The effect of cold blockade of the medullary chemoreceptors on the CO2 modulation of vascular tone and heart rate

1979 ◽  
Vol 57 (5) ◽  
pp. 461-468 ◽  
Author(s):  
Brian D. Hanna ◽  
Franco Lioy ◽  
Canio Polosa
Keyword(s):  
Heart Rate ◽  
Vascular Tone ◽  
Perfusion Pressure ◽  
Respiratory Control ◽  
Ventral Surface ◽  
Sodium Pentobarbital ◽  
Artificial Cerebrospinal Fluid ◽  
Chemosensitive Areas ◽  
Ventral Medullary Surface

We have previously reported that a direct relationship exists between neurogenic vascular tone in the cat hindlimbs and arterial CO2 tension [Formula: see text]. Since this relationship is not appreciably changed by deafferentiation of peripheral chemoreceptors, we have studied the possible role of structures on the ventral surface of the medulla in mediating the CO2 sensitivity of neurogenic tone. The vagosympathetic trunks and the carotid sinus nerves were sectioned bilaterally in cats under sodium pentobarbital anesthesia. The ventral surface of the medulla was perfused with artificial cerebrospinal fluid of physiological [Formula: see text], pH, and temperature. The animals were hyperventilated with different mixtures of CO2 (0, 4, and 10% in O2), so as to change [Formula: see text] from 12.6 ± 1.2 to 57.4 ± 1.8 mmHg (mean ± SE). The perfusion pressure of the hindlimbs, vascularly isolated and perfused at constant flow, was positively correlated with [Formula: see text]. Bilateral chemosensitive areas of the ventral surface of the medulla oblongata (7 mm caudal to the foramen coecum and 3 mm lateral to the midline) were cooled to a temperature of 12 °C by means of small thermodes. This maneuver decreased the heart rate and perfusion pressure present at each level of [Formula: see text] and also the sensitivity of the perfusion pressure to changes in [Formula: see text]. Cold blockade (12 °C) of the rest of the ventral medullary surface induced a further decrease in heart rate and perfusion pressure but not in the slope of the [Formula: see text] – perfusion pressure relation. Similar results were obtained in a group of adrenalectomized animals. These experiments suggest that the medullary areas which mediate the central CO2-sensitivity of respiratory control systems also play a role in cardiovascular control.

Site of central chemosensitivity in fetal sheep

1975 ◽  
Vol 39 (1) ◽  
pp. 1-6 ◽  
Author(s):  
A. H. Jansen ◽  
V. Chernick
Keyword(s):  
Blood Pressure ◽  
Spinal Cord ◽  
Heart Rate ◽  
Respiratory Response ◽  
Fetal Sheep ◽  
Central Chemosensitivity ◽  
Cord Clamping ◽  
Chemosensitive Areas ◽  
Ventral Medullary Surface ◽  
Histotoxic Hypoxia

The heart rate, blood pressure, and respiratory response to topically applied cyanide on the ventrolateral medullary surface and upper spinal cord was studied on exteriorized sinaortic-denervated fetal lambs under pentobarbital anesthesia. On all sites tested cyanide produced a rapid increase in heart rate and blood pressure (P smaller than 0.05) which was most pronounced from the area adjacent to the nerve roots IX to XI (mean 32%). Respiratory efforts consisting of 1–8 gasps were induced in half the applications to the medulla but never when the pledgets were applied to the spinal cord. The mean delay to response was 43 s (range 13–102 s). After cautery of the chemosensitive areas, topical application of cyanide failed to stimulate gasping, whereas intravenous cyanide or cord clamping still produced a vigorous respiratory response. It is concluded that sympathetic stimulation of the heart and blood vessels can originate centrally in response to local histotoxic hypoxia of the ventral medulla and upper spinal cord. Furthermore, it is proposed that in the apneic fetus histotoxic hypoxia of the medulla initiates respiration possibly by stimulating a special gasping mechanism which is separate from the respiratory center responsible for rhythmic breathing after birth. The responsible neurons must be located at least 2 mm beneath the ventral medullary surface.

Human placental acetylcholine

1991 ◽  
Vol 3 (4) ◽  
pp. 405 ◽  
Author(s):  
RG King ◽  
NM Gude ◽  
BR Krishna ◽  
S Chen ◽  
SP Brennecke ◽  
...  
Keyword(s):  
Blood Flow ◽  
Amino Acid ◽  
Cholinergic System ◽  
Vascular Tone ◽  
Perfusion Pressure ◽  
Acid Transport ◽  
Ach Release ◽  
Fetal Vessels

The human placenta contains both acetylcholine (ACh) and choline acetyltransferase, and in vitro bilaterally perfused placental lobules release ACh. The function of this placental cholinergic system has not yet been clearly defined, although changes occur in it during parturition and it may be linked to placental prostaglandin generation at this time. It has also been suggested that ACh may regulate placental amino-acid transport and/or blood flow. It has been found that ACh release from fetal vessels of bilaterally perfused placental lobules is reduced during preeclampsia but is not necessarily correlated with any change in perfusion pressure or materno-fetal transfer of the nonmetabolizable amino acid alpha-aminoisobutyric acid. However, a correlation has been found between releases from human placental explants of ACh (when inhibited by (2-benzoylethyl)trimethylammonium or vesamicol) and of prostaglandins E2 and F2 alpha. Thus, although the evidence for a role of ACh in the control of placental amino-acid transfer or vascular tone is not conclusive, inhibition of the human placental cholinergic system has been shown to be associated with reduced output of prostaglandins from this tissue.

Neurons of C1 area mediate cardiovascular responses initiated from ventral medullary surface

1986 ◽  
Vol 250 (5) ◽  
pp. R932-R945 ◽  
Author(s):  
E. E. Benarroch ◽  
A. R. Granata ◽  
D. A. Ruggiero ◽  
D. H. Park ◽  
D. J. Reis
Keyword(s):  
Heart Rate ◽  
Electrical Stimulation ◽  
Arterial Pressure ◽  
Cardiovascular Responses ◽  
Ventral Surface ◽  
Aminobutyric Acid ◽  
Ventrolateral Medulla ◽  
Gamma Aminobutyric Acid ◽  
Pressor Responses ◽  
Ventral Medullary Surface

We sought to establish whether neurons of the C1 area of the rostral ventrolateral medulla (RVL) mediate changes in arterial pressure and heart rate evoked by topical application of drugs to the ventral medullary surface of the rat. Animals were anesthetized, paralyzed, and ventilated. The ventral surface was mapped with L-glutamate, and a restricted zone was identified from which L-glutamate, as well as kainic acid, bicuculline, strychnine, carbachol, or physostigmine, increased arterial pressure and heart rate. The hypertensive effects of carbachol and physostigmine were blocked by previous local application of atropine but not hexamethonium. Application of gamma-aminobutyric acid (GABA) or glycine to this area produced hypotension and bradycardia. Located caudal to the trapezoid bodies and lateral to the pyramids, this area corresponded to points with lowest threshold for pressor responses evoked by electrical stimulation and overlapped the distribution of epinephrine-synthesizing cells of the RVL. Processes arising from these neurons were identified reaching and contacting the ventral surface. Unilateral lesions involving the C1 area or phenylethanolamine-N-methyltransferase-labeled descending axons derived from this area imparied by greater than 70% the response to ipsilateral application of L-glutamate, GABA, or glycine to the ventral surface. We suggest that neurons within the C1 area of RVL adjacent to or including epinephrine cells may mediate cardiovascular changes elicited from a restricted chemosensitive zone of the ventral medullary surface of the rat.

Role of endogenous centrally released NO in cardiovascular adaptation to hypovolemia in WKY and SHR

1997 ◽  
Vol 272 (5) ◽  
pp. H2282-H2288 ◽  
Author(s):  
P. Paczwa ◽  
A. S. Budzikowski ◽  
E. Szczepanska-Sadowska
Keyword(s):  
Heart Rate ◽  
Spontaneously Hypertensive Rats ◽  
Hypotensive Effect ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Time Control ◽  
Artificial Cerebrospinal Fluid ◽  
In Series ◽  
Wistar Kyoto

The role of endogenous centrally released nitric oxide (NO) during hypovolemia was investigated in normotensive Wistar-Kyoto (WKY) and spontaneously hypertensive rats (SHR). Bleeding of the rats (1.3% of blood volume) was performed after intracerebroventricular (ICV) administration of: 1) artificial cerebrospinal fluid (series 1, time control, 8 WKY and 8 SHR); 2) 0.5 mg NG-nitro-L-arginine (L-NNA, 2.3 nmol), an inhibitor of NO synthesis (series 2, 8 WKY and 7 SHR); and 3) 0.5 mg L-NNA followed by 1 mg (5.8 nmol) of L-arginine (L-Arg) (6 WKY and 5 SHR). In WKY, hypotension was associated with significant bradycardia (P < 0.001), whereas in SHR slight acceleration of heart rate was observed. In series 2 hemorrhage resulted in a small but significant increase of mean arterial pressure (MAP; P < 0.05) and considerable tachycardia (P < 0.001). In SHR, L-NNA did not modify the decrease of MAP during hypovolomia, and bleeding resulted in a significant bradycardia (P < 0.001). Pretreatment with L-Arg in series 3 was able to reverse the effects of L-NNA on changes of MAP and heart rate during hypovolemia. The results indicate that the central nitroxidergic system plays a significant role in eliciting hypotension and bradycardia in normotensive WKY during hemorrhage. Function of the central nitroxidergic system is significantly altered in SHR in which NO appears to prevent hemorrhagic bradycardia and to reduce the hypotensive effect.

Central effects of endothelin on respiratory output during development

1995 ◽  
Vol 79 (2) ◽  
pp. 420-427 ◽  
Author(s):  
I. A. Dreshaj ◽  
M. J. Miller ◽  
P. Ernsberger ◽  
B. Haxhiu-Poskurica ◽  
R. J. Martin ◽  
...  
Keyword(s):  
Specific Binding ◽  
Respiratory Control ◽  
Ventral Surface ◽  
Inhibitory Effect ◽  
Ventrolateral Medulla ◽  
Postnatal Life ◽  
Receptor Blockade ◽  
Endothelin 1 ◽  
Chemosensitive Areas ◽  
Endothelin A

Both endothelin-1 protein and endothelin-1 specific binding sites have been identified in areas of the medulla oblongata involved in respiratory control. We examined whether endothelin acting centrally affects respiratory output during early postnatal life. We initially examined the effect of intracisternally administrated endothelin on respiratory output in 10 2- to 18-day-old piglets. Endothelin-1 administration at 50 nmol to 1 mumol caused respiratory inhibition. We subsequently examined whether this response is mediated through chemosensitive areas of the ventral medulla. Endothelin-1 was microinjected into specific ventral or dorsal medullary regions in 31 14- to 22-day-old piglets. Microinjection of endothelin-1 (10 fmol to 0.1 pmol) just above the hypoglossal roots, lateral to the pyramids, and within 1 mm from the surface (n = 24) attenuated respiratory output, and complete apnea occurred with 1 pmol in all animals. However, microinjection of endothelin-1 3 mm below the ventral surface (n = 5) and into the dorsal medulla (n = 3) had no inhibitory effect. Comparable doses of angiotensin II (n = 5) and norepinephrine (n = 5) microinjected into the endothelin-1 sensitive area also did not influence respiratory output. These effects of endothelin-1 were not altered by prior endothelin-B receptor blockade (IRL-1038) but could be reversed by endothelin-A receptor blockade (BQ-610). These results suggest that endothelin-1 release may cause ventilatory depression mediated through endothelin-A receptors located in the chemosensitive areas of the ventrolateral medulla.

Relaxation during the evening and next-morning energy: The role of hassles, uplifts, and heart rate variability during work.

2020 ◽  
Vol 25 (2) ◽  
pp. 83-98
Author(s):  
Stacey L. Parker ◽  
Sabine Sonnentag ◽  
Nerina L. Jimmieson ◽  
Cameron J. Newton
Keyword(s):  
Heart Rate ◽  
Heart Rate Variability

Pre-emptive Analgesia for Postoperative Pain Relief in Children – Role of Paracetamol

2009 ◽  
pp. 9-16
Author(s):  
Rubina Yasmin ◽  
AKM Akhtaruzzaman ◽  
Paresh Chandra Sarker ◽  
Neaz Ahmed ◽  
Ranadhir Kumar Kundu ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Postoperative Pain ◽  
Diclofenac Sodium ◽  
Total Duration ◽  
Pain Scale ◽  
Prospective Clinical Study ◽  
High Dose ◽  
Induction Of Anaesthesia

This prospective clinical study was carried out in the Dept. of Anaesthesia, Analgesia and Intensive Care Medicine, BSMMU, Dhaka, during the period of May 2003 to July 2003. The study was done to emphasize the importance of giving analgesics preemptively instead of waiting for the child to complain of pain and to produce smooth recovery after surgery by decreasing immediate postoperative pain in children by a simple, safe acceptable drug. The children scheduled for tonsillectomy under general anaesthesia were recruited in this study. The analgesic efficiency of rectal paracetamol in two doses, 25 mg/kg bodywt.(Gr-P25) and 50 mg/kg. bodywt. (Gr-P50) were compared with Diclofenac Sodium suppository 1mg/ kg body weight (Gr-D) given half an hour before induction of anaesthesia. Pain scoring was done by TPPPS (Toddler Pre-schooler postoperative pain scale). Heart rate and blood pressure were stable in Gr-P50 and Gr-D. Time of first demand of analgesic was delayed in Gr-P50 and Gr-D. Total paracetamol consumption in 24 hours was less in Gr-P50(181±14.25) and Gr-D (212±25) than Gr-P25(318± 26.39). Total duration of analgesia in Gr- P50 (657±9.94) mins. and in Gr- D(502±10.63) mins. and in Gr-P25(288±23.17) mins. Pre-emptive high dose rectal paracetamol appears to be more effective than diclofenac sodium suppository for postoperative analgesia in children undergoing tonsillectomy. Journal of BSA, Vol. 18, No. 1 & 2, 2005 p.9-16

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