Carotid Sinus Area Research Articles

Structural organization of the carotid sinus under the influence of monosodium glutamate in the experiment: analysis of changes in dynamics

Carotid artery pathology is one of the leading causes of cerebral stroke. Among the pathogenetic factors in the development of carotid artery damage, disorders of lipid metabolism, atherosclerosis, and metabolic syndrome occupy a prominent place. The alimentary factor is extremely important in this context. Monosodium glutamate is one of the most common food additives, which is often used uncontrollably and can cause changes in the structure and functions of organs and tissues. The purpose of the study: to analyze the dynamics of morphological changes in the carotid sinus area under the influence of monosodium glutamate when administered orally in an experiment. The area of the carotid sinus of 20 male laboratory white rats that received sodium glutamate orally at a dose of 10 mg/kg/day for 8 weeks was studied by morphological methods at the macro- and microstructural levels after 6 and 8 weeks of the experiment. The obtained data are compared with the results of a morphological study of the same area in 20 animals of the control group. Statistical processing of animal weight was performed using MS Excel 2007 software. Mean ± standard deviation was determined. After 6 weeks of the experiment, when evaluating the histological structure of the wall of the internal carotid artery in the area located directly above the bifurcation, when compared with the control group, multiplication and folding of the intima were found in the experimental group, presumably associated with the proliferation of endothelial cells under the influence of sodium glutamate, detachment of the endothelium and lysis of individual endotheliocytes, as well as uneven thickening of elastic media fibers and disruption of their structure. Attention was drawn to the accumulation of white fat perivasally and in the zone of the carotid glomus, as well as the disorganization of nerves and the expansion of vessels of the microcirculatory channel. After 8 weeks of the experiment, the negative dynamics of structural changes were noticeable: signs of increased inflammatory infiltration, deformation of the vessels of the microcirculatory bed with thickening of their walls and narrowing of the lumen, stasis, noticeable degranulation of cells of type I carotid glomus cells, the appearance of single labrocytes (mast cells) in the infiltrate. The amount of adipose tissue (white fat) in the area of the carotid sinus and the perivasal bifurcation of the carotid arteries, as well as in the immediate vicinity of the carotid glomus, also increased markedly, and a tendency towards thickening of adipose tissue was noted. Thus, monosodium glutamate with systematic oral use can cause a violation of the structural organization of the carotid sinus, the wall of the carotid arteries and the carotid glomus, and the severity of changes in dynamics increases. Further research is needed to clarify the nature of the structural changes in the carotid sinus under the conditions of withdrawal of monosodium glutamate, as well as to find possible ways of correction.

Morphometry of the Entire Internal Carotid Artery on CT Angiography.

Background and Objectives: Knowledge of the internal carotid artery’s (ICA) morphometric features is influential in outlining surgical and minimally invasive procedures in the neurovascular field. Many studies have shown divisive numbers regarding the ICA’s caliber, with the measuring point of the artery sometimes differing. This study presents ICA dimensions based on computed tomography angiography in each of its seven segments as per Bouthillier’s classification, correlating vascular dimensions with anthropometric parameters. Materials and Methods: A thorough CT angiography analysis was performed on 70 patients with internal carotid vessels unaffected by atherosclerotic disease. The extracranial part of the ICA was measured in four locations—carotid bulb, post-bulbar dilation, at its cervical midpoint, and below its entrance into the carotid foramen. Single landmarks were used for measurements in the intracranial segments. ICA length was assessed in the neck region and also in the cranial cavity. Craniometric measurements were performed on sagittal and coronal CT reconstructions. Patient height was taken into consideration. Results: The largest ICA portion is near its origin in the carotid sinus area (7.59 ± 1.00 mm), with a steep decline in caliber following its extracranial course. Distal ICA presented values somewhat similar to its proximal intracranial segment diameters (4.67 ± 0.47 mm). Dimensions of the ICA in the intracranial segments start from a value of 4.53 ± 0.47 mm and decrease by approximately 40% when reaching the origin of the middle cerebral artery (2.71 ± 0.37 mm), showing a marked decrease in caliber after the emergence of the most critical collateral artery, the ophthalmic branch. The length of the ICA varies between genders, with the male ICA being about 10 mm longer in total length than female ICA; this difference is also correlated with patient height and skull dimensions. Conclusions: Both intra- and extracranial ICA have variable dimensions and length related to gender and anthropometric parameters, with no significant differences obtained concerning side or age.

Anatomical meningo-orbital band evaluation and clinical implications: a cadaveric dissection study.

The meningo-orbital band (MOB) is a dural structure which runs around the superior orbital fissure (SOF) tethering the frontotemporal basal dura to the periorbita, through the SOF. MOB division is important to expose and remove the anterior clinoid process, to access to proximal carotid artery and cavernous sinus area. The aim of this study was to measure how the MOB could be safely incised without cranial nerves and cavernous sinus injuries. Anatomical dissections and extradural exposure of the anterior clinoid process was performed on 20 cadavers (40 sides). Measurement of the MOB thickness was performed before its incision, after dura propria dissection, and retraction off the inner cavernous membrane, to expose the cranial nerves. We analyzed 20 cadaveric formalin-fixed heads injected with colored silicone, 11 man and 9 women of Caucasian race. The average length of a safe incision of the MOB was 10.6±1.1 mm on the right side, and 10.65±1.09 mm on the left side. In our study the average length of a safe incision of the MOB was 10.6±1.1 mm. Thus, the incision length of the MOB should not exceed 9 mm; the peeling of the anterior cavernous sinus and of the SOF, dissecting the two layers of the dura throughout the incision of the MOB, is a useful technique to avoid cranial nerves and cavernous sinus lesions.

Facilitation of Chronic Intermittent Hypobaric Hypoxia on Carotid Sinus Baroreflex in Anesthetized Rats

Our previous study showed that chronic intermittent hypobaric hypoxia (CIHH) could prevent decreases in systemic arterial blood pressure (SABP) during acute hypoxia. However, the mechanism was not clear. The purpose of the present study was to observe whether the carotid sinus baroreflex (CSB) was involved in the antagonizing effect of CIHH on SABP decrease induced by acute hypoxia and to explore the underlying mechanism using perfusion technique in rat isolated carotid sinus area. After 14-day and 28-day CIHH exposure, the CSB in rats was enhanced markedly, manifesting as increases in PS and RD, and decreases in TP and SP. This facilitation of CSB was partly abolished by Glibenclamide (Gli, 10 μM), a K ATP channel blocker, but was not influenced by L-NAME (100 μM), a nitric oxide synthase (NOS) inhibitor. The results of the study suggested that CIHH facilitated CSB through opening the K ATP channels in carotid sinus of anesthetic rats and might be one of mechanisms of CIHH keeping SABP homeostasis during acute hypoxia.

Determinants and Outcomes of Asystole During Carotid Artery Stenting

To examine the predictors and outcomes of asystole in patients who undergo carotid artery stenting (CAS). Forty-three patients (24 men; median age 69 years) with asystole were identified after reviewing the case records of 884 patients who underwent CAS at our institution between 1997 and 2009. The control group comprised 678 patients who underwent stenting in the carotid sinus area without asystole. Univariate and multivariate logistic analyses were used to determine the predictors and outcomes of asystole. A right-sided procedure was more likely to result in asystole [odds ratio (OR) 11.4, 95% CI 4.0 to 32.7, p<0.0001] compared with a left-sided procedure. Patients with a contralateral carotid stenosis (OR 1.7, 95% CI 1.0 to 2.8, p = 0.04) and a left ventricular ejection fraction (LVEF) of <40% (OR 2.2, 95% CI 1.1 to 4.5, p = 0.03) were also more likely to suffer asystole. Smokers appeared less likely to develop asystole (OR 0.25, 95% CI 0.12 to 0.56, p = 0.0006). Periprocedural stroke (14% vs. 1.3%, p<0.001), length of stay during index hospitalization (2.2 vs. 1.2 days, p = 0.002), and 30-day mortality (11.6% vs. 4.1%, p = 0.02) were significantly higher in the asystole group. Asystole during CAS is more likely to occur in patients undergoing procedures in the right carotid sinus area, in those who have significant contralateral carotid stenosis, and in those with a reduced LVEF. More caution should be exercised during right-sided than left-sided CAS procedures.

Effect of carotid sinus nerve blockade on hemodynamic stability during carotid endarterectomy under local anesthesia

To find out whether routine carotid sinus nerve blockade with lidocaine during carotid endarterectomy under local anesthesia results in perioperative changes in blood pressure and heart rate. This was a prospective, randomized, single-center study, conducted in a university hospital. A total of 120 patients undergoing carotid endarterectomy under local anesthesia were randomly assigned to three equal groups. Patients with previous carotid endarterectomy were excluded from the study. During the operation the carotid sinus area was infiltrated as follows: group 1 received 2 mL of 1% lidocaine; group 2 received 2 mL of 0.9% NaCl; and group 3 received no infiltration. The carotid sinus nerve was spared in all patients. Blood pressure and heart rate were invasively monitored during the operation and 12 hours postoperatively over the radial artery cannula. Preoperative values were calculated as a mean of three noninvasive measurements on the day before surgery. Data comprised of arterial blood pressures and heart rates from 32 time point measurements for each patient were analyzed. There was no significant difference among the groups regarding the mean arterial blood pressures and mean heart rates during the follow-up period. There was no significant difference among groups regarding the number of patients that required vasoactive therapy at any time of measurement. Routine infiltration of carotid sinus area with 1% lidocaine during carotid endarterectomy performed under local anesthesia has no significant impact on mean arterial blood pressure and heart rate during the operative procedure and the following 12 postoperative hours.

Effect of lignocaine injection in carotid sinus on baroreceptor sensitivity during carotid endarterectomy

Objectives This study was undertaken to test the hypothesis that there is a neural basis for baroreceptor deterioration during carotid endarterectomy (CEA), by investigating intraoperative hemodynamic changes induced by intraluminal carotid stretch stimulation, before and after application of local anesthetic to the adventitial layer of the carotid sinus region. Methods This was a prospective study of 20 patients undergoing elective CEA. During CEA, before removal of the atheroma, intraluminal stretch simulation of the carotid baroreceptors (rub test) was performed before and after injection of 1% lignocaine into adventitial tissue of the artery in the region of the carotid sinus. Continuous measurements of mean arterial blood pressure (MAP), electrocardiographic r-r intervals (R-R), heart rate, cardiac vagal tone, and carotid sinus baroreflex were recorded to determine alterations in baroreceptor function. Results Rub test before injection of lignocaine was associated with a decrease in MAP and heart rate and an increase in R-R, cardiac vagal tone, and carotid baroreflex response, indicating a functioning baroreflex. After lignocaine injection and repetition of the rub test, no significant change was seen in MAP, heart rate, R-R, cardiac vagal tone, or carotid baroreflex response, indicating a nonfunctioning baroreflex. Comparing the peak responses to the rub test stimulus before and after lignocaine injection showed significant differences for all variables ( P < .05), with carotid baroreflex response and heart rate being highly significant ( P < .0005). Conclusions The baroreflex response to intraluminal stretch stimulation of the carotid sinus area is operational in patients undergoing CEA, and this response is abolished by infiltration of local anesthetic into the periadventitial tissue around the carotid sinus.

Intraoperative change in baroreceptor function during carotid endarterectomy

Abstract Background Labile blood pressure following carotid endarterectomy (CEA) is common and is associated with perioperative myocardial infarction and intracranial haemorrhage. Previous studies have identified that alteration in carotid baroreceptor function is responsible for the blood pressure changes although the mechanism remains unclear. This study aimed to identify the mechanism by which CEA affects baroreceptor function. Methods Fifty patients were recruited prospectively and underwent estimation of baroreceptor sensitivity (BRS) during a 10-min period of supine bed rest using electrocardiography and Finapres, 2 days before and 2 days to 6 weeks after surgery. During surgery continuous measurements of blood pressure (intra-arterial) and heart rate were recorded on to digital audio tape for postoperative analysis. During analysis the operation was divided into different stages to identify at which stage baroreceptor function altered. Particular attention was paid to initial clamping of the carotid artery, performance of the endarterectomy and final restoration of blood flow. In addition the carotid sinus area was stimulated by stroking the inside of the artery before and after removal of the plaque. Autonomic activity was calculated using power spectral analysis of beat-to-beat blood pressure and the R–R interval from the electrocardiograph. BRS was estimated by calculation of the square root of the ratio of the powers of R–R interval and systolic blood pressure to give the alpha index which has been shown to correlate well with BRS calculated by means of standard pharmacological techniques. Results For this cohort of patients BRS was significantly reduced 2 days after surgery compared with the preoperative recordings (2·8(0·4) to 5·6(0·8)). Six weeks after operation BRS had improved but had not achieved preoperative levels (3·8(0·6) to 5·6(0·8)). During surgery, patients with good baroreceptor function identified before operation experienced a rise in blood pressure on initial carotid clamping indicating that dissection had not affected the baroreceptor mechanism. Similarly, intraluminal stimulation of the carotid sinus area with the plaque in situ produced a decrease in blood pressure indicating good baroreceptor function. After removal of the plaque, repeating the intraluminal stimulation did not produce a decrease in blood pressure indicating disruption of the baroreceptor mechanism. Conclusion Removal of the atheromatous plaque during CEA adversely affects carotid baroreceptor function. The baroreceptor mechanism is disrupted but not completely destroyed and gradually improves in the weeks following surgery.

The effects of carotid sinus nerve blockade on hemodynamic stability after carotid endarterectomy

Objective : To determine whether intraoperative administration of bupivacaine reduces the incidence of hypotension after carotid endarterectomy (CEA). Design : Prospective, double-blinded, randomized controlled trial. Setting : A single-institute, tertiary-care medical center. Participants : Patients ( n = 135) who were referred for CEA without prior ipsilateral CEA, diabetes mellitus, or allergies to local anesthetics. Interventions : 2 mL of 0.25% bupivacaine or 2 mL NaCl (control) injected by the surgeon at the carotid sinus immediately after CEA. Measurements and Main Results : Blood pressure and heart rate were measured before induction, before carotid reperfusion, 2 minutes after reperfusion, before carotid sinus injection, and every 15 minutes thereafter for 2 hours. Anesthesia was induced and maintained with fentanyl, pancuronium, and 0.5% to 1% enflurane. Hypertension was defined as a systolic blood pressure 30% above baseline or greater than 180 mmHg. Hypotension was defined as a systolic blood pressure 30% below baseline or less than 100 mmHg. Postoperative incidences of hypertension, hypotension, and the associated use of corrective medications were compared in both groups using the chi-squared test to determine statistical significance. Patients in the bupivacaine group ( n = 61) had a similar incidence of postoperative hypotension as controls ( n = 74) but a higher incidence of hypertension (40% v 24%; p = 0.043). The bupivacaine group required vasodilators more often (33% v 18%; p = 0.04). Baseline hypertension and preoperative use of β-blockers also were predictive of postoperative hypertension. Conclusions : Carotid sinus area infiltration with bupivacaine after CEA does not reduce the incidence of postoperative hypotension but significantly increases the incidence of postoperative hypertension. Thus, its routine use cannot be recommended in carotid endarterectomy.

The evolution of surgery for the treatment and prevention of stroke. The Willis Lecture.

Thomas Willis, the man for whom this lecture is named, was an Englishman and a leading neuroanatomist of the 17th century. Born in 1621, he attended Oxford University, graduating from Christ Church College in 1639. While still at Oxford, he became Sedleian Professor of Natural History in 1660. He did much experimental work with his associate Richard Lower. He performed injection experiments on cadavers and noted that if he injected the carotid artery on one side, the dye solution would come forth from the carotid on the opposite side. In 1664 Willis published his monumental work Cerebri Anatome , the most complete and accurate account of the nervous system that had hitherto appeared. In it he contributed the term “neurology” to medicine, a word derived from the Greek, meaning “sinew,” “tendon,” or “bowstring.” The word was translated and introduced into the English language in 1681 in Samuel Pordage's translation of Willis' work. Cerebri Anatome contains a classification of the cerebral nerves, the first description of the eleventh nerve, and a description of the hexagonal network of arteries at the base of the brain that we know as the circle of Willis. Although others had described the circle before Willis, he was the first to grasp its physiological and pathological significance. He records the clinical histories of two patients in whom he suggests that the anatomic configuration of the arteries at the base of the brain could prevent apoplexy. The book was illustrated by Christopher Wren, an associate of Willis at Oxford, later to become England's leading architect and designer of St Paul's Cathedral, numerous other English churches, and many historic secular buildings. Willis moved to London in 1666 and acquired the largest fashionable practice of his day. He continued his careful clinical observations and made a number of other important …

Depressed baroreflex in heart failure is not due to structural change in carotid sinus nerve fibers

It is well known that the baroreceptor reflex is blunted in the heart failure state. However, the mechanisms for this depression are not well understood. The aim of the present study was to determine if carotid sinus nerve fiber density is decreased in the heart failure state. Experiments were carried out in pacing-induced heart failure and normal dogs. The carotid sinus nerve (CSN) was dissected and the CSN discharge responses to changes in arterial pressure with nitroglycerin (25 μg/kg, i.v.) or phenylephrine (10 μg/kg, i.v.) were recorded. Thereafter, the carotid sinus area was isolated and perfused with oxygenated Krebs-Henseleit solution. Carotid sinus baroreceptor single-unit activity was recorded and a carotid sinus pressure-discharge curve was constructed using either static or pulsatile pressure. Finally, the carotid sinus nerve was removed and fixed at its in situ length in 3% glutaraldehyde. The fixed carotid sinus nerve was cut transversely in 0.5–1.0-μm sections and prepared for electron microscopy. A photographic collage of the CSN was then analyzed at 4000 × magnification. The total number, diameter and area of myelinated and non-myelinated fibers were measured with a digitizer and the density and diameter distribution were calculated. Carotid sinus nerve discharge responses to change in arterial pressure were significantly blunted in dogs with pacing-induced heart failure. Furthermore, single-unit baroreceptor responses to both static and pulsatile pressurization were markedly depressed in dogs with heart failure. However, there was no change in either fiber density or the ratio of myelinated fibers to unmyelinated fibers in the carotid sinus nerve in heart failure. In addition, there was no change in the distribution of either fiber diameter or cross-sectional area in the carotid sinus nerve in dogs with heart failure. These data indicate that there is no significant change in the number or type of fibers in the CSN of dogs with heart failure. Therefore, the depressed baroreceptor reflex in heart failure is not due to structural changes in fibers of the CSN. The depressed baroreflex is most likely due to desensitization of individual baroreceptors.

Static Magnetic Field Effect on Sinocarotid Baroreceptors in Humans

This research is an extension of our previous animal studies where we showed that sinocarotid baroreceptors react to static magnetic field (SMF) in unconscious and conscious rabbits (1-8). The objective was to study SMF cardiovascular effect on sinocarotid baroreceptors in conscious healthy volunteers by the analyzing heart rate variability using a fast Fourier transform (FR). After a 5-min resting period in the supine position, R-R intervals were measured in cycles comprising 300 heartbeats during blank control, sham, and 0.12 T iron bar magnet local application over the right and left carotid sinus areas. We found that SMF increased heart rate variability, accompanied by significant shift of the power spectrum amplitude peak to lower-frequency regions, which is associated with increased sinocarotid baroreceptor activity. On the basis of this and our previous (1-8) research, we conclude that sinocarotid baroreceptors react to SMF. SMF might stabilize cellular membranes, leading to an increase in sinocaro...

Static Magnetic Field Effects on Sinocarotid Baroreceptors in Rabbits Exposed under Conscious Conditions

This research is an extension of our previous studies, where we showed that sinocarotid baroreceptors react to a static magnetic field (SMF) in unconscious rabbits (1–7).The objective was to study the cardiovascular effect of SMF on sinocarotid baroreceptors in conscious rabbits. Two groups of experiments with different protocols were carried out in 18 healthy adult male rabbits. The first group included 31 experimental runs. In this group 0.24 T static bar magnets were positioned under rabbits' carotid sinus areas for 30 min. The second group included 20 experimental runs. In this group 0.5 T static bar magnets were positioned under carotid sinus areas for 40 min. We found that SMF significantly decreased blood pressure and heart rate and increased blood pressure variability and microcirculation during its local application to the sinocarotid baroreceptor region. SMF might stabilize cellular membranes, leading to an increase of buffer capacity of the sinocarotid baroreceptors to blood pressure variations.

Geomagnetic Field and Artificial 0.2 T Static Magnetic Field Combined Effect on Blood Pressure

We investigated the influence of the external time-varying component of the natural geomagnetic field–geomagnetic activity–on the degree of the 0.2 T static magnetic field (SMF) hypotensive effect. We showed previously that 0.2 T SMF applied to the carotid sinus area of anesthetized rabbits had a hypotensive effect under norepinephrine-induced hypertensive conditions (1).We found that the degree of the 0.2 T SMF hypotensive effect depends on the level of the geomagnetic activity at the time of the experiment and is maximal for days with disturbed geomagnetic activity.We concluded that in the evaluation of artificial electromagnetic fields biological effects, geomagnetic field activity must be taken into consideration, because of a possible modulating effect.

Rapid resetting of baroreflexes in hypertensive dogs.

The hypothesis tested was that the rapid resetting of the arterial baroreflex control of arterial pressure in normotension could be demonstrated in experimental hypertension. After the development of experimental hypertension (using a bilateral renal wrap technique), rapid resetting of arterial pressure and heart rate (HR) was acutely assessed under pentobarbital sodium anesthesia in hypertensive and normotensive vagotomized dogs. The carotid sinus area was isolated and perfused at controlled carotid sinus pressures (CSPs). Baroreflex response [mean arterial pressure (MAP) and HR] curves were measured after three carotid sinus conditioning pressures (50, 125, and 200 mmHg) were applied. For the MAP response, the CSPo (CSP at point of maximum reflex gain) increased significantly to the same extent in both groups with increasing conditioning pressures (with 22.2 and 16.7% resetting in the normotensive group, and 20.3 and 14.2% resetting in the hypertensive group). We conclude that short-term adjustments to changes in prevailing pressure (rapid resetting) occur in the arterial pressure response in experimental hypertension to the same extent seen in normotension.

Aldosterone reduces baroreceptor discharge in the dog.

We have previously demonstrated that baroreceptor discharge sensitivity is depressed in dogs with experimental heart failure and that this depressed sensitivity can be reversed by the Na+,K(+)-ATPase inhibitor ouabain. This suggests that enhanced Na+,K(+)-ATPase activity in baroreceptors is responsible for the blunted baroreceptor discharge sensitivity seen in heart failure state. Because aldosterone, a known stimulator of Na+,K(+)-ATPase, is elevated in heart failure the present study was undertaken to determine the effects on baroreceptor discharge of perfusion of the carotid sinus with aldosterone in normotensive dogs. Single unit baroreceptor activity was recorded as well as carotid sinus pressure and the diameter of the carotid sinus. Perfusion of the carotid sinus with aldosterone (in Krebs-Henseleit solution) significantly elevated threshold pressure (108.5 +/- 3.1 mm Hg versus 92.7 +/- 4.6 mm Hg, p less than 0.05) and reduced peak discharge rate (40.3 +/- 3.9 spikes/sec, p less than 0.05). These effects appeared 15 minutes after aldosterone perfusion and remained constant for the next 60 minutes. There was no change in the carotid sinus pressure-diameter curve during perfusion with aldosterone. Perfusion of the carotid sinus with ouabain (0.1 microgram/ml) during aldosterone perfusion did not reverse the blunted baroreceptor discharge. The blunted baroreceptor activity induced by perfusion of the carotid sinus with aldosterone was prevented by removal of the endothelial cells in the carotid sinus area with a balloon-tipped catheter or by perfusion with saponin. Finally, perfusion of the carotid sinus with spironolactone (10 ng/ml), a mineralocorticoid receptor antagonist, prevented the inhibitory effect of aldosterone. These data suggest that aldosterone reduces maximum baroreceptor discharge.(ABSTRACT TRUNCATED AT 250 WORDS)

Low-pressure-sensitive baroreceptor fibers recorded from rabbit carotid sinus nerves.

Activity was recorded from physiologically identified baroreceptor or chemoreceptor fibers in carotid sinus nerves of urethane-anesthetized spontaneously breathing rabbits. A carotid sinus area was vascularly isolated so that carotid sinus pressure and perfusion medium (Locke's solution or rabbit blood) could be controlled. The cervical sympathetic, vagus, and aortic depressor nerves were bilaterally cut to eliminate vagal and cardiopulmonary reflexes. Baroreceptor fibers could be divided into two groups: fibers with a mean firing threshold of 47.6 +/- 1.9 mm Hg and no activity below this threshold (37 fibers) and fibers that were active at low intrasinus pressures (18.1 +/- 2.2 impulses/sec at an intrasinus pressure of 0 mm Hg). The baroreceptor fibers that were spontaneously active at low pressures were also chemically sensitive: discharge rate was increased by 5-hydroxytryptamine (10 fibers, p less than 0.01), nicotine (10 fibers, p less than 0.01), or hypercapnia (13 fibers, p less than 0.001). The activity of baroreceptor fibers with a clear pressure threshold was usually decreased by hypercapnia (26 of 27 fibers, from 18.8 +/- 3.1 to 13.2 +/- 3.9 impulses/sec). Chemoreceptor fibers failed to respond to intrasinus pressure changes from 0 to 100 mm Hg (n = 25 fibers, p greater than 0.5) but were sensitive to chemical changes, as expected. Thus, there is a subset of baroreceptor fibers that, under certain conditions, is spontaneously active at very low intrasinus pressures and responds to changes in the chemical milieu.

Influence of substance P on carotid sinus nerve baro- and chemoreceptor activity in rabbits

Substance P (SP) is abundant in the carotid sinus nerve (CSN) and has been implicated in baro- and chemoreceptor reflexes. We examined the effect of SP on blood pressure, heart rate, phrenic nerve activity, hindlimb perfusion pressure, and cardiac contractile strength in urethane-anesthetized rabbits with bilaterally cut cervical sympathetic, vagus, and aortic depressor nerves. Retrograde simultaneous injection of SP (0.5–2.7 μg/kg in 0.2–0.3 ml saline) into both carotid sinus areas via the internal carotid arteries decreased blood pressure (by 56%), heart rate (by 13%), cardiac contractility (by 25%) and phrenic nerve activity (by 77%). The effect on hindlimb perfusion pressure was variable. There was both a reflex effect and direct hindlimb vasodilation. In another group of rabbits, the carotid sinus areas were vascularly isolated and perfused with SP (0.19 μg/min dissolved in Locke's solution) or Locke's solution alone for 5 min. While carotid sinus perfusion pressure was maintained in the range of 80–120 mmHg, mean arterial blood pressure, heart rate, and unit activity from the CSN were recorded. SP increased the activity of 11 of 18 baroreceptor fibers and inhibited all of 20 chemoreceptor fibers. SP decreased mean arterial blood pressure and heart rate, but the changes were less than those obtained with injection of SP into nonisolated carotid sinus arteries because systemic effects of SP, which in some cases counteracted the reflex effects, were eliminated.

Observations on the structure and innervation of the carotid sinus complex in the African porcupine (Hystrix cristata)

The carotid arterial system of the porcupine Hysitrix cristota has been studied using light and electron microscopy. Emphasis has been placed on describing the structure and innervation of the carotid sinus area located at the origin of the internal carotid artery. The sinus wall has a largely elastic structure and a reduced smooth muscle content. A functional relationship is proposed between the elastic structure of the sinus wall and baroreceptor mechanisms.

Interaction of canine carotid sinus and aortic arch baroreflexes in the control of total peripheral resistance.

Interaction of carotid sinus and aortic arch reflex control of total peripheral resistance was studied in eight dogs anesthetized with sodium pentobarbital and placed on constant flow cardiac bypass. Carotid sinus and aortic arch baroreceptor areas were isolated and separately perfused at controlled pressures. Combinations of carotid sinus and aortic arch pressures were delivered at random in steps of 25 mm Hg over the 50-225 mm Hg pressure range, and systemic arterial pressure was measured. Changes in arterial pressure reflected changes in total peripheral resistance. A multiple linear regression showed that both carotid sinus and aortic arch pressures exhibited a sigmoidal relationship with arterial pressure. Independent of carotid and aortic baroreceptor pressures, arterial pressure was found to be a periodic function of time (period = 2 hours) in all dogs. The average carotid sinus reflex open loop gain was found to be 0.231 +/- 0.092, while average aortic arch open loop gain was 0.141 +/- 0.088. The gain of either the carotid sinus or aortic arch reflex was not influenced by the absolute pressure level of the other receptor area. In a separate series of experiments performed in the same dogs, we tested the hypothesis that a nonlinear temporal summation of the reflex control of total peripheral resistance might exist when the inputs to carotid and aortic baroreceptors are changed simultaneously. With both inputs held at the region of maximum gain, 25 mm Hg step changes were imposed first on carotid sinus pressure, then on aortic arch pressure, and then on both simultaneously. A temporal inhibition of the two reflexes showed that simultaneous excitation of both receptors resulted in a smaller reflex response than the sum of individual responses.