Central neural mechanisms of the cerebral ischemic response. Characterization, effect of brainstem and cranial nerve transections, and simulation by electrical stimulation of restricted regions of medulla oblongata in rabbit.

Dampney, R.A.L.; Kumada, Mamoru; Reis, Donald J.

doi:10.1161/01.res.45.1.48

Cited by 105 publications

(20 citation statements)

References 32 publications

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“…In contrast with the rapid cessation of the cortical electrical activity by ischemia, the vasomotor center in the ventrolateral medulla as well as the cardioinhibitory center, i.e., nucleus ambiguus or dorsal motor nucleus, are excited by ischemia to produce the characteristic cerebral ischemic response (22)(23)(24)(25)(26)(27)(28).…”

Section: Discussionmentioning

confidence: 99%

Deterioration of baroreceptor reflex by transient global cerebral ischemia in dogs.

et al. 1989

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Abstract-Influence of transient global cerebral ischemia on baroreceptor reflex sensitivity (BRS) was investigated in anesthetized dogs. Cerebral ischemia was produced by the combined occlusions of the left subclavian (LSA) and the brachio cephalic (BCA) arteries with preceding ligations of the intercostal arteries (ICA). BRS was assessed by phenylephrine-induced reflex bradycardia. Ischemia of 5 and 10-min duration produced a significant decrease in BRS during the reperfusion period of 60-120 min. On the other hand, such a change was not observed follow ing the ischemia of less than 2_-min or occlusions of LSA and BCA without preced ing ligations of ICA. Heart rate response to the electrical stimulation of the vagal afferent nerve was attenuated by 10-min ischemia, while response to the vagal efferent nerve stimulation and ECG parameters were not influenced. These results indicate that some regions vulnerable to the relatively short duration of cerebral ischemia may be involved in the central pathway of the baroreflex mechanism.

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Section: Discussionmentioning

confidence: 99%

Deterioration of baroreceptor reflex by transient global cerebral ischemia in dogs.

et al. 1989

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“…Cerebral hypoxia or ischemia elicits a rapid, patterned, autonomic response, which originates in the lower brainstem (Dampney et al, 1979;Guyenet and Brown, 1986) and includes sympathetic excitation, visceral and muscular vasoconstriction, bradycardia, and expiratory apnea (Dampney et al, 1979;Dampney and Moon, 1980;Guyenet and Brown, 1986;. In addition, there is a widespread increase in regional cerebral blood flow (rCBF) without change in a cerebral metabolism [as evaluated by regional cerebral glucose utilization (rCGU)] and synchronization of the EEG (Underwood et al, 1992(Underwood et al, , 1994Golanov and Reis, 1996;Golanov et al, 2000b;).…”

mentioning

confidence: 99%

Neurons of a Limited Subthalamic Area Mediate Elevations in Cortical Cerebral Blood Flow Evoked by Hypoxia and Excitation of Neurons of the Rostral Ventrolateral Medulla

2001

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Sympathoexcitatory reticulospinal neurons of the rostral ventrolateral medulla (RVLM) are oxygen detectors excited by hypoxia to globally elevate regional cerebral blood flow (rCBF). The projection, which accounts for Ͼ50% of hypoxic cerebral vasodilation, relays through the medullary vasodilator area (MCVA). However, there are no direct cortical projections from the RVLM/MCVA, suggesting a relay that diffusely innervates cortex and possibly originates in thalamic nuclei. Systematic mapping by electrical microstimulation of the thalamus and subthalamus revealed that elevations in rCBF were elicited only from a limited area, which encompassed medial pole of zona incerta, Forel's field, and prerubral zone. Stimulation (10 sec train) at an active site increased rCBF by 25 Ϯ 6%. Excitation of local neurons with kainic acid mimicked effects of electrical stimulation by increasing rCBF. Stimulation of the subthalamic cerebrovasodilator area (SVA) with single pulses (0.5 msec; 80 A) triggered cortical EEG burst-CBF wave complexes with latency 24 Ϯ 5 msec, which were similar in shape to complexes evoked from the MCVA. Selective bilateral lesioning of the SVA neurons (ibotenic acid, 2 g, 200 nl) blocked the vasodilation elicited from the MCVA and attenuated hypoxic cerebrovasodilation by 52 Ϯ 12% ( p Ͻ 0.05), whereas hypercarbic vasodilation remained preserved. Lesioning of the vasodilator site in the basal forebrain failed to modify SVA-evoked rCBF increase. We conclude that (1) excitation of intrinsic neurons of functionally restricted region of subthalamus elevates rCBF, (2) these neurons relay signals from the MCVA, which elevate rCBF in response to hypoxia, and (3) the SVA is a functionally important site conveying vasodilator signal from the medulla to the telencephalon.

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“…13 25 -28 produce increases in arterial blood pressure and coronary vasoconstriction, which is often marked. In the present study, coronary vasoconstriction was observed during cerebral ischemia, but the neurogenic component of this vasoconstriction resulted from concurrent changes in baroreceptor activity and was not an independent effect of cerebral ischemia.…”

Section: Physiological Importancementioning

confidence: 99%

Coronary vascular response to the cerebral ischemia reflex.

Boel

Gutterman

1993

Hypertension

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Most centrally mediated sympathoexcitatory reflexes produce increases in arterial pressure, heart rate, and peripheral vascular resistance, including coronary vasoconstriction. Cerebral ischemia also causes large increases in arterial pressure and peripheral vasoconstriction but with modest or variable changes in heart rate. To examine the effect of cerebral ischemia on coronary vascular resistance, we produced cerebral ischemia in 14 cats by occluding the right brachiocephalic and left subclavian arteries for 30 seconds. After vagotomy and ^-blockade, a marked increase in arterial pressure (89±14%) and coronary vascular resistance (52 ±7%) was seen. After inhibition of the carotid baroreceptor reflex by surgical denervation and application of topical lidocaine, the increase in arterial pressure to cerebral ischemia was not affected, but the increase in coronary vascular resistance was attenuated (33 ±6%; p<0.05 versus before denervation) to a level expected with autoregulation. To evaluate the possible contribution of the chemoreflex on coronary blood flow during cerebral ischemia, we conducted separate experiments in which nicotine was injected into both carotid arteries. Coronary constriction was not observed. Adrenalectomy and upper extremity ischemia likewise did not alter coronary vascular resistance. We conclude that cerebral ischemia elicits neurally mediated coronary vasoconstriction as a result of baroreceptor hypotension rather than directly. The relative absence of neurogenic coronary constriction and changes in heart rate suggest that sympathoexcitation during cerebral ischemia is directed more toward the peripheral vasculature than the heart. {Hypertension 1993;21:216-221) KEY WORDS • vasoconstriction • pressoreceptors • sympathetic nervous system • cerebral ischemiaA variety of reflex stimuli produce a-adrenergicmediated coronary vasoconstriction. Barore->. ceptor hypotension, 1 activation of carotid chemoreceptors, 2 and nociceptive reflexes, 3 as well as static 4 and dynamic exercise, 5 all increase systemic arterial pressure, heart rate, and coronary vascular resistance through sympathetic activation.Cerebral ischemia, produced by interruption of perfusion to the head, is a potent stimulus for sympathetic discharge. However, unlike most sympathoexcitatory reflexes, tachycardia is not a consistent feature of the ischemic response. The effect of cerebral ischemia on coronary flow is difficult to predict. The large pressor response to cerebral ischemia suggests that neurogenic coronary constriction accompanies the sympathoexcitation. However, other sympathoexcitatory reflexes producing coronary constriction include tachycardia. BradyFrom the Veterans Administration

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Central neural mechanisms of the cerebral ischemic response. Characterization, effect of brainstem and cranial nerve transections, and simulation by electrical stimulation of restricted regions of medulla oblongata in rabbit.

Abstract: THE CEREBRAL ischemic response consists of an elevation of arterial pressure

Cited by 105 publications

References 32 publications

Deterioration of baroreceptor reflex by transient global cerebral ischemia in dogs.

Deterioration of baroreceptor reflex by transient global cerebral ischemia in dogs.

Neurons of a Limited Subthalamic Area Mediate Elevations in Cortical Cerebral Blood Flow Evoked by Hypoxia and Excitation of Neurons of the Rostral Ventrolateral Medulla

Coronary vascular response to the cerebral ischemia reflex.

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