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Biomedical subjects

J E Kendrick

Publications and source records attributed to J E Kendrick.

At least 19 recordsLinked to original sources
PubMed1984

Reduced effectiveness of the carotid baroreflex during arterial hypoxia in dogs.

The ability of the carotid baroreflex to produce cardiac slowing during arterial hypoxia was investigated in dogs anesthetized with morphine-chloralose. The heart rate response to baroreflex stimulation decreased by about 20% at an arterial O2 tension (PaO2) of 65-70 Torr and by over 60% at a PaO2 of 15-20 Torr. After the aortic nerves were cut bilaterally, baroreflex stimulation produced greater cardiac slowing (P less than 0.001) during arterial hypoxia (PaO2 20 Torr) than at the same PaO2 with intact aortic nerves. The systemic depressor response to baroreflex stimulation was reduced in a qualitatively similar manner but with greater variability. After atropine (0.2 mg/kg iv) or vagal transection the heart rate response to baroreflex stimulation during hypoxia was not suppressed from its control. Perfusion of the head with hypoxic blood in carotid-denervated animals also reduced the baroreflex bradycardia. The results suggest that the vagal component of the baroreflex bradycardia is suppressed during arterial hypoxia both by a reflex mediated by the aortic chemoreceptors and by a direct effect of hypoxia on the central nervous system.

Animals↗
PubMed1984

Interaction between depressor and pressor reflexes arising from the aorta in dogs.

In 18 dogs anesthetized with morphine-chloralose the interaction between the aortic nerve (AN) pressor and depressor reflexes was studied. Low-intensity, high-frequency electrical stimulation of the AN causes large decreases in heart rate and systemic pressure characteristic of baroreflex responses. High-intensity, low-frequency stimulation of the AN causes modest increases in heart rate and systemic pressure similar to the responses observed to intraaortic nicotine. Simultaneous electrical stimulation of these antagonistic reflexes results in much smaller (P less than 0.001) reductions in heart rate and systemic pressure that can be explained on the basis of simple addition of the individual responses. Similarly the AN depressor reflexes are suppressed during intraaortic infusions of nicotine (40 micrograms/min). The results suggest that the inhibitory effects of the AN baroreflexes are suppressed by the aortic chemoreflexes . This interaction occurs in the CNS rather than at the level of the heart or vascular smooth muscle.

Animals↗
PubMed1984

Nonalgebraic interaction between pressor and depressor reflexes in dogs: evidence for a central site of action.

In a previous study (Kendrick, JE and Matson, G 1979, Amer J Physiol 327:H662-H667) we demonstrated that the vascular responses in dogs to electrical stimulation of aortic nerve (AN) pressor and carotid sinus nerve (CSN) depressor afferents did not sum algebraically. We suggest this results from a reflex interaction which occurs in the central nervous system. The present study extends earlier studies by recording sympathetic vasomotor in chloralose-anesthetized dogs. Stimulation of the CSN reduced sympathetic activity by 51 +/- 20 (SD)%. AN stimulation (2 Hz) caused a 17 +/- 12% increase in sympathetic activity. Combined stimulation of the ipsilateral CSN and AN caused 0 +/- 28% change rather than a 34% decrease expected by an additive interaction. The interaction recorded in this study from the sympathetic outflow is therefore consistent with the previously reported vascular responses (cited above) and implicates central nervous site(s) of action. A conditioning stimulus train to CSN inhibited sympathetic discharges to AN test stimuli. This inhibition was prevented by pairing an AN stimulus with the CSN stimulus train. The AN pressor reflexes act in part by increasing sympathetic activity and in part by suppressing the baroreflexes.

Afferent Pathways↗
PubMed1982

Inhibition of baroreflex bradycardia by aortic nerve excitatory afferents in dogs.

In dogs anesthetized with morphine-chloralose, low-frequency high-intensity stimulation of the aortic nerve (AN) causes a modest reflex tachycardia and a rise in systemic pressure. Stimulation of the carotid sinus nerve or raising pressure in the isolated carotid sinus causes reflex bradycardia and a fall in systemic pressure. Combined stimulation of these reflexes resulted in less bradycardia and a smaller decrease in systemic pressure than the sum of the responses to separate stimulation (P less than 0.001). This suggests that the opposing reflexes interact in a manner whereby the carotid baroreflex responses are inhibited by the AN stimulation. This interaction occurs in the medullary centers and appears to involve primarily suppression of the vagal efferents to the heart. Baroreflex inhibition of sympathetic vasomotor activity also appears to be suppressed by AN stimulation. It is concluded that aortic cardiac sympathetic activity and in part by suppressing baroreflex-induced bradycardia.

Afferent Pathways↗
PubMed1979

Central interaction between the baroreceptor reflexes from the carotid sinus and aortic arch.

The cardiovascular response to combined stimulation of the aortic nerve (AN) and carotid sinus nerve (CSN) with trains of electrical stimuli was studied in dogs under morphine-chloralose anesthesia. Combined stimulation of both nerves ipsilaterally resulted in systemic arterial depressor responses and cardiac slowing that were 59% and 77% greater (P less than 0.05) than the respective sum of the responses to separate stimulation of these nerves. The depressor response to combined stimulation of these nerves contralaterally was not different (P greater than 0.05) from the sum of the separate responses. However, cardiac slowing to contralateral stimulation of the nerves remained 43% greater (P less than 0.05) than the sum of the individual responses. The results suggest that an interaction between the aortic and carotid baroreceptor reflexes occurs centrally, which causes a greater than additive effect on the autonomic output. The degree of interaction between the reflexes did not change as the delay between the stimulus trains was varied over an interval of 0 and 100 ms. At intervals greater than 100 ms the reflex responses were additive.

Animals↗
PubMed1979

Interaction between carotid sinus baroreceptor and aortic nerve pressor reflexes in the dog.

In dogs anesthetized with morphine-chloralose, strong, low-frequency (2 Hz) electrical stimulation of the aortic nerve (AN) causes pressure in the perfused hindlimbs to rise. This pressor response is followed by a large depressor phase upon cessation of stimulation. Simultaneous stimulation of the ipsilateral carotid sinus nerve (CSN) with intermittent trains of stimuli enhanced the AN pressor response by 113%. Similar stimulation of the contralateral CSN had little effect on the AN pressor response. Constant-frequency stimulation of the ipsilateral CSN also failed to enhance this response. Possible mechanisms of the interaction between these antagonistic reflexes were investigated. The results suggest that the augmentation of the AN pressor response results from a central neuronal interaction between these antagonistic reflexes.

Animals↗
PubMed1975

Central summation of barosensory impulses over both carotid sinus nerves in the dog.

Stimulation of both CSN in dogs with continuous stimuli decreased blood pressure and heart rate as effectively as intermittent bursts of stimuli. The temporal separation between the stimulus bursts to the two CSN was without effect on the reflex response. Similarly perfusion of both carotid sinuses with pressure pulses which were in phase was no more effective in eliciting the reflex than perfusion with pressure pulses 180 degree out of phase. These results suggest that the barosensory fibers project centrally to independent neuronal pools. Pulsatile perfusion of the carotid sinuses lowered systemic pressure more than nonpulsatile pressure at the same mean level. The greater efficacy of pulsatile pressure appears to result from baroreceptor recruitment and not from the impulse pattern.

Animals↗