Fetal responses to carotid occlusion: immaturity of buffering systems

1995 ◽  
Vol 268 (2) ◽  
pp. R343-R348 ◽  
Author(s):  
C. E. Wood
Keyword(s):  
Late Gestation ◽  
Vagal Afferents ◽  
Carotid Occlusion ◽  
Fetal Sheep ◽  
Hormonal Responses ◽  
Arterial Blood ◽  
Bilateral Carotid Occlusion ◽  
Bilateral Carotid ◽  
Functional Immaturity ◽  
Vagal Afferent

In postnatal animals, carotid occlusion does not stimulate reflex hormonal responses, because decreases in carotid arterial baroreceptor activity are balanced by reflex-mediated increases in vagal afferent traffic from aortic and cardiac receptors. The present experiments were designed to test the hypothesis that hormonal responses to carotid occlusion in fetal animals are not inhibited by vagal afferents. In thirteen chronically catheterized fetal sheep (125-146 days), bilateral carotid occlusion (n = 11) increased arterial blood pressure from 44.0 +/- 2.4 to 55.2 +/- 3.3 mmHg, decreased heart rate from 189 +/- 5 to 165 +/- 12 beats/min, increased plasma adrenocorticotropin from 71 +/- 15 to 248 +/- 79 pg/ml and vasopressin from 3.0 +/- 1.0 to 7.4 +/- 2.6 pg/ml but did not significantly alter renin. Plasma hormone concentrations were not significantly altered in control (n = 7) experiments or in response to unilateral carotid occlusion (n = 4). The results of these experiments demonstrate the functional immaturity of the vagal afferent buffering systems in the late-gestation fetus compared with the postnatal animal.

Constriction of lymphatics by catecholamines, carotid occlusion, or hemorrhage

1988 ◽  
Vol 255 (3) ◽  
pp. H514-H524
Author(s):  
J. M. Dabney ◽  
M. J. Buehn ◽  
D. E. Dobbins
Keyword(s):  
Lymphatic Vessel ◽  
Perfusion Pressure ◽  
Sympathetic Nerves ◽  
Carotid Occlusion ◽  
Central Venous ◽  
Lymphatic Function ◽  
Hemorrhagic Hypotension ◽  
Arterial Blood ◽  
Bilateral Carotid Occlusion ◽  
Bilateral Carotid

Regulation of lymphatics by sympathetic nerves or hormones seems probable. To elucidate this, we perfused a lymphatic vessel in the paw of the anesthetized dog while measuring lymphatic perfusion pressure. We studied the effects of norepinephrine, epinephrine, hemorrhage, and carotid occlusion on lymphatic pressure. Blood was pumped to the forelimb via the brachial artery. Cannulas were placed to measure systemic, central venous, and forelimb vascular pressures. Catecholamines, whether added to the lymphatic perfusate or infused into the forelimb arterial blood, and bilateral carotid occlusion significantly increased lymphatic perfusion pressure. Perfusion of prenodal lymphatics disconnected from downstream vessels and nodes indicated that this increase occurred primarily in prenodal lymph vessels. Hemorrhagic hypotension to 55 mmHg did not affect lymphatic pressure but reduction to 35 mmHg did. The increase in lymphatic pressure produced by epinephrine and norepinephrine was blocked by phentolamine. Increased lymphatic perfusion pressure subsequent to exogenous catecholamines, severe hemorrhagic hypotension, or bilateral carotid occlusion supports the possibility that lymphatic function is modulated by adrenergic mechanisms in physiological and/or pathophysiological states.

Effect of Bilateral Occlusion of Common Carotid Arteries on Cardiac Output and Oxygen Content of Arterial and Venous Blood in the Anesthetized Dog

1956 ◽  
Vol 185 (3) ◽  
pp. 483-486 ◽  
Author(s):  
Shirley H. Brind ◽  
Joseph R. Bianchine ◽  
Matthew N. Levy
Keyword(s):  
Cardiac Output ◽  
Oxygen Content ◽  
Venous Blood ◽  
Carotid Occlusion ◽  
Systemic Hypertension ◽  
Arterial Blood ◽  
Venous Oxygen Content ◽  
Bilateral Carotid Occlusion ◽  
Bilateral Carotid ◽  
Common Carotid Arteries

Changes in cardiac output, mean arterial blood pressure, hematocrit ratio, and arterial and venous oxygen content resulting from bilateral carotid occlusion were investigated. Cardiac output exhibited no significant alteration during endosinusal hypotension, and the systemic hypertension engendered was attributed to an increase in vasomotor tone. Arterial and venous oxygen content, as well as hematocrit ratio, increased significantly during the period of carotid occlusion. This increase was ascribed to splenic contraction evoked by carotid occlusion, since no comparable augmentation was observed when the splenic circulation was temporarily interrupted.

Carotid arterial control of vasopressin secretion in sheep

1984 ◽  
Vol 247 (3) ◽  
pp. R589-R594 ◽  
Author(s):  
C. E. Wood ◽  
L. C. Keil ◽  
A. M. Rudolph
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Plasma Concentrations ◽  
Carotid Occlusion ◽  
Arterial Blood ◽  
Plasma Vasopressin ◽  
Bilateral Carotid Occlusion ◽  
Bilateral Carotid ◽  
Vasopressin Secretion ◽  
Carotid Arterial

The purpose of this study was to test the role of carotid arterial mechanoreceptors in the control of vasopressin secretion in conscious 6- to 7-wk-old lambs. Bilateral carotid occlusion decreased lingual arterial pressure and stimulated reflex increases in heart rate and femoral arterial blood pressure but did not significantly alter plasma concentrations of vasopressin. Acute vagosympathetic blockade, produced by injection of 2% lidocaine onto the vagosympathetic trunks, did not significantly alter heart rate or blood pressure but did stimulate a slow increase in plasma vasopressin concentration, suggesting that afferent vagal fibers tonically inhibit vasopressin secretion. Bilateral carotid occlusion after vagosympathetic blockade stimulated a brisk increase in plasma vasopressin that was larger than the response to vagosympathetic blockade alone. These results suggest that vasopressin secretion in lambs is partially controlled by arterial mechanoreceptors in the carotid sinus and by extracarotid receptors with vagosympathetic afferent fibers.

Reversible vascular isolation of carotid sinuses in conscious dogs

1980 ◽  
Vol 238 (6) ◽  
pp. H809-H814 ◽  
Author(s):  
R. B. Stephenson ◽  
D. E. Donald
Keyword(s):  
Carotid Sinus ◽  
Carotid Occlusion ◽  
Response Curves ◽  
Stimulus Response ◽  
Arterial Blood ◽  
Bilateral Carotid Occlusion ◽  
Bilateral Carotid ◽  
Before And After ◽  
Surgical Preparation ◽  
Sinus Pressure

A surgical technique has been developed that permits reversible vascular isolation of both carotid sinuses in the conscious dog. Seven dogs so prepared were studied over periods of 4-12 wk. Repeatable stimulus-response curves relating arterial blood pressure to carotid sinus pressure were obtained for sinus pressures of 40-240 mmHg. Two studies gave evidence that the ability of the carotid baroreceptors to influence arterial pressure was not or was minimally affected by the surgical dissection. In 10 dogs one sinus was surgically prepared; 3 wk later the dogs were anesthetized and vagotomized. The steady-state stimulus-response curves for the chronically prepared sinuses showed no consistent differences from the curves for the opposite, acutely prepared sinuses. In 8 other dogs the hypertensive responses to bilateral carotid occlusion were compared before and after surgical preparation of both sinuses. The responses to carotid occlusion tended to be decreased after surgery but the differences were small and were significant only in 3 dogs.

Effect of myocardial ischemia on hemodynamic response to carotid occlusion

1989 ◽  
Vol 256 (3) ◽  
pp. H672-H680
Author(s):  
G. E. Billman ◽  
D. H. Marsh
Keyword(s):  
Contractile Function ◽  
Left Ventricular Pressure ◽  
Hemodynamic Response ◽  
Left Ventricular ◽  
Vagal Afferents ◽  
Carotid Occlusion ◽  
Aortic Blood Flow ◽  
Bilateral Carotid Occlusion ◽  
Bilateral Carotid ◽  
Bilateral Vagotomy

Fourteen mongrel dogs were anesthetized and instrumented to measure arterial pressure (AP), left ventricular pressure (LVP), aortic blood flow, and heart rate (HR). Hydraulic occluders were placed around the left anterior descending (LAD, n = 9) and left circumflex (LCC, n = 14) coronary arteries. A bilateral carotid occlusion (BCO) was made before and during either anterior (LAD occlusion) or posterior (LCC occlusion) ischemia. Posterior ischemia significantly (P less than 0.01) reduced the BCO-induced increases in mean AP (by 44.3 +/- 7.3%), systolic LVP (by 65.5 +/- 6.9%), first derivative of LVP (dLVP/dt, by 95.7 +/- 44.3%), and aortic resistance (by 117.7 +/- 26.9%). In contrast, anterior ischemia failed to alter significantly the hemodynamic response to BCO. Bilateral vagotomy attenuated or eliminated many of the effects of posterior ischemia on the BCO response. In fact, the change in aortic resistance was no longer affected by the ischemia and increased to the same extent, as noted during the control BCO. However, mean AP (38.7 +/- 6.8%), systolic LVP (40.3 +/- 8.7%), and dLVP/dt (62.4 +/- 11.0%) remained significantly reduced when compared with the control (no coronary occlusion) response. These data suggest that 1) posterior ischemia elicits a greater reduction in the BCO response than anterior ischemia, and 2) vagal afferents as well as depression of contractile function may both contribute to the BCO response inhibition noted during posterior ischemia.

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