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Biomedical subjects

K Matsukawa

Publications and source records attributed to K Matsukawa.

At least 19 recordsLinked to original sources
PubMed2004

Noninvasive evaluation of cardiac output during postural change and exercise in humans: comparison between the modelflow and pulse dye-densitometry.

To investigate whether the Model-flow method, by simulating the aortic input impedance model from a noninvasive monitoring of arterial blood pressure, reflected a reliable measure of cardiac output (CO) during postural change and whole-body exercise occurring in daily life, we compared the Modelflow-estimated CO with a simultaneous reference determined by the pulse dye-densitometry. Nine healthy volunteers performed postural change from supine to upright and dynamic stepping exercise. The Modelflow-estimated CO decreased to 4.8 +/- 0.5 l/min, from 5.8 +/- 0.6 l/min, during the postural change and increased to 12.8 +/- 1.3 l/min during a stepping exercise, returning to 5.1 +/- 0.4 l/min at 5 min after exercise. When comparing the pooled data of CO during resting and following exercise between the Modelflow and pulse dye-densitometry, we found that the average CO did not differ between the two estimates and that there was a significant correlation between them; the slope of the linear regression line corresponded to approximately 1.0. Although such linear relationship was also observed in an individual subject, the slope of the regression line varied from 0.737 to 1.588 among the subjects. The calibration of the Modelflow-estimated CO with the dye-densitometry value at supine or upright improved a correlation between the two estimates. Thus it is likely that the noninvasive Modelflow simulation from arterial blood pressure can provide a reliable estimation of group-average cardiac output during postural change and stepping exercise occurring in daily life. It will be recommended for a more accurate estimation of cardiac output in a given subject to calibrate the Modelflow data with an independent measure.

Adult↗
PubMed2001

Cardiac vagal and sympathetic efferent discharges are differentially modified by stretch of skeletal muscle.

We directly measured cardiac vagal efferent nerve activity (CVNA) and cardiac sympathetic efferent nerve activity (CSNA) in cats decerebrated at the level of the precollicular-premammillary body while the hindlimb or the triceps surae muscle was passively stretched. CVNA gradually decreased during passive stretch of the hindlimb, and this decrease was sustained throughout the stretch. CSNA increased at the onset of passive stretch, but this increase was not sustained. CVNA and CSNA responded differentially to graded passive stretches of the triceps surae muscle as well as the hindlimb. The sustained decrease in CVNA but not the initial increase in CSNA became greater depending on muscle length and developed tension. The time course and direction of the cardiac autonomic responses to muscle stretch were not affected by partial sinoaortic denervation, although the magnitude of the CSNA response was augmented. We conclude that the muscle mechanoreflex contributes to differential regulation of cardiac parasympathetic and sympathetic efferent discharges during passive stretch of skeletal muscle irrespective of arterial baroreceptor input.

Animals↗
PubMed2001

Reflex responses in plasma catecholamines caused by static contraction of skeletal muscle.

To examine a hypothesis of whether static muscle contraction produces a release of catecholamines from the adrenal medulla via reflex stimulation of preganglionic adrenal sympathetic nerve activity induced by receptors in the contracting muscle, we compared the reflex responses in a concentration of epinephrine (Ep) and norepinephrine (NEp) in arterial plasma during static contraction and during a mechanical stretch of the hindlimb triceps surae muscle in anesthetized cats. Static contraction was evoked by electrically stimulating the peripheral ends of the cut L(7) and S(1) ventral roots at 20 or 40 Hz. Mean arterial pressure (MAP) and heart rate (HR) increased 23 +/- 3.1 mmHg and 19 +/- 4.3 beats/min during static contraction. Ep in arterial plasma increased 0.18 +/- 0.072 ng/ml over the control of 0.14 +/- 0.051 ng/ml within 1 min from the onset of static contraction, and NEp increased 0.47 +/- 0.087 ng/ml over the control of 0.71 +/- 0.108 ng/ml. Following a neuromuscular blockade, although the same ventral root stimulation failed to produce the cardiovascular and plasma catecholamine responses, the mechanical stretch of the muscle increased MAP, HR, and plasma Ep, but not plasma NEp. With bilateral adrenalectomy, the baseline Ep became negligible (0.012 +/- 0.001 ng/ml) and the baseline NEp was lowered to 0.52 +/- 0.109 ng/ml. Neither static contraction nor mechanical stretch produced significant responses in plasma Ep and NEp following the adrenalectomy. These results suggest that static muscle contraction augments preganglionic adrenal sympathetic nerve activity, which in turn secretes epinephrine from the adrenal medulla into plasma. A muscle mechanoreflex from the contracting muscle may play a role in stimulation of the adrenal sympathetic nerve activity.

Adrenal Medulla↗
PubMed1999

Effects of mental stress on cardiac and motor rhythms.

To identify whether spontaneous cardiac rhythm and voluntary motor rhythm are modified in parallel or influenced separately when imposing mental stress, we recorded simultaneously the two rhythms during finger tapping as a simple model of rhythmical motion in 10 healthy human subjects (6 males, 4 females each). Each subject performed finger tapping with an arbitrary tapping rhythm. Mental stress was given intermittently three times for 10-15 s at intervals of 40 s during tapping for 150 s. Heart rate (HR) and tapping rate (TR) and their variations (standard deviation; SD) during finger tapping with and without mental stress were compared. HR and TR increased significantly in response to mental stress during tapping. After mental stress was ended, HR returned rapidly to the initial level, but TR remained at a higher level. Moreover, SD of TR, but not SD of HR, during tapping was increased by mental stress. The present results indicate that the cardiac and motor rhythms are influenced simultaneously by mental stress. However, a difference was seen about the sustained effect of mental stress on the two rhythms.

Adult↗
PubMed1999

Effect of renal denervation on the compensatory renal growth following nephrectomy in the cat.

The purpose of this study was to clarify the effect of denervation on the mass of the remaining kidney with or without unilateral nephrectomy using adult cats. The animals were divided into 4 groups: (1) control group, the weights of the right and left kidneys were measured intact in 5 cats; (2) nephrectomy group (Nx, n = 5 cats), the right kidney was removed and the left kidney was weighed 3-5 d after nephrectomy; (3) nephrectomy and denervation group (Nx+Dx, n = 7 cats), the left kidney was weighed on the 7th day after surgery in which the left kidney was denervated and the right kidney was removed; and (4) denervation group (Dx+Dx, n = 5 cats), both kidneys were weighed on the 7th day after denervation of the kidneys. In the control group, the left and right kidney weights per body weight (LKW and RKW) were the same (LKW, 0.74 +/- 0.06%; RKW, 0. 74 +/- 0.07%). In the Nx group, LKW increased to 0.90 +/- 0.03% 3-5 d after nephrectomy, although RKW of the removed kidney was 0.66 +/- 0.01%. In the Nx+Dx group, LKW increased to 0.97 +/- 0.15%, which was similar to that of the Nx group. In the Dx+Dx group, LKW (0.56 +/- 0.05%) and RKW (0.54 +/- 0.05%) were significantly less than those in the control group. We conclude that the renal nerves may contribute to maintaining the renal mass and that the neural effect on compensatory growth following nephrectomy may be covered by other growth factors.

Adaptation, Physiological↗
PubMed1998

Augmented renal sympathetic nerve activity by central command during overground locomotion in decerebrate cats.

We examined whether the cerebrum is essential for producing the rapid autonomic adjustment at the onset of spontaneous overground locomotion. Renal sympathetic nerve activity (RSNA), mean arterial pressure (MAP), heart rate (HR), and electromyogram of the forelimb triceps brachialis were measured when freely moving, decerebrate cats spontaneously produced overground locomotion, supporting body weight. Decerebration was performed at the level of the precollicular-premammillary body. RSNA increased 95 +/- 14 impulses/s (68 +/- 10% of baseline value) at the onset of spontaneous locomotion, which was followed by rises in MAP and HR (7 +/- 1 mmHg and 18 +/- 2 beats/min, respectively). Concomitantly with the MAP rise, RSNA declined toward control values and then increased again during the subsequent period of locomotion. The same rapid increase in RSNA at the onset of locomotion was observed after sinoaortic denervation and vagotomy. It is concluded that some central site(s), other than the cerebrum and the rostral part of the diencephalon, can generate the centrally induced autonomic adjustment at the onset of spontaneous overground locomotion, which is independent of arterial baroreceptor and vagal afferents.

Afferent Pathways↗
PubMed1997

Direct observations of sympathetic cholinergic vasodilatation of skeletal muscle small arteries in the cat.

1. The aim of this study was to examine the actual changes of the internal diameter (i.d.) of arterial vessels of skeletal muscle evoked by activation of sympathetic cholinergic nerve fibres during stimulation of the hypothalamic defence area in anaesthetized cats. 2. For this purpose, we have used our novel X-ray TV system for visualizing small arteries (100-500 microm i.d.) of the triceps surae muscle and larger extramuscular arteries (500-1400 microm i.d.) of the hindlimb (the femoral (FA), popliteal (PA) and distal caudal femoral (DCFA) arteries). The passage of a contrast medium from the large extramuscular arteries to the smaller intramuscular arteries was serially measured before and during hypothalamic stimulation. 3. Hypothalamic stimulation increased mean arterial blood pressure, heart rate and femoral vascular conductance. The i.d. of FA, PA, and DCFA did not change during the hypothalamic stimulation, whereas the i.d. of small arteries in the triceps surae muscle increased by 48 +/- 2% (mean +/- S.E.M.) and the cross-sectional area increased concomitantly by 118%. The maximum increase in i.d. of 78 +/- 6%, was observed in arteries of 100-200 microm. These increases in diameter were markedly reduced by intra-arterial injection of atropine or by cutting the sciatic nerve, but not by phentolamine and propranolol given together. 4. The vasodilatation evoked by hypothalamic stimulation was seen in almost all the sections of the small arteries observed under control conditions and was distributed along the entire length of the vessel. In addition, the number of arterial vessels that could be detected increased by 42% during hypothalamic stimulation. The newly detected arterial branches, which ranged from 100 to 300 microm in diameter, mostly arose from the branching points. 5. It is concluded that stimulation of sympathetic cholinergic nerve fibres dilates the small arteries of skeletal muscle ranging from 100 to 500 microm, but not the larger extramuscular arteries.

Animals↗
PubMed1997

Cardiovascular responses during spontaneous overground locomotion in freely moving decerebrate cats.

To examine whether the cerebrum is essential for producing the rapid cardiovascular adjustment at the beginning of overground locomotion, we examined heart rate (HR), mean arterial blood pressure (MAP), and integrated electromyogram (iEMG) of the forelimb triceps brachialis muscle in freely moving decerebrate cats during locomotion. Two to four days after decerebration surgery performed at the level of the precollicular-premammillary body, the animals spontaneously produced coordinated overground locomotion, supporting body weight. HR began to increase immediately before the onset of iEMG, and MAP began to rise almost simultaneously with the iEMG onset. Their increases in HR and MAP (24 +/- 3 beats/min and 22 +/- 4 mmHg) were sustained during locomotion. Sinoaortic denervation (SAD) did not affect the abrupt changes in HR and MAP at the beginning of locomotion (0-4 s from the onset of iEMG), whereas SAD had a contrasting effect during the subsequent period, a decrease in the HR response (9 +/- 1 beats/min) and an increase in the MAP response (30 +/- 3 mmHg). These results suggest that the cerebrum and the rostral part of the diencephalon are not essential for producing the rapid cardiovascular adjustment at the beginning of spontaneous overground locomotion. The arterial baroreflex does not contribute to this rapid adjustment but plays an important role in regulating the cardiovascular responses during the later period of spontaneous locomotion.

Animals↗
PubMed1996

Tissue distribution of human gliostatin/platelet-derived endothelial cell growth factor (PD-ECGF) and its drug-induced expression.

Human tissue contents of gliostatin/platelet-derived endothelial cell growth factor (PD-ECGF) and its drug-induced expression in tumor cells were currently examined by a sandwich enzyme immunoassay (EIA) system and a reverse transcription-polymerase chain reaction (RT-PCR) method. Gliostatin/PD-ECGF was found to distribute in rather ubiquitous than specific human tissues and organs, with a relatively high levels in the tissues of digestive system (esophagus and rectum), brain, spleen, bladder and lung, but not in gall bladder, aorta, muscle, fat and kidney. Most of examined human tumor cell lines showed 4- or 5-fold higher contents (21.5 +/- 3.9 ng/mg protein) than normal tissue contents (4.4 +/- 1.1 ng/mg protein) on the average. While gliostatin/PD-ECGF is known to lack a signal sequence, some tumor cells (A431 and MKN74) appeared to release it into the conditioned medium. Expression of gliostatin/PD-ECGF in epidermoid carcinoma cell (A431) and stomach cancer cell (MKN45) was induced by dibutyryl cyclic AMP and phorbol ester, and uniquely in MKN45 by hydrocortisone. In particular, this hydrocortisone specifically caused an increase of the apparent secretion of MKN74 without its cytotoxic effects, suggesting a possible secretion of gliostatin/PD-ECGF in the restricted but not universal cell line. Biological significance on the chemical induction of gliostatin/PD-ECGF in tumor cells and on its extracellular secretion are discussed.

Cell Line↗
PubMed1996

Divergence of ventilatory responses to isometric contraction in anesthetized cats.

The purpose of this study was to determine if the initial ventilatory and phrenic nerve responses to isometric contraction of the triceps surae muscle of anesthetized cats are influenced by the pattern of the contraction. To address this, three different types of muscle contraction were evoked: (1) a high tension, continuous tetanic (HT-CT) contraction; (2) a moderate tension, continuous tetanic (MT-CT) contraction; and (3) high tension, intermittent tetanic (HT-IT) contractions. The duration of each contraction period was 60 sec. The MT-CT and HT-IT contractions increased minute volume (VE; 19 +/- 4% and 15 +/- 5%, respectively) within the first 15 sec. These increases were the result of rises in breathing frequency and tidal volume. However, only the MT-CT contraction increased phrenic activity (pVE) in the first 15 sec. By contrast, ventilation and phrenic nerve activity failed to increase within the first 15 sec of the HT-CT contraction. If fact, 'tidal' phrenic activity (pVT; -14 +/- 5%) decreased during the first 5 sec, and there was a tendency for tidal volume (VT; -8 +/- 5%), VE (-8 +/- 6%), and pVE (-16 +/- 8%) to fall. These data suggest that stimulation of muscle afferent fibers by static contraction can initially inhibit phrenic nerve activity, provided the activation is sustained and of sufficient intensity.

Anesthesia, General↗
PubMed1995

Differential effects of clonidine on renal sympathetic nerve activity and heart rate at onset of static exercise.

The effects of the alpha 2-adrenergic agonist clonidine on the increase in renal sympathetic nerve activity (RSNA) and heart rate (HR) at the onset of voluntary static exercise were studied using conscious cats. Five cats were trained to press a bar with one forelimb. A total of 60 exercise trials were performed before and after injection of clonidine (5-10 micrograms/kg i.v.). Before clonidine, RSNA and HR increased immediately before or at the onset of exercise, which was followed by a rise in arterial blood pressure (AP). The initial increases in RSNA and HR are likely to be caused by descending input from higher brain centers. After clonidine, baseline RSNA was decreased to 21 +/- 5% of the control before clonidine, probably due to a central action of clonidine. HR and AP were decreased from 221 +/- 4 to 178 +/- 5 bpm and from 108 +/- 2 to 82 +/- 4 mmHg, respectively. The increase in RSNA at the onset of exercise and the rise in AP during exercise were blunted to 56-57% of the responses before clonidine injection. In contrast, the increase in HR at the onset of exercise was not altered by clonidine. Thus, it is suggested that clonidine, administered intravenously, attenuates the centrally-induced increase in RSNA at the onset of static exercise but does not affect the increase in HR.

Adrenergic Fibers↗
PubMed1995

Effects of baroreceptor reflex on efferent pulmonary sympathetic nerve activity in anesthetized cat.

We analyzed the baroceptor reflex effect on efferent pulmonary sympathetic nerve activity (PSNA) in anesthetized cats. PSNA was recorded from the central end of the cut nerve bundle, which was isolated from the lobar artery supplying the diaphragmatic lobe. Renal sympathetic nerve activity (RSNA) and aortic blood pressure (AP) were also simultaneously measured. There were grouped discharges synchronous with cardiac cycle and its respiratory modulation in PSNA. In a given cardiac cycle, the discharge patterns differed between the pulmonary and renal nerves. Average sympathetic nerve activity and AP obtained from 100 consecutive cardiac cycles showed that the baroreceptor reflex delay time on the pulmonary nerve (266 ms) was longer than that on the renal nerve (195 ms). The data indicate nonuniformity in the cardiac-related PSNA and RSNA. The grouped PSNA disappeared with hexamethonium bromide, indicating that PSNA originates from postganglionic efferent fibers. To examine the baroreflex response of PSNA, AP was increased by 70 mmHg with phenylephrine and decreased by 70 mmHg with nitroprusside. PSNA changed inversely to the changes in mean aortic pressure (MAP). In the delta MAP-delta PSNA curve, delta PSNA reached the maximum level (74%) and the noise level at -56 +/- 4 and 58 +/- 4 mmHg, respectively. The mean slope of the curve was 1.5 +/- 0.1%/mmHg. RSNA also responded inversely to the MAP change.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1995

Changes in efferent pulmonary sympathetic nerve activity during systemic hypoxia in anesthetized cats.

Changes in efferent sympathetic nerve activity to the pulmonary vessels during systemic hypoxia have yet to be elucidated. The purpose of this study was to determine the pulmonary sympathetic nerve activity (PSNA) changes in response to acute systemic hypoxia before and after sinoaortic denervation plus vagotomy in anesthetized cats. The denervation was performed to estimate the central nervous system-mediated peripheral chemoreceptor- and baroreceptor-independent PSNA change. PSNA was recorded from the central end of the cut nerve bundle, which was isolated from the lobar artery supplying the diaphragmatic lobe. Renal sympathetic nerve activity (RSNA) and systemic and pulmonary arterial pressures were also measured simultaneously. The animals were submitted to approximately 3-min periods of graded hypoxia (16, 12, 8, 5, and 3% O2 inhalations). PSNA did not change from normoxia down to an arterial O2 partial pressure (PaO2) of approximately 45 Torr (with 12-21% O2 inhalations). Below this level, PSNA began to increase, and markedly so (approximately 2.5-fold) at a PaO2 of approximately 15 Torr (with 3% O2). The hypoxic PSNA increase was significantly larger than that for RSNA, with a PaO2 of less than approximately 30 Torr (with 3-8% O2). Particularly at a PaO2 of approximately 15 Torr, the magnitude of the PSNA increase was two times greater than that for RSNA. After denervation, the hypoxic PSNA increase was significantly attenuated at a PaO2 of approximately 25 to approximately 45 Torr (with 5-12% O2), but the attenuation was very small; therefore most of the PSNA increase persisted. The hypoxic RSNA increase, in contrast, was mostly abolished after denervation. The data indicate that the neural reflex effect of systemic hypoxia on PSNA is significantly greater than that on RSNA and suggest that the hypoxic PSNA increase is mostly mediated by central mechanisms, whereas that for RSNA is chiefly caused by peripheral chemoreceptors.

Animals↗
PubMed1995

Spontaneous diabetes mellitus associated with persistent bovine viral diarrhea (BVD) virus infection in young cattle.

Histologic and immunohistochemical studies were carried out on four young cattle with diabetes mellitus associated with persistent bovine viral diarrhea (BVD) virus infection. Clinical findings included persistent hyperglycemia, decreased glucose tolerance, glycosuria, polydipsia, and severe emaciation. Macroscopically, multiple erosions and ulcers in the mucosa of upper and lower alimentary tracts and swollen lymph nodes were commonly observed. Erosions and ulcers in the mucosa of tongue, esophagus, and forestomach were represented histologically by necrosis of squamous epithelium with neutrophilic infiltration. In the small and large intestines, villous atrophy and suppurative cryptitis were often observed, along with diffuse infiltration of lymphocytes and macrophages and fibroplasia in the lamina propria. In the pancreas of all cattle, there was a reduction in the number of islet cells, and most of the residual islet cells had hydropic degeneration and a decreased number of secretory granules. Immunohistochemical examination confirmed that these cells were severely degranulated beta-cells. In addition, many islets containing necrotic islet cells were observed. These islet cells had increased eosinophilia and shrinkage of cytoplasm, as well as pyknotic nuclei. Inflammation of the islets with mild infiltration of lymphocytes was observed in all pancreatic lobes. In addition, bovine IgG-immunoreactive cells were identified immunohistochemically in the affected pancreatic islets. The BVD virus antigen was not identified in the cytoplasm of the islet cells by immunohistochemical study, although it was identified in the epithelial cells of the small intestine. The histologic and immunohistochemical studies demonstrated that the pancreatic lesions in these animals were similar to those caused by acute insulin-dependent diabetes mellitus (IDDM) in human beings.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1995

Attenuation of the reflex responses to muscle contraction by the coadministration of antagonists to substance P and somatostatin into the dorsal horn.

OBJECTIVE: The aim was to determine if the coadministration of antagonists to substance P and somatostatin into the L7 dorsal horn blunts the reflex cardiovascular responses to static contraction to a greater extent than each antagonist alone. The possibility that this attenuation is mediated by blunting the contraction evoked increases in sympathetic outflow was also tested. METHODS: Using alpha chloralose anaesthetised cats (n = 8), static contraction and stretch of the triceps surae muscle were performed before and after microinjecting (1 microliter) 250 ng of the substance P antagonist, D-Pro2-D-Phe7-D-Trp9-substance P, and the somatostatin antagonist, cyclo(7-amino-heptanoyl-phenylalanyl-D-tryptophyl-lysyl-threonyl-[ benzyl]). The muscle was contracted by electrically stimulating the peripheral end of the cut L7 ventral root. RESULTS: Before injecting the antagonists, static muscle contraction increased mean arterial blood pressure by 40(SEM 6) mm Hg, heart rate by 13(2) beats.min-1, and renal sympathetic nerve activity (RSNA) by 41(7)%. These changes were blunted by the antagonists since the increases in blood pressure, heart rate, and RSNA were reduced to 21(3) mm Hg, 8(1) beats.min-1, and 23(5)%, respectively. In contrast, antagonist administration did not affect the pressor [33(5) v 31(5) mm Hg], heart rate [9(2) v 10(2) beats.min-1], or RSNA [23(4)% v 25(5)%] responses to muscle stretch. Microinjection of 2% lignocaine into the dorsal horn virtually abolished the reflex changes elicited by muscle stretch. CONCLUSIONS: The release of substance P and somatostatin in the spinal cord plays a role in mediating the cardiovascular changes caused by static contraction, but the release of other neurotransmitters/neuromodulators is also involved. The attenuation produced by these antagonists is mediated, at least in part, by reducing sympathetic outflow.

Animals↗
PubMed1994

Aberrant production of gliostatin/platelet-derived endothelial cell growth factor in rheumatoid synovium.

OBJECTIVE: To purify a protein inhibitor from rheumatoid arthritis (RA) synovial fluids which suppresses the apparent incorporation of 3H-thymidine into fibroblasts and synovial cells, and to define its biochemical features that have clinical relevance to the pathogenesis of RA. METHODS: Several standard chromatographic techniques were employed for the purification of the protein. Immunochemical methods with monoclonal antibody were used to quantify and visualize the protein in sera, synovial fluids, and tissues from RA patients. RESULTS: The chemical properties of purified inhibitor from RA synovial fluids confirmed its identity as gliostatin/platelet-derived endothelial cell growth factor (PD-ECGF), a potent angiogenic factor. The gliostatin/PD-ECGF level in synovial fluid and serum was higher in RA patients than in osteoarthritis controls. CONCLUSION: These findings strongly suggest that gliostatin/PD-ECGF might play an important role in the aberrant neovascularization of rheumatoid synovium.

3T3 Cells↗
PubMed1994

Origin of cardiac-related synchronized cardiac sympathetic nerve activity in anaesthetized cats.

To study the origin of cardiac-related rhythm in cardiac sympathetic nerve activity (CSNA), ECG, aortic pressure and CSNA were recorded when cardiac interval was changed by artificial pacing, or when the aortic nerve was stimulated after baroreceptor denervation in anaesthetized cats. CSNA was averaged by using the R-wave of ECG, or stimulus pulse as a trigger. Delay times from arterial pulse or stimulus pulse to the onset and half amplitude of inhibition and to the maximal inhibition were measured from the averaged data. The delay of inhibition in CSNA was constant and independent of pacing interval. Stimulation of the aortic nerve with single shocks caused an inhibition in averaged CSNA. The delay of inhibition was constant and independent of stimulus frequency. These results indicate that the cardiac-related rhythm in CSNA is produced reflexly by inhibiting the transmission of the fundamental rhythmicity due to periodic baroreceptor input.

Anesthesia↗