Biomedical subjects

H N Sapru

Publications and source records attributed to H N Sapru.

At least 37 records · Page 2Linked to original sources

PubMed1995

Chemical stimulation of the nucleus tractus solitarii decreases spinal cord blood flow in anesthetized rats.

L-Glutamate was microinjected into the nucleus tractus solitarii (NTS) in anesthetized (chloralose and urethane), paralyzed and artificially ventilated rats, and spinal cord blood flow (SCBF) was determined using a combination of labeled microspheres. Unilateral chemical stimulation of the NTS (n = 13) significantly decreased SCBF in the cervical cord from 43 +/- 6 (mean +/- SEM) to 28 +/- 4 (P < 0.05), in the thoracic cord from 35 +/- 3 to 24 +/- 4 (P < 0.01), and in the lumbar cord from 49 +/- 3 to 40 +/- 3 ml min-1 (100 g)-1 (P < 0.05). The decrease in SCBF was not due to the decrease in arterial blood pressure (ABP) because the SCBF during the chemical stimulation of the NTS was significantly smaller (P < 0.05) than the SCBF during controlled hemorrhagic hypotension (n = 11). Chemical stimulation of the NTS did not affect the reactivity of the spinal cord vessels to hypercapnia (n = 5). Microinjection of the vehicle solution into the NTS had no effects on spinal cord circulation (n = 9). These results suggest that the cell bodies within the NTS may play a role in the control of spinal cord circulation.

Animals↗

PubMed1995

Chemoreceptor-sensitive neurons in commissural subnucleus of nucleus tractus solitarius of the rat.

Experiments were carried out in pentobarbital-anesthetized, vagotomized, paralyzed, and artificially ventilated male Wistar rats with a pneumothorax. Blood pressure, heart rate, and phrenic nerve activity were recorded. Extracellular neuronal recordings were made by glass micropipettes in a midline area in the commissural subnucleus of the nucleus tractus solitarius. At the end of the experiment, the recording sites were marked. Chemoreceptors were stimulated by tracheal administration of N2 or injection of CO2-saturated saline (50 microliters) near the carotid body. The baroreceptors were stimulated by an intravenous injection of phenylephrine (1-3 micrograms). Neurons that were excited by chemoreceptor stimulation but not baroreceptor stimulation were found in the commissural subnucleus of nucleus tractus solitarius and were designated as chemoreceptor-sensitive neurons. They exhibited a continuous discharge (9.9 +/- 1.3 spikes/s) that showed no apparent relation to either phrenic nerve bursts or arterial pulses. Such neurons were not found in the rostral portions of the nucleus tractus solitarius. These results confirm and extend our previous reports in which a discrete chemoreceptor projection site was identified in the commissural subnucleus of the rat.

Animals↗

PubMed1994

A midline area in the nucleus commissuralis of NTS mediates the phrenic nerve responses to carotid chemoreceptor stimulation.

The carotid body chemoreceptor afferents have been reported to project to a discrete area located in the nucleus commissuralis of nucleus tractus solitarius [A. Vardhan et al., Am. J. Physiol., 264 (1993) R41-R50]. The afore-mentioned study was done in spontaneously breathing rats and the afferents and efferents located in the chest wall and the respiratory tract of these animals were intact. In order to exclude the role, if any, of these afferents and efferents, in the present experiments respiratory changes were monitored by recording the phrenic nerve activity instead of tracheal airflow. Experiments were carried out in pentobarbital-anesthetized, bilaterally vagotomized, paralyzed and artificially ventilated rats with a pneumothorax. The carotid body chemoreceptors were stimulated with tracheal administration of nitrogen for 7-10 s. The chemoreceptor stimulation induced an increase in the frequency and amplitude of phrenic nerve bursts. A decrease in the duration of inspiratory (T1), expiratory (TE) and total cycles (TTOT) was observed in the phrenic nerve activity. Inhibition of neuronal cell bodies by microinjections of muscimol (140 pmol/20 nl) into a discrete area in the commissural subnucleus of the nucleus tractus solitarius (coordinates in mm: 0.3 rostral to 0.5 caudal, 0 to 0.5 lateral and 0.3 to 0.5 deep with respect to the calamus scriptorius), attenuated the phrenic nerve responses to the carotid body stimulation. On the other hand, control injections of saline (0.9%) into this site did not alter the phrenic nerve response to the carotid body stimulation.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1994

Medullary cardiovascular center and acute brain swelling.

Acute brain swelling is reported to be due to acute vasodilatation of cerebral vessels. One of the causes of acute brain swelling may be disturbance of central control mechanisms of cerebral vessels. It has been reported that the anatomical location of the area which controls cerebral circulation is related to the area which controls systemic circulation. However, the role of the cardiovascular center on cerebral circulation has not been clear. The present study was, therefore, undertaken to examine the effects of chemical stimulation of the medullary cardiovascular center [nucleus tractus solitarius (NTS), ventrolateral depressor area (VLDA), and ventrolateral pressor area (VLPA)] on cerebral circulation. In anesthetized, paralyzed and artificially ventilated rats, the neurons in the NTS, VLDA, and VLPA were chemically stimulated and the cerebral blood flow (CBF) was determined using labeled microspheres. The CBF decreased significantly and the cerebrovascular resistance (CVR) increased significantly by chemical stimulation of the NTS, VLDA, and VLPA. These results suggest that the neurons within the NTS, VLDA, and VLPA control cerebral vessels vasoconstrictively. There is a possibility that the dysfunction of the NTS, VLDA, and VLPA may cause acute brain swelling.

Animals↗

PubMed1994

Dysfunction of the medullary cardiovascular center may cause acute spinal cord swelling.

Acute brain swelling is well known to be acute vasodilatation of cerebral vessels and sometimes results from brain injury. One of the causes of acute brain swelling may be disturbance of central control mechanisms of cerebral vessels. However, the presence of acute spinal cord swelling is little noticed. We present here a possibility that acute spinal cord swelling may be occur following the dysfunction of the cardiovascular center of the medulla. In urethane-anesthetized, paralyzed and artificially ventilated rats, the neurons in the rostral ventrolateral pressor area (VLPA), origin of the sympathetic nerve activities in the brain stem, were chemically stimulated by microinjection of L-glutamate and the spinal cord blood flow (SCBF) was determined using labeled microspheres. The SCBFs of cervical, thoracic, and lumbar cord decreased significantly from 27 +/- 3 (mean +/- S.E.M.) to 20 +/- 2 (p < 0.01), from 22 +/- 1 to 17 +/- 2 (p < 0.05), and from 41 +/- 5 to 26 +/- 3 (p < 0.05) ml.min-1.(100 g)-1, respectively (n = 12). The spinal cord vascular resistances (SCVRs) of cervical, thoracic, and lumbar cord increased significantly from 3.7 +/- 0.4 to 5.0 +/- 0.6 (p < 0.05), from 4.2 +/- 0.2 to 5.9 +/- 0.7 (p < 0.05), and from 2.5 +/- 0.2 to 3.8 +/- 0.4 (p < 0.05) mmHg per [ml.min-1.(100 g)-1], respectively (n = 12). These results suggest that the neurons within the VLPA may play a role in the control of spinal cord circulation. There is a possibility that the dysfunction of the VLPA may cause acute spinal cord swelling.

Animals↗

PubMed1994

Caudal ventrolateral medullary depressor area controls cerebral circulation via rostral ventrolateral medullary pressor area.

The cerebral blood flow (CBF) was determined by radiolabeled microsphere technique in urethane (1.1-1.5 g.kg-1, i.p.) anesthetized Wistar rats. Microinjection of L-glutamate (1.7 nmol) into the ventrolateral medullary depressor area (VLDA) produced a significant (P < 0.01) decrease in CBF from 64 +/- 9 (mean +/- S.E.M.) to 48 +/- 9 ml.min-1.(100g)-1 and a significant (P < 0.01) increase in cerebrovascular resistance (CVR) from 1.7 +/- 0.2 to 2.4 +/- 0.4 mmHg per [ml.min-1.(100g)-1] in the cerebral cortex ipsilateral to the stimulated VLDA side but not in other structures such as brain stem and cerebellum (n = 9). Cervical sympathectomy blocked the decrease in CBF and increase in CVR elicited by chemical stimulation of the VLDA (n = 10). Depression of the ventrolateral medullary pressor area (VLPA) neurons induced by microinjection of muscimol into the VLPA blocked the CBF decrease and CVR increase following chemical stimulation of the VLDA (n = 11). Microinjection of the vehicle solution into the VLDA had no effects on systemic and cerebral circulation (n = 7). These results suggest that a vasoconstrictor pathway to control cerebral vessels involves an excitatory projection from the VLDA to the VLPA and the changes in cerebral circulation are mediated by the cervical sympathetic nerves.

Animals↗

PubMed1994

Cerebral vasoconstrictive response produced by chemical stimulation of the caudal ventrolateral medullary depressor area is mediated via the rostral ventrolateral medullary pressor area and the cervical sympathetic nerves.

It was investigated that the cerebral blood flow (CBF) decrease response elicited by chemical stimulation of the caudal ventrolateral medullary depressor area (VLDA) is mediated via the rostral ventrolateral medullary pressor area (VLPA) and the cervical sympathetic nerve. The CBF was determined by radiolabeled microsphere technique in urethane (1.1-1.5 g.kg-1, i.p.) anesthetized Wistar rats. (i) Microinjection of L-glutamate (1.7 nmol) into the VLDA produced a significant (P < 0.01) decrease in CBF from 64 +/- 9 (mean +/- SEM) to 48 +/- 9 ml.min-1.(100 g)-1 and a significant (P < 0.01) increase in cerebrovascular resistance (CVR) from 1.7 +/- 0.2 to 2.4 +/- 0.4 mmHg per [ml.min-1.(100 g)-1] in the cerebral cortex ipsilateral to the stimulated VLDA side (n = 9). (ii) After cervical sympathectomy, L-glutamate was unilaterally microinjected into the VLDA. The CBF and CVR did not change significantly (n = 10). (iii) After depression of the VLPA neurons with muscimol (GABA agonist), L-glutamate was unilaterally microinjected into the VLDA. The CBF and CVR did not change significantly (n = 14). These results suggest that the pathway from the VLDA to control cerebral vessels may be mediated via the VLPA and the cervical sympathetic nerves.

Animals↗

PubMed1994

Effects of microinjection of N-methyl-D-aspartic acid into the nucleus tractus solitarii on cerebral blood flow in anesthetized rats.

N-Methyl-D-aspartic acid (NMDA) (10 pmol in 100 nl of 0.9% sodium chloride solution) was microinjected into the nucleus tractus solitarii (NTS) of urethane-anesthetized, paralyzed and artificially ventilated rats, and cerebral blood flow (CBF) was determined using a combination of labeled microspheres. Moderate hypertension within the upper limit of cerebral autoregulation was induced by blood transfusion in order to measure CBF at normotension. Arterial blood pressure (ABP) was decreased by unilateral microinjection into the NTS in these rats but remained within normotensive range. The CBF in the cerebral cortex ipsilateral to the stimulated NTS significantly (P < 0.01) decreased from 38 +/- 4 (mean +/- S.E.M) to 27 +/- 4 ml.min-1.(100 g)-1(n = 9). The cerebrovascular resistance (CVR) in the cerebral cortex ipsilateral to the stimulated NTS significantly (P < 0.01) increased from 2.6 +/- 0.3 to 4.1 +/- 0.7 mmHg per [ml.min-1.(100 g)-1]. Blockade of NMDA receptors in the NTS with D,L-2-amino-5-phosphonovalerate (AP5, 500 pmol) abolished the CBF decrease and CVR increase responses elicited by microinjection of NMDA into the NTS (n = 9). Blockade of non-NMDA receptors in the NTS with 6,7-dinitro-quinoxaline-2,3-dione (DNQX, 100 pmol) had little effect on the CBF decrease and CVR increase responses elicited by microinjection of NMDA into the NTS (n = 10). Microinjection of the vehicle solution into the NTS had no effects on cerebral circulation (n = 7). Cerebral autoregulation was well maintained at moderate hypertension induced by blood transfusion and at normotension returned from moderate hypertension following controlled hemorrhage (n = 8). These results suggest that the NMDA receptors in the NTS may be involved in the control of cerebral circulation.

2-Amino-5-phosphonovalerate↗

PubMed1993

Role of alpha 1-adrenergic receptors in the intermediolateral column in mediating the pressor responses elicited by the stimulation of ventrolateral medullary pressor area.

Microinjections of alpha 1-adrenergic receptor agonists into the intermediolateral cell column of the spinal cord (IML) elicit sympathoexcitatory responses. This observation, together with the identification of projections of epinephrine-containing cells in the rostral ventrolateral medullary pressor area (VLPA) to the IML, has prompted speculation that epinephrine may mediate pressor responses to the stimulation of the VLPA. This hypothesis was tested in pentobarbital-anesthetized, artificially ventilated, male Wistar rats. A mesenteric arterial branch was cannulated for monitoring blood pressure. Pressor responses were elicited predominantly from T8-T10 by injections (1.7 nmol/20 nl) of L-glutamate into the IML; maximum pressor responses (29.3 +/- 4 mmHg) were elicited from T9. Pressor responses were also elicited by injections of epinephrine into the IML at T9; maximum pressor effect (16.3 +/- 1.2 mmHg) was elicited by a dose of 0.05 pmol/20 nl. This effect of epinephrine at T9 was blocked by prior injections of prazosin (a selective alpha 1-adrenergic receptor blocker; 0.125 pmol/20 nl) at the same site. Stimulation of the VLPA by unilateral microinjections of glutamate elicited pressor responses (56 +/- 12 mmHg). Bilateral injections of prazosin at T8-T10, in the dose (0.125 pmol) that blocked a maximally effective dose of epinephrine, did not block the pressor responses to subsequent injections of glutamate into the VLPA. On the other hand, bilateral microinjections of AP-7 (an NMDA receptor blocker; 1 nmol/20 nl), but not DNQX (10 pmol; a non-NMDA receptor blocker), into the IML at T8-T10 blocked the pressor effects of the subsequent injections of glutamate into the VLPA.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenal Glands↗

PubMed1993

Excitatory amino acid receptors in the nucleus tractus solitarius mediate the responses to the stimulation of cardio-pulmonary vagal afferent C fiber endings.

Stimulation of cardio-pulmonary vagal afferent C fiber endings by right atrial injections of phenylbiguanide (PBG, 40 micrograms/kg) elicited apnea, bradycardia and hypotension. These responses were abolished by bilateral vagotomy low in the neck. Stimulation of neurons in a specific nucleus tractus solitarius site (0.5 mm rostral, 0.5 mm lateral and 0.5 mm deep with reference to the calamus scriptorius) by injections of L-glutamate produced responses similar to those following the stimulation of cardio-pulmonary vagal afferent C fiber endings by PBG. Inhibition of neurons in this NTS site by injections of muscimol abolished the responses to PBG. Specific blockade of NMDA receptors by microinjections of AP-7 (100 pmol) or non-NMDA receptors (KA and AMPA) by injections of DNQX (10-25 pmol) into this NTS site did not block the responses to PBG. Microinjections of kynurenic acid (1-4 nmol) into this NTS site blocked the responses to right atrial injections of PBG. These results indicate that: (1) blockade of either NMDA receptors or non-NMDA receptors (KA and AMPA) alone in the above-mentioned NTS site does not abolish the responses to the stimulation of cardio-pulmonary vagal afferent C fiber endings; (2) it is necessary to block NMDA as well as non-NMDA receptors in this NTS site for abolishing the responses to the stimulation of these nerve endings.

Afferent Pathways↗

PubMed1993

Cardiac effects of injections of epinephrine into the spinal intermediolateral column.

Small doses of epinephrine (0.008, 0.05, and 0.1 pmol, i.e., 20-nl volumes of 0.40, 2.5, and 5 microM solutions) produced a dose-dependent increase in heart rate when micro-injected into the right intermediolateral column (IML) at T2 spinal level. These effects were mediated via alpha 1-adrenergic receptors because prazosin blocked them. The presence of alpha 1-adrenergic receptors at this site was confirmed by microinjections of phenylephrine (a specific agonist for these receptors); phenylephrine elicited tachycardia. Larger doses of epinephrine (320, 2,000, and 3,200 pmol, i.e., 20-nl volumes of 16, 100, and 160 mM solutions) caused bradycardia when microinjected into the IML. These effects were mediated via alpha 2-adrenergic receptors because idazoxan blocked them. The presence of alpha 2-adrenergic receptors at this site was confirmed by microinjections of clonidine (a specific agonist for these receptors); clonidine elicited bradycardia. Injections of the vehicle (20 nl of normal saline containing 0.3% ascorbic acid, pH 7.4) did not evoke a response. Epinephrine, prazosin, or idazoxan did not alter the responses to L-glutamate. None of the doses of epinephrine elicited any response when injected intravenously. The aforementioned results provide pharmacological evidence for the presence of alpha 1- and alpha 2-adrenergic receptors in the IML at T2. Thus a basis is provided for investigating the role, if any, of alpha-adrenergic receptors in the IML in mediating cardiovascular responses elicited by the stimulation of different brain stem areas.

Animals↗

PubMed1993

Excitatory amino acid receptors in commissural nucleus of the NTS mediate carotid chemoreceptor responses.

Stimulation of carotid body chemoreceptors by saline saturated with 100% CO2 elicited an increase in mean arterial pressure, respiratory rate, tidal volume, and minute ventilation (VE). Microinjections of L-glutamate into a midline area 0.5-0.75 mm caudal and 0.3-0.5 mm deep with respect to the calamus scriptorius increased VE. Histological examination showed that the site was located in the commissural nucleus of the nucleus tractus solitarii (NTS). The presence of excitatory amino acid receptors [N-methyl-D-aspartic acid (NMDA); kainate, quisqualate/alpha-amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid (AMPA) and trans 1-amino-cyclopentane-trans-1,3-dicarboxylic acid (ACPD)] in this area was demonstrated by microinjections of appropriate agonists. Simultaneous blockade of NMDA and non-NMDA receptors by combined injections of DL-2-aminophosphonoheptanoate (AP-7; 1 nmol) and 6,7-dinitro-quinoxaline-2,3-dione (DNQX; 1 nmol) abolished the responses to stimulation of carotid body on either side. Combined injections of AP-7 and DNQX did not produce a nonspecific depression of neurons because the responses to another agonist, carbachol, remained unaltered. Inhibition of the neurons in the aforementioned area with microinjections of muscimol (which hyperpolarizes neuronal cell bodies but not fibers of passage) also abolished the responses to subsequent carotid body stimulation on either side.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1993

Cardiovascular responses to global cerebral ischemia: role of excitatory amino acids in the ventrolateral medullary pressor area.

The object of this study was to investigate the role of the ventrolateral medullary pressor area in mediating the cardiovascular responses to experimentally induced global cerebral ischemia, and to test if excitatory amino acids or acetylcholine are the transmitters released in this brain region during these responses. The cerebral ischemic response was elicited in pentobarbital-anesthetized, artificially ventilated male Wistar rats by bilateral ligation of vertebral arteries followed by temporary clamping of the common carotid arteries. The pressor area was identified by microinjections of L-glutamate. Inhibition of neurons in this area by microinjections of muscimol, a gamma-aminobutyric acid receptor agonist, abolished the ischemic response, which demonstrated that this area is important in mediating these responses. Microinjections of a broad-spectrum excitatory amino acid receptor blocker (kynurenate), of specific antagonists for N-methyl-D-aspartic acid (NMDA) and non-NMDA receptors (injected alone or in combination), and of atropine failed to block the ischemic responses. These results indicate that: 1) the ventrolateral medullary pressor area mediates pressor responses to cerebral ischemia, and 2) excitatory amino acids or acetylcholine in this area do not mediate the cardiovascular responses to cerebral ischemia.

Acetylcholine↗

PubMed1992

Spinal cord blood flow decreases following chemical stimulation of the rostral ventrolateral medullary pressor area in anesthetized rats.

In urethane-anesthetized, paralyzed and artificially ventilated rats, the neurons in the rostral ventrolateral medullary pressore area (VLPA) were chemically stimulated by microinjections of L-glutamate (1.7-5.0 nmol in 100 nl of 0.9% sodium chloride solution) and the spinal cord blood flow (SCBF) was determined using a combination of labeled microspheres (57Co, 113Sn and 46Sc). In order to measure SCBF at normotension, moderate hypotension within the lower limit of spinal cord autoregulation was induced by controlled hemorrhage (n = 12). Unilateral chemical stimulation of the VLPA in these rats increased arterial blood pressure (ABP) but it remained within normotensive range. The SCBFs of cervical, thoracic and lumbar cord decreased significantly from 27 +/- 3 (mean +/- S.E.M.) to 20 +/- 2 (P less than 0.01), from 22 +/- 1 to 17 +/- 2 (P less than 0.05), and from 41 +/- 5 to 26 +/- 3 (P less than 0.05) ml.min-1.(100 g)-1, respectively. The spinal cord vascular resistances (SCVRs) of cervical, thoracic and lumbar cord increased significantly from 3.7 +/- 0.4 to 5.0 +/- 0.6 (P less than 0.05), from 4.2 +/- 0.2 to 5.9 +/- 0.7 (P less than 0.05), and from 2.5 +/- 0.2 to 3.8 +/- 0.4 (P less than 0.05) mmHg per [ml.min-1.(100 g)-1], respectively. During the chemical stimulation of the VLPA, SCBF increased in response to the changes in arterial PaCO2 indicating that the reactivity of spinal cord vasculature was intact (n = 5).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1991

Chemical stimulation of the rostral ventrolateral medullary pressor area decreases cerebral blood flow in anesthetized rats.

In urethane-anesthetized, paralyzed and artificially ventilated rats, the neurons in the rostral ventrolateral medullary pressor area (VLPA) were chemically stimulated by microinjections of L-glutamate (1.7-5.0 nmole in 100 nl of 0.9% sodium chloride solution) and the cerebral blood flow (CBF) was determined using a combination of labeled microspheres (57Co, 113Sn and 46Sc). In one group of rats (n = 11), unilateral chemical stimulation of the VLPA produced a significant (P less than 0.01) increase in arterial blood pressure (ABP), a significant (P less than 0.05) decrease in CBF, and a significant (P less than 0.01) increase in cerebrovascular resistance (CVR) in the cerebral cortex ipsilateral to the stimulated VLPA. The CBF was 52 +/- 3 (mean +/- S.E.M.) and 48 +/- 4 ml.min-1.(100 g)-1 before and during the chemical stimulation of VLPA; the CVR was 1.9 +/- 0.1 and 2.6 +/- 0.3 mmHg per ml.min-1.(100 g)-1 before and during the stimulation. In order to measure CBF at normotension, moderate hypotension was induced by controlled hemorrhage in another group of rats (n = 8). Unilateral chemical stimulation of the VLPA in these rats increased ABP but it remained within normotensive range. The CBFs of ipsilateral and contralateral cerebral cortices decreased significantly (P less than 0.05) from 57 +/- 14 to 41 +/- 9 and from 50 +/- 12 to 39 +/- 9 ml.min-1.(100 g)-1, respectively. The CVRs of ipsilateral and contralateral cortices increased significantly (P less than 0.05) from 2.6 +/- 0.6 to 3.5 +/- 0.8 and from 2.7 +/- 0.5 to 3.5 +/- 0.8 mmHg/[ml.min-1.(100 g)-1], respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia↗

PubMed1991

Chemical stimulation of the ventrolateral medullary depressor area decreases ipsilateral cerebral blood flow in anesthetized rats.

In anesthetized (chloralose and urethane), paralyzed and artificially ventilated rats, the neurons in the ventrolateral medullary depressor area (VLDA) were chemically stimulated by microinjections of L-glutamate (2.5-5 nmole in 100 nl of 0.9% sodium chloride solution) and the cerebral blood flow (CBF) was determined using a combination of labeled microspheres (57Co, 113Sn and 46Sc). Unilateral chemical stimulation of the VLDA (n = 11) produced a significant (P less than 0.05) decrease in CBF of the cerebral cortex ipsilateral to the stimulated VLDA; the CBF was 41 +/- 5 (mean +/- S.E.M.) and 29 +/- 4 ml.min-1.(100 g)-1 before and during the chemical stimulation of VLDA. The decrease in CBF was not due to the decrease in arterial blood pressure (ABP) caused by the chemical stimulation of the VLDA because the CBF during the chemical stimulation of the VLDA was significantly smaller (P less than 0.01) than the CBF during controlled hemorrhagic hypotension (n = 10). In another group of rats (n = 6), moderate hypertension was induced by blood transfusion. Unilateral chemical stimulation of the VLDA in these rats decreased ABP but it remained within normotensive range. A significant (P less than 0.05) decrease in CBF (from 46 +/- 12 to 29 +/- 7 ml.min-1.(100 g)-1) and a significant (P less than 0.01) increase in cerebrovascular resistance (from 2.7 +/- 0.4 to 4.3 +/- 0.6 mmHg per [ml.min-1.(100 g)-1]) was observed in the ipsilateral cerebral cortex of these rats. Chemical stimulation of the VLDA did not affect the reactivity of the cerebral vessels to hypercapnea (n = 5).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1990

Chemical stimulation of the nucleus tractus solitarii decreases cerebral blood flow in anesthetized rats.

In anesthetized (chloralose and urethane), paralyzed and artificially ventilated rats, the neurons in the nucleus tractus solitarius (NTS) were chemically stimulated by microinjections of L-glutamate and the cerebral blood flow (CBF) was determined using a combination of labeled microspheres (either 57Co, 113Sn and 46Sc or 141Ce, 85Sr and 46Sc). Unilateral chemical stimulation of the NTS (n = 14) decreased CBF significantly in most brain areas. The decrease in CBF was not due to the decrease in arterial blood pressure (ABP) because the CBF of the whole cerebral cortex during the chemical stimulation of the NTS was significantly smaller (P less than 0.05) than the CBF during controlled hemorrhagic hypotension (n = 10). In another group of rats (n = 6), moderate hypertension was induced by blood transfusion. Unilateral chemical stimulation of the NTS in these rats decreased ABP but it remained within normotensive range. A significant (P less than 0.05) decrease in CBF (from 62 +/- 28 (mean +/- S.D.) to 48 +/- 23 ml.min-1.(100 g)-1) and increase in cerebrovascular resistance (from 1.9 +/- 1.2 to 2.6 +/- 1.2 mm Hg per [ml.min-1.(100 g)-1]) was observed in the whole cerebral cortex of these rats. Chemical stimulation of the NTS did not affect the reactivity of the cerebral vessels to hypercapnea (n = 5). These results suggest that the cell bodies within the NTS may play a role in the control of cerebral circulation.

Animals↗

PubMed1989

Cardiovascular effects of substance P receptor stimulation in the ventrolateral medullary pressor and depressor areas.

The pressor (VLPA) and the depressor (VLDA) areas in the ventrolateral medulla were identified with the microinjection of L-glutamate (1.77 nmol/site) in artificially ventilated urethane-anesthetized male Wistar rats. Bilateral microinjection of a stable substance P (SP) agonist [pGlu5, MePhe8, Sar9]-SP(5-11)], abbreviated as DiMe, into the VLPA (6-600 pmol/site) produced a dose-dependent increase in blood pressure (BP). The effects on heart rate (HR) were variable. Intravenous pretreatment with a ganglionic blocker chlorisondamine (3.0 mg/kg, i.v.), but not with a vasopressin antagonist, blocked these responses. Similar microinjection of DiMe (6-600 pmol/site) into the VLDA produced a dose-dependent decrease in HR but had no effect on BP levels. The DiMe-induced bradycardic response elicited from the VLDA was blocked by i.v. pretreatment with atropine methylbromide (0.5 mg/kg, i.v.). These findings indicate that there are SP receptors localized on sympathoexcitatory neurons in the VLPA and that SP may be an excitatory neurotransmitter in this area. In the VLDA, the SP receptors appear to be localized on a subpopulation of neurons that affect vagal, but not sympathetic, outflow to the heart.

Adrenergic Fibers↗