is that the dopaminergic system in the carotid body keeps chemoreceptor responses to blood gas stimuli suppressed and hence cardiorespiratory oscillations damped. 2) Hypotension and circulatory delay induced by the partial occlusion of venous return led to cardiorespiratory oscillations at low but not at high arterial PO2. 3) A few cats developed cardiorespiratory oscillations without any particular experimental intervention. These oscillations were independent of arterial PO2 and chemoreceptor activity. Thus it is reasonable to conclude that the peripheral chemoreflex can play a critical role in developing cardiorespiratory oscillations in certain instances.

Animals↗
PubMed1984

Contemporary gastroenteritis of infancy: clinical features and prehospital management.

In a prospective survey carried out over 12 months 447 children aged under 2 years were admitted to the Manchester Regional Infectious Diseases Unit for treatment of gastroenteritis. Comparison of the children with those in a survey 15 years previously in the same unit showed that the illness was milder than in the earlier series, with no deaths and with lower incidences of hypernatraemia (1%), uraemia (8%), and dehydration (14%). These improved findings occurred despite several deficiencies of care in the prehospital phase of the illness, particularly poor compliance with the widely recommended guidelines for fluid and dietary management in infantile gastroenteritis.

Child, Preschool↗
PubMed1984

Dopaminergic efferent inhibition of carotid body chemoreceptors in chronically hypoxic cats.

The observations that the dopamine concentration of the carotid body and efferent inhibition of carotid chemoreceptors are increased during chronic hypoxia led to the hypothesis that the inhibition was due to the effect of an increased dopamine release by the activity of carotid sinus nerve (CSN) efferents. The hypothesis was tested by measuring the effect of dopamine receptor blockade on efferent inhibition of carotid chemosensory responses to graded levels of arterial O2 partial pressure in chronically hypoxic and normoxic cats. Chronically hypoxic cats were prepared by exposing the cats to 10% O2 at sea level for 30-34 days. Carotid chemosensory activity was first measured from a slip of an otherwise intact CSN. The measurements were then repeated after sectioning the remaining nerve trunk. The effect of sectioning the CSN provided the measure of efferent inhibition. In each group of cats the effects of sectioning the CSN with and without dopamine receptor blockade by haloperidol were also studied. CSN section augmented the chemosensory responses in the chronically hypoxic cats. Haloperidol, a dopamine antagonist, augmented the responses further, indicating that a part of the endogenous dopamine effect was independent of the CSN efferents. After haloperidol treatment CSN section did not influence the chemosensory responses. This study confirmed that the efferent inhibition significantly increased in the chronically hypoxic cats and demonstrated that haloperidol blocked the efferent inhibition, suggesting that the mechanism of the augmented inhibition is dopaminergic.

Animals↗
PubMed1983

Efferent inhibition of carotid body chemoreception in chronically hypoxic cats.

The effects of chronic hypoxia on carotid chemoreceptor afferent activity before and after sectioning the carotid sinus nerves (CSN) were studied in cats exposed to 10% O2 for 21-49 days in a chamber at sea level. For comparison, chronically normoxic cats at sea level were also studied. The cats were anesthetized, paucifiber preparation for the measurement of carotid chemosensory activity from a small slip of CSN was made, and their steady-state responses to 4-5 levels of arterial pressure of O2 (PaO2) at a constant PaCO2 and to 3-4 levels of PaCO2 in hyperoxia were measured before and after sectioning the CSN. The chemosensory response to hypoxia in the cats with intact CSN after chronic exposure to hypoxia was not reduced relative to the cats that breathed room air at sea level. Sectioning the CSN significantly augmented the chemosensory responses to hypoxia in all the chronically hypoxic but not significantly in the normoxic cats. The responses to moderate hypercapnia during hyperoxia were not significantly changed by cutting the CSN in either group. We conclude that there is a significant CSN efferent inhibition of chemosensory activity due to chronic hypoxia in the cat. This implies that without the efferent inhibition the hypoxic chemosensitivity is increased by chronic hypoxia.

Animals↗
PubMed1982

Adaptive response of carotid body chemoreceptors to CO2.

Carotid body chemoreceptor responses to sudden changes in pETCO2 (end-tidal tracheal CO2 partial pressure) and paCO2 (arterial CO2 partial pressure) from one stable state to another at a constant level of PETO2 (end-tidal tracheal O2 partial pressure) and paO2 (arterial O2 partial pressure) were studied in 18 anesthetized cats. Chemoreceptor activity was recorded from single or pauci-fiber filaments of a cut sinus nerve. During a hypercapnic stimulus by CO2 inhalation the discharge rate rapidly increased to a peak and then adapted to a lower level in 20-30 s showing an overshoot in the response. Likewise, withdrawal of the hypercapnic stimulus was followed by an undershoot in chemoreceptor activity. Hypoxia decreased the latency of the response and increased the overshoot and stable state responses to hypercapnia. The responses to step paCO2 increases by blood perfusion were qualitatively similar but the latency and time to peak amplitude were shorter and the peak amplitude was larger at any given perfusate pO2. The stable state responses to a given paCO2 achieved by CO2 inhalation or by blood perfusion were similar. The transient overshoot and undershoot in the activity produced by the increase and decrease in paCO2 were blocked by acetazolamide, a carbonic anhydrase inhibitor. The results are best explained by postulating that in the carotid body tissue, H+ is generated from CO2 in one compartment in the presence of carbonic anhydrase and is transported to another containing the receptor site in a pO2 dependent way--a high pO2 attenuating and a low pO2 augmenting it.

Acclimatization↗
PubMed1982

Stimulation of carotid chemoreceptors and ventilation by doxapram in the cat.

Small doses of doxapram (less than 0.5 mg . kg-1 iv) were used to study its effect on carotid chemoreceptor activity and ventilation in cats anesthesized with alpha-chloralose. The effects were studied at several levels of partial pressures of O2 and CO2 in arterial blood (PaO2 and PaCO2). It was found that doxapram stimulated discharge rate of the carotid chemoreceptor afferents by the same magnitude at all levels of PaO2 and PaCO2 studied. However, the ventilatory effect of doxapram was more than additive to the concomitant stimulation by hypoxia or hypercapnia. This ventilatory effect was eliminated by sectioning the carotid sinus and aortic nerves. These results led to the conclusion that the ventilatory stimulus interaction due to doxapram is dependent on the excitatory input from the peripheral chemoreceptors.

Anesthesia↗
PubMed1981

Relative responses of aortic body and carotid body chemoreceptors to carboxyhemoglobinemia.

The effects of carbon monoxide inhalation and of consequent carboxyhemoglobinemia (HbCO) on the discharge rates of aortic body and carotid body chemoreceptor afferents were investigated in 18 anesthetized cats. In 10 experiments both aortic and carotid chemoreceptor activities were monitored simultaneously. Carbon monoxide inhalation during normoxia always stimulated aortic chemoreceptors before carotid chemoreceptors, and the steady-state response of aortic chemoreceptors to HbCO was greater than that of most carotid chemoreceptors. Only 2 of the 18 carotid chemoreceptor fibers tested showed a distinct increase in activity in response to moderate increases in HbCO%. Thus, oxyhemoglobin contributed substantially to maintain tissue PO2 of all aortic chemoreceptors and of a few carotid chemoreceptors. Hyperoxia diminished the response of both aortic and carotid chemoreceptors to HbCO, indicating a lowered tissue PO2 as the stimulus source. We hypothesize that the aortic bodies have a much lower perfusion relative to their O2 utilization compared to the carotid bodies. As a consequence, the aortic chemoreceptors are able to act as a sensitive monitor of O2 delivery and to generate a circulatory chemoreflex for O2 homeostasis. carotid chemoreceptors monitor O2 tension and initiate strong reflex effects on the level of ventilation.

Animals↗
PubMed1981

Comparison of aortic and carotid chemoreceptor responses to hypercapnia and hypoxia.

A quantitative comparison of the responses between aortic and carotid chemoreceptors to steady-state levels of arterial CO2 and O2 partial pressure was made in 35 cats anesthetized, paralyzed, and artificially ventilated. The measurements on the two receptors were made simultaneously in 6 cats and separately in 29 cats. The response of aortic chemoreceptors to a CO2 stimulus was a fraction of that of carotid chemoreceptors, and the response to hypoxia was relatively blunted. The differences between the two chemoreceptors are quantitative rather than qualitative. Since a low arterial CO2 partial pressure stimulus is known to attenuate the hypoxic response of carotid chemoreceptors, it is suggested that the low CO2 response of aortic body chemoreceptors is responsible for their blunted hypoxic response.

Animals↗
PubMed1981

Responses of aortic chemoreceptors before and after pneumothorax in the cat.

That the response of aortic chemoreceptors to hypercapnia is considerably smaller than that of carotid chemoreceptors is well accepted, but the mechanism for the difference is not known. It has been suggested that surgical exposure of the carotid body may contribute to the difference. Accordingly, the response of aortic body chemoreceptors to CO2 would be expected to resemble quantitatively that of carotid chemoreceptors after exposure of the aortic bodies by pneumothorax. The effect of opening the chest on aortic and carotid chemoreceptor responses to several levels of arterial CO2 and O2 tension and arterial blood pressure were studied in anesthetized cats. The activity of aortic chemoreceptors increased in spite of a decreased stimulus level in the thoracic cavity after pneumothorax. The activity remained higher than the control at all levels of arterial CO2 and O2 tension and arterial blood pressure. However, the slopes of CO2 response curves, which were initially small, did not change after pneumothorax. Thus a change in the normal environment of the aortic bodies by experimental manipulation did not cause the aortic chemoreceptor responses to resemble those of carotid chemoreceptors.

Animals↗
PubMed1980

Relative latency of responses of chemoreceptor afferents from aortic and carotid bodies.

Discharges from aortic and carotid body chemoreceptor afferents were simultaneously recorded in 18 anesthetized cats to test the hypothesis that aortic chemoreceptors, because of their proximity to the heart, respond to changes in arterial blood gases before carotid chemoreceptors. We found that carotid chemoreceptor responses to the onset of hypoxia and hypercapnia, and to the intravenously administered excitatory drugs (cyanide, nicotine, and doxapram), preceded those of aortic chemoreceptors. Postulating that this unexpected result was due to differences in microcirculation and mass transport, we also investigated their relative speed of responses to changes in arterial blood pressure. The aortic chemoreceptors responded to decreases in arterial blood pressure before the carotid chemoreceptors, supporting the idea that the aortic body has microcirculatory impediments not generally present in the carotid body. These findings strengthened the concept that carotid bodies are more suited for monitoring blood gas changes due to respiration, whereas aortic bodies are for monitoring circulation.

Action Potentials↗
PubMed1980

Relative responses of aortic body and carotid body chemoreceptors to hypotension.

Responses to acute arterial blood pressure changes of a single or a few chemoreceptor afferents from the aortic body and carotid body at constant arterial blood gases and pH were measured in 16 adult cats. During normocapnic normoxia and moderate hypoxia (arterial oxygen tension of 60 Torr) an induced hypotension of 80 Torr increased strikingly the discharge rate of all aortic chemoreceptors but not of most carotid chemoreceptors; hypotension down to the level of 50 Torr stimulated most carotid chemoreceptors only slightly. Hyperoxia eliminated the stimulatory effect of this degree of hypotension on carotid chemoreceptors; it did not affect aortic chemoreceptors to the same extent. Hypoxia augmented the effect on aortic chemoreceptors more than the effect on carotid chemoreceptors. Thus the effect of hypotension was dependent on arterial oxygen tension. The greater effect of hypotension on aortic body chemoreceptor activity indicates a greater normal circulatory constraint for the aortic body. Accordingly, aortic chemoreceptors are more suited to monitor circulatory changes in O2 flow, and carotid chemoreceptors are more suited to monitor arterial gas pressure changes due to respiration.

Animals↗
PubMed1980

Interaction of dopamine and haloperidol with O2 and CO2 chemoreception in carotid body.

Effects of dopamine and of a dopaminergic blocker, haloperidol, on the responses of carotid body chemoreceptors to hypoxia and hypercapnia were investigated in 16 anesthetized cats. Intravenous infusion of dopamine (10-20 micrograms.min-1) decreased carotid body chemoreceptor responses to hypoxia and hypercapnia. The effect was greater at higher levels of arterial oxygen and carbon dioxide tension (PaO2 and PaCO2) stimulus. Thus, the magnitude of the dopamine effect depended on the degree of both PO2- and PCO2-mediated excitation of the receptors. Haloperidol potentiated responses to both hypoxia and hypercapnia but apparently did not stimulate the receptors in the absence of these stimuli. Potentiation by haloperidol and inhibition by dopamine of excitatory effects due to PaO2 decrease and PaCO2 increase are complementary. The data suggest that chemoreception of dopamine, O2, and CO2 converge at some site in the carotid body. Persistence of hypoxic and hypercapnic responses, following dopamine-blocking doses of haloperidol, does not support the theory that regulation of dopamine release is responsible for O2 and CO2 chemoreception in carotid body of the cat.

Afferent Pathways↗