Effect of nembutal on arterial pressure responses evoked by stimulation of the hypothalamus, medulla, and lateral horns of the spinal cord

1968 ◽  
Vol 65 (6) ◽  
pp. 649-652 ◽  
Author(s):  
V. A. Tsyrlin
Keyword(s):  
Spinal Cord ◽  
Arterial Pressure ◽  
Stimulation Of

scholarly journals Dissociation by Chloralose of the Cardiovascular and Cerebrovascular Responses Evoked from the Cerebellar Fastigial Nucleus

1990 ◽  
Vol 10 (3) ◽  
pp. 375-382 ◽  
Author(s):  
Costantino Iadecola ◽  
Mary E. Springston ◽  
Donald J. Reis
Keyword(s):  
Spinal Cord ◽  
Heart Rate ◽  
Arterial Pressure ◽  
Initial Dose ◽  
Cardiovascular Responses ◽  
Fastigial Nucleus ◽  
Neural Pathways ◽  
Cerebrovascular Autoregulation ◽  
Brain And Spinal Cord ◽  
Stimulation Of

We studied the effects of chloralose anesthesia on the elevation in arterial pressure (AP), heart rate (HR), and regional CBF (rCBF) elicited by stimulation of the cerebellar fastigial nucleus (FN). Rats were anesthetized with an initial dose of chloralose (40 mg/kg s.c), paralyzed, and artificially ventilated. The FN was stimulated (50–100 μA, 50 Hz, 1 s on/1 s off) with microelectrodes stereotaxically implanted. During the stimulation AP was carefully maintained within cerebrovascular autoregulation. CBF was measured by the [14C]iodoantipyrine technique with regional dissection. In rats that received only the initial dose of chloralose, FN stimulation elevated rCBF in brain and spinal cord, up to 209 ± 13% of control in frontal cortex (n = 5; p < 0.01, analysis of variance). Administration of additional chloralose (10 mg/kg i.v., 30 min prior to measurement of CBF) did not affect resting rCBF (n = 5), the EEG, or the elevation in AP and HR elicited by FN stimulation (n = 4). However, the additional chloralose abolished the elevations in rCBF (n = 5; p > 0.05). Thus, the cerebrovasodilation elicited from the FN is more susceptible to the effects of additional anesthesia than the elevation in AP and HR. These results indicate that the cerebrovascular and cardiovascular responses elicited from the FN are functionally distinct and provide additional evidence for the notion that these responses are mediated by different neural pathways and transmitters.

Spinal vasopressin mechanisms of cardiovascular regulation

1986 ◽  
Vol 251 (3) ◽  
pp. R510-R517 ◽  
Author(s):  
J. P. Porter ◽  
M. J. Brody
Keyword(s):  
Spinal Cord ◽  
Arterial Pressure ◽  
Neural Control ◽  
Intrathecal Injection ◽  
Cardiovascular Regulation ◽  
Spinal Subarachnoid Space ◽  
Vascular Beds ◽  
Vasopressinergic Neurons ◽  
Stimulation Of ◽  
Related Increase

Extrahypothalamic vasopressin-containing neurons have been implicated in the central neural control of the cardiovascular system. In the present study we investigated the possibility that vasopressinergic neurons arising from the paraventricular nucleus (PVN) and terminating in the spinal cord are involved in the regulation of vasomotor functions. Vasopressin (1-17 pmol) was injected into the spinal subarachnoid space of conscious rats instrumented with Doppler flow probes and indwelling intrathecal catheters. The peptide produced a dose-related increase in arterial pressure accompanied by vasoconstriction in the mesenteric, renal, and hindquarter vascular beds. Pretreatment, intrathecally, with 0.5 nmol of the vasopressin antagonist d(CH2)5Me(Tyr)AVP completely prevented the increase in arterial pressure expected after subsequent intrathecal injection of vasopressin. However, the changes in arterial pressure and vascular resistances produced by stimulation of the PVN were not affected by the intrathecal antagonist. Stimulation of the PVN in Brattleboro rats, which lack hypothalamic and spinal vasopressin, produced hemodynamic responses similar to those produced in Long-Evans control rats. Taken together, these data suggest that spinal vasopressin can act within the spinal cord to alter vasomotor functions; however, the hemodynamic effects evoked by stimulation of the PVN do not appear to depend on spinal vasopressinergic mechanisms.

Fastigial stimulation releases vasopressin in amounts that elevate arterial pressure

1983 ◽  
Vol 244 (5) ◽  
pp. H687-H694 ◽  
Author(s):  
A. Del Bo ◽  
A. F. Sved ◽  
D. J. Reis
Keyword(s):  
Spinal Cord ◽  
Heart Rate ◽  
Electrical Stimulation ◽  
Arterial Pressure ◽  
Pressor Response ◽  
Stimulus Train ◽  
Specific Antagonist ◽  
6 Hydroxydopamine ◽  
Stimulation Of ◽  
Intact Rats

Electrical stimulation of the cerebellar fastigial nucleus (FN) in anesthetized, paralyzed, and artificially ventilated rat with a 10-s stimulus train (50 Hz) resulted in a stimulus-locked elevation in arterial pressure (AP) and heart rate, the fastigial pressor response (FPR). Blockade of autonomic effectors by chemosympathectomy (produced by treatment with 6-hydroxydopamine) combined with adrenalectomy, or by spinal cord transection at C1, abolished the FPR but unmasked an elevation of AP with longer latency (10-12 s) and duration (2-4 min), termed the residual FPR. The residual FPR was 1) abolished by midbrain transection, 2) blocked by administration of a specific antagonist of the vasopressor response to arginine vasopressin (AVP) [1,d(CH2)5Tyr(Me)AVP], and 3) was absent in homozygous and attenuated in heterozygous rats of the Brattleboro strain. FN stimulation elevated AVP threefold (from 13 +/- 1 to 38 +/- 8 pg/ml, P less than 0.02; n = 6) in intact rats and sevenfold in rats with combined chemosympathectomy and adrenalectomy (from 14 +/- 1 to 96 +/- 11 pg/ml, P less than 0.001; n = 9). Stimulation of the cerebellar FN can release AVP. In the absence of sympathoadrenal effectors, the amount so released is enhanced and capable of elevating AP.

Electrical stimulation of the carotid sinus lowers arterial pressure and improves heart rate variability in l-NAME hypertensive conscious rats

2020 ◽  
Vol 43 (10) ◽  
pp. 1057-1067 ◽  
Author(s):  
Gean Domingos-Souza ◽  
Fernanda Machado Santos-Almeida ◽  
César Arruda Meschiari ◽  
Nathanne S. Ferreira ◽  
Camila A. Pereira ◽  
...  
Keyword(s):  
Heart Rate ◽  
Heart Rate Variability ◽  
Electrical Stimulation ◽  
Arterial Pressure ◽  
Carotid Sinus ◽  
Conscious Rats ◽  
Stimulation Of

The role of cutaneous afferents in controlling locomotion evoked by epidural stimulation of the spinal cord in decerebrate cats

2008 ◽  
Vol 38 (7) ◽  
pp. 695-701 ◽  
Author(s):  
I. Yu. Dorofeev ◽  
V. D. Avelev ◽  
N. A. Shcherbakova ◽  
Yu. P. Gerasimenko
Keyword(s):  
Spinal Cord ◽  
Cutaneous Afferents ◽  
Epidural Stimulation ◽  
Decerebrate Cats ◽  
Stimulation Of

Drastic Decrease in Isoflurane Minimum Alveolar Concentration and Limb Movement Forces after Thoracic Spinal Cooling and Chronic Spinal Transection in Rats

2005 ◽  
Vol 102 (3) ◽  
pp. 624-632 ◽  
Author(s):  
Steven L. Jinks ◽  
Carmen L. Dominguez ◽  
Joseph F. Antognini
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Minimum Alveolar Concentration ◽  
Tail Flick ◽  
Noxious Stimulation ◽  
Partial Recovery ◽  
Spinal Transection ◽  
Thoracic Spinal ◽  
Cord Injury ◽  
Stimulation Of

Background Individuals with spinal cord injury may undergo multiple surgical procedures; however, it is not clear how spinal cord injury affects anesthetic requirements and movement force under anesthesia during both acute and chronic stages of the injury. Methods The authors determined the isoflurane minimum alveolar concentration (MAC) necessary to block movement in response to supramaximal noxious stimulation, as well as tail-flick and hind paw withdrawal latencies, before and up to 28 days after thoracic spinal transection. Tail-flick and hind paw withdrawal latencies were measured in the awake state to test for the presence of spinal shock or hyperreflexia. The authors measured limb forces elicited by noxious mechanical stimulation of a paw or the tail at 28 days after transection. Limb force experiments were also conducted in other animals that received a reversible spinal conduction block by cooling the spinal cord at the level of the eighth thoracic vertebra. Results A large decrease in MAC (to &lt;/= 40% of pretransection values) occurred after spinal transection, with partial recovery (to approximately 60% of control) at 14-28 days after transection. Awake tail-flick and hind paw withdrawal latencies were facilitated or unchanged, whereas reflex latencies under isoflurane were depressed or absent. However, at 80-90% of MAC, noxious stimulation of the hind paw elicited ipsilateral limb withdrawals in all animals. Hind limb forces were reduced (by &gt;/= 90%) in both chronic and acute cold-block spinal animals. Conclusions The immobilizing potency of isoflurane increases substantially after spinal transection, despite the absence of a baseline motor depression, or "spinal shock." Therefore, isoflurane MAC is determined by a spinal depressant action, possibly counteracted by a supraspinal facilitatory action. The partial recovery in MAC at later time points suggests that neuronal plasticity after spinal cord injury influences anesthetic requirements.

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