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H N Sapru

Publications and source records attributed to H N Sapru.

At least 55 records · Page 3Linked to original sources
PubMed1989

Cholinergic mechanisms subserving cardiovascular function in the medulla and spinal cord.

This investigation was designed to study the role of muscarinic receptor subtypes in the cardiovascular responses elicited by microinjection of cholinergic agonists in the intermediate portion of the NTS, the VLPA and VLDA areas and the IML of the spinal cord. Microinjections of L-glutamate (1.77 nmol in 20-50 nl in 0.9% sodium chloride solution) were used to identify these areas. Bilateral microinjections (0.02-2 nmol/site) of a potent M2 muscarinic receptor agonist, CD, but not those of a relatively selective M1 receptor agonist (McNA343; 3 nmol/site), into the intermediate portion of NTS and the VLDA induced depressor and bradycardic responses. In the VLPA these agonists elicited pressor and tachycardic effects while in the IML at T1-T3 only increase in HR was observed. Previous microinjections of a selective competitive M2 receptor antagonist (AFDX-116; 0.8-1.6 nmol/site), but not those of a potent selective M1 receptor antagonist (PZ; 1.5-2.0 nmol/site), into these areas blocked the effects of CD. These results indicate that the muscarinic receptors of M2 type may play a part in the regulation of cardiovascular function in the above-mentioned cardiovascular areas in a yet unidentified manner.

Animals↗
PubMed1988

Putative neurotransmitters involved in medullary cardiovascular regulation.

Experiments were carried out in artificially ventilated pentobarbital-anesthetized male Wistar rats. Following microinjection of muscimol (GABA-mimetic) or kynurenic acid (KYN; glutamate antagonist) into the ventrolateral medullary depressor area (VLDA), microinjection of L-glutamate (GLU; 4.5 nmol) into the NTS elicited a pressor response. This pressor response was attenuated in a dose-dependent manner by microinjection of KYN (0.5-5 nmol) into the ventrolateral medullary pressor area (VLPA). A GLU-induced pressor response could also be elicited from the NTS when GABA receptors in the VLPA were blocked with the microinjection of bicuculline (GABA antagonist, 200 pmol) into this site. The same dose of bicuculline in the VLPA also blocked the depressor responses elicited from the VLDA. With the VLDA or VLPA functionally unimpaired, microinjection of GLU (4.5 nmol) into the NTS elicited a fall in blood pressure and heart rate. This depressor response was attenuated in a dose-dependent manner by the microinjections of KYN (2-20 nmol) into the VLDA. These results indicate that: (1) The NTS sends glutamatergic inputs to both the VLDA and the VLPA; the projection from the NTS to the VLPA mediates pressor responses while that from the NTS to the VLDA represents one component of the pathway mediating the depressor responses elicited from the NTS. (2) The pathway from the VLDA to the VLPA is GABA-ergic and represents another component of the pathway mediating depressor responses evoked from the NTS. (3) The bradycardia evoked from the NTS may involve a pathway from the NTS to the VLDA.

Animals↗
PubMed1988

Evidence for a sympathoexcitatory pathway from the nucleus tractus solitarii to the ventrolateral medullary pressor area.

The role of the ventrolateral medullary pressor (VLPA) and depressor (VLDA) areas in mediating cardiovascular responses evoked from the nucleus tractus solitarius (NTS) was investigated. Male Wistar rats, anesthetized with pentobarbital or urethane, were artificially ventilated and blood pressure (BP) and heart rate (HR) were monitored. The VLPA, VLDA, and the NTS were identified bilaterally with microinjections of L-glutamate. Unilateral microinjections of muscimol or lidocaine into the VLPA or the VLDA blocked the decrease in BP produced by microinjections of L-glutamate (1.77 nmol) into the NTS. These findings indicate that both areas are essential for mediating depressor responses elicited from the NTS. When neuronal activity in the VLDA was depressed unilaterally (leaving the ipsilateral VLPA intact), with the microinjection of muscimol or lidocaine, microinjection of a larger dose (5.0 nmol) of L-glutamate into the ipsilateral NTS elicited a pressor response. This response was blocked by depressing neuronal activity in the ipsilateral VLPA by microinjection of muscimol into this site. This pressor response evoked from the NTS was not due to non-specific effects of L-glutamate since repeated microinjections of L-glutamate (5.0 nmol/site) into the NTS consistently produced decreases in BP and HR. The stimulation of the contralateral NTS by glutamate continued to elicit the usual decreases in BP and HR. Microinjections of either dose (1.77 or 5 nmol) of L-glutamate into the areas adjacent to the NTS (e.g. 1.0 mm rostral or lateral to the NTS, the gracile or cuneate nuclei and area postrema) failed to evoke any cardiovascular responses indicating that the responses were mediated by neurons localized within the intermediate one-third of the NTS. These results indicate that: (1) the depressor responses elicited from the NTS involve the pathways from the NTS to the VLDA and VLDA to VLPA and (2) there may be a pathway from the NTS to the VLPA which is sympathoexcitatory and is unmasked when neuronal activity in the VLDA is depressed.

Animals↗
PubMed1988

Stimulation of opiate receptors in the dorsal pontine tegmentum inhibits reflex contraction of the urinary bladder.

In urethane-anesthetized rats the i.v. administration of the potent short-acting opioid, fentanyl, elicited inhibition of rhythmic spontaneous reflex increases in vesical pressure (VP) evoked by urinary bladder distension. The duration of fentanyl-induced inhibition was dose-related between 0.8 and 8.0 micrograms/kg i.v. Pretreatment with the opiate receptor antagonist, naloxone HCl (250 micrograms/kg i.v.), antagonized completely fentanyl's effect on VP rhythm. Results similar to those obtained with fentanyl were observed after the bilateral stimulation of opiate receptors in the dorsolateral tegmental-subceruleus region of the pons (DLT-SC region) with D-Ala2-Met5-enkephalinamide (DAMA) microinjections. These inhibitory effects were dose-related and significant between 1.0 and 100.0 ng/site. DAMA in the DLT-SC did not alter basal cardiorespiratory parameters. The systemic and local administration of naloxone reversed rapidly the VP effects elicited by DAMA in the DLT-SC region. Naloxone alone, administered either i.v. or locally in the DLT-SC region, increased the frequency of spontaneous reflex increases in VP. Moreover, pretreatment of the DLT-SC region with naloxone microinjections significantly (55% reduction) decreased the duration of fentanyl (8.0 micrograms/kg i.v.)-induced inhibition of VP rhythm. Neurons in DLT-SC region whose discharge increased just before and throughout spontaneous increases in VP (vesical contraction-related units), were inhibited rapidly and completely by the systemic administration of fentanyl. However, fentanyl elicited a prolonged decremental discharge in neurons of the DLT-SC region with discharge patterns related to vesical relaxation (vesical relaxation-related units).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

Ventrolateral medullary pressor area: site of hypotensive action of clonidine.

Intravenous injections of clonidine produce an initial transient increase in blood pressure followed by a long-lasting hypotension and bradycardia. The initial pressor response is due to activation of vascular alpha 1-adrenergic receptors while the hypotension and bradycardia are caused by the central actions of clonidine. Although, hypothalamus, nucleus tractus solitarius (NTS), ventrolateral medulla and the intermediolateral cell column of the thoracolumbar spinal cord (IML) have been implicated, the exact site of these actions of clonidine in the central nervous system is not established. The results of this investigation suggest that the pressor area in the ventrolateral medulla (VLPA) is the site of hypotensive and bradycardic actions of intravenously administered clonidine. This conclusion is based on the observation that microinjections of idazoxan, a specific alpha 2-adrenergic receptor blocker, into the VLPA prevented and reversed the hypotension and bradycardia despite the fact that other proposed sites of these actions (NTS, hypothalamus and IML) were intact and accessible to intravenously administered clonidine.

Animals↗
PubMed1987

Differential regulation of regional vascular resistance by the rostral and caudal ventrolateral medulla in the rat.

Regional vascular resistance changes were determined following chemical excitation and inhibition of the rostral vasopressor (RVLM) and caudal vasodepressor (CVLM) areas in the ventrolateral medulla. Mesenteric, renal and hindquarter vascular resistances were assessed in paralyzed and artificially ventilated urethane-anesthetized rats instrumented with pulsed-Doppler flow probes. Microinjection of the excitatory amino acid L-glutamate in the RVLM elicited a significant dose-related transient increase in blood pressure, heart rate and resistance of mesenteric, renal and hindquarter vascular beds. A similar dose-related hemodynamic profile was obtained following microinjection of muscimol, a GABAmimetic, in the CVLM. In contrast, significant dose-related decrease in blood pressure, heart rate and resistance in mesenteric and hindquarter vascular beds was observed following glutamate-induced excitation of the CVLM and muscimol-induced inhibition of the RVLM. Changes in renal vascular resistance were inconsistent in this second hemodynamic profile. Intravenous administration of the alpha 1 adrenergic antagonist, prazosin, abolished all of the hemodynamic effects elicited by excitation of the RVLM except the tachycardia. Intravenous atropine methylnitrate blocked the bradycardia associated with excitation of the CVLM but did not alter the vascular resistance changes. These results indicate that the changes in heart rate did not contribute significantly to the resistance profiles described. The changes in vascular resistance elicited by excitation and inhibition of the RVLM were correlated with increase and decrease in the greater splanchnic nerve activity, respectively. In conclusion, neuron pools in the RVLM and CVLM exert differential effects upon resistance in different vascular beds via changes in sympathetic outflow.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

Activation of cholinergic mechanisms in the medulla oblongata reverse intravenous opioid-induced respiratory depression.

The role of cholinergic mechanisms in opioid-induced respiratory depression was investigated in isoflurane-anesthetized rats. In these animals, the i.v. administration of fentanyl, a clinically useful potent opioid analgesic/anesthetic, induced a prolonged period of apnea and subsequent rise in the end-tidal CO2, hypotension and bradycardia. The centrally acting anticholinesterase, physostigmine, significantly decreased fentanyl-induced respiratory and circulatory depression. The beneficial respiratory and circulatory effects of physostigmine could be abolished by the administration of muscarinic antagonists, e.g., scopolamine hydrobromide or atropine sulfate. Inhibition of inspiratory phrenic nerve activity by fentanyl and restoration of this activity by the subsequent i.v. administration of physostigmine indicates that the origin of this opioid-cholinergic interaction is the central nervous system. Similar effects on phrenic nerve discharge were observed when the systemic administration of fentanyl was followed by microinjection of physostigmine or carbachol in the rostral ventrolateral medulla. In conclusion, opioid-induced respiratory depression after systemic administration is obtunded greatly by facilitation of muscarinic mechanisms in the ventrolateral medulla. Inhibition of a cholinergic link in the central chemosensor may underlie opioid-induced respiratory depression. Manipulation of this cholinergic link could lead to the use and development of analgesics devoid of respiratory depression.

Analgesia↗
PubMed1986

Medullary pressor area: site of action of intravenous physostigmine.

Physostigmine, a choline-esterase inhibitor, is known to elevate endogenous levels of acetylcholine. Intravenously administered physostigmine causes a rise in blood pressure via its action in the central nervous system. Exact site of this action of physostigmine is not known. In this paper, it was demonstrated that microinjections of tetrodotoxin (a fast sodium channel blocker), lidocaine (a local anesthetic) and scopolamine (a cholinergic muscarinic receptor blocker) into the rostral ventrolateral medullary pressor area abolished the pressor action of intravenously administered physostigmine. These results demonstrate that the rostral ventrolateral medulla is the site of action of intravenously administered physostigmine and this action is mediated via cholinergic muscarinic receptors.

Animals↗
PubMed1985

Blockade of cholinergic receptors in the C1 area abolishes hypertensive response to opiates in the A1 area of the ventrolateral medulla.

Opiate receptor stimulation by microinjections of a delta-receptor agonist, D-Ala2-D-Leu5-enkephalin (DADLE) into the caudal depressor (A1) area of the ventrolateral medulla produced a hypertensive response which was prevented as well as reversed by the blockade of cholinergic receptors in the rostral pressor (C1) area. These results suggest that the hypertensive responses to opiates in the A1 area are mediated via cholinergic mechanisms in the rostral C1 area of the ventrolateral medulla and acetylcholine may be the neurotransmitter released in the ventrolateral pressor area.

Acetylcholine↗
PubMed1984

Interdependence of rostral and caudal ventrolateral medullary areas in the control of blood pressure.

Pharmacologic experiments were carried out to test the degree of interdependence of rostral vasopressor and caudal vasodepressor neuron pools in the ventrolateral medulla (VLPA and VLDA, respectively). In two groups of urethane-anesthetized rats, the gamma-aminobutyric acid (GABA) agonist muscimol (10 ng/site) was bilaterally microinjected into both the VLPA and VLDA to inhibit neuronal activity at these sites. In one group of experiments, muscimol was microinjected first into the VLPA and then into the VLDA. Following muscimol microinjection in the VLPA the mean arterial pressure (MAP) and heart rate (HR) decreased to 40 +/- 6 mm Hg and 310 +/- 21 beats/min (bpm) from a control level of 90 +/- 3 mm Hg and 403 +/- 23 bpm. Subsequent microinjection of muscimol in the VLDA had no significant effect on BP or HR. This lack of response was not due to severe fall in BP caused by microinjection of muscimol into the VLPA. In the second group of experiments muscimol was first injected into the VLDA followed by muscimol microinjection into the VLPA. In the VLDA muscimol significantly increased MAP and HR to 139 +/- 4 mm Hg and 427 +/- 4 bpm from a control level of 87 +/- 2 mm Hg and 356 +/- 23 bmp. The aortic depressor nerve response (-37 +/- 1 mm Hg and -47 +/- 4 bpm) was converted to an aortic 'pressor' response (+20 +/- 1 mm Hg and -13 +/- 6 bpm). Subsequent microinjection of muscimol into the VLPA caused MAP and HR to fall to 43 +/- 5 mm Hg and 338 +/- 17 bpm. The aortic 'pressor' response was also abolished (2 +/- 2 mm Hg). These results indicate that neuronal activity in the rostral VLPA is an important determinant for changes in BP and its reflex regulation mediated by the VLDA. However, BP changes mediated by the rostral VLPA are independent of the level of neuronal activity in the VLDA. Sites of VLPA and VLDA interaction are discussed.

Animals↗
PubMed1984

Cardiovascular response to injections of enkephalin in the pressor area of the ventrolateral medulla.

The cardiovascular effects of the injection of an enkephalin analogue, [D-ala2-met5]enkephalinamide (DAME) into the pressor area of the rostral ventrolateral medulla were studied in urethane-anesthetized and decerebrate rats. The excitatory amino acid L-glutamate was used to identify the ventrolateral medulla. The pressor responses to L-glutamate were elicited from an area that included the nucleus reticularis gigantocellularis, the medial aspect of the nucleus reticularis parvocellularis and the dorsal portion of the nucleus reticularis lateralis. Injection (0.1 microliter volume) of DAME (2.5-500.0 ng/site) into the ventrolateral medulla elicited a dose-related decrease in arterial blood pressure and heart rate and attenuated the carotid occlusion response (COR). Control injections (0.1-0.2 microliter vol) of saline into the same area failed to produce any response. The specificity of this opiate response was tested with naloxone HCl, an opiate antagonist, which prevented, as well as reversed, the action of DAME both by intravenous (i.v.) administration and by injection into the ventrolateral medulla. It was concluded that the ventrolateral medulla plays a role in the generation of vasomotor tone and that stimulation of opiate receptors in this area by an enkephalin analogue produced hypotension, bradycardia and modification of cardiovascular reflexes.

Animals↗
PubMed1984

Hypertensive response following stimulation of opiate receptors in the caudal ventrolateral medulla.

In urethane-anesthetized rats, vasodepressor neuron pools were located bilaterally in and adjacent to the A1 area of the ventrolateral medulla by injecting the neuroexcitatory amino acid, L-glutamate. Ventrolateral vasodepressor areas included the caudalateral part of the nucleus reticularis gigantocellularis, the rostrolateral part of the nucleus reticularis ventralis, and the dorsal nucleus reticularis lateralis. In the ventrolateral vasodepressor areas L-glutamate elicited a transient fall in blood pressure (BP) and heart rate (HR). The opiate agonist (D-ala2-met5)-enkephalinamide (DAME) was used to stimulate opiate receptors in vasodepressor sites, identified with L-glutamate. In these sites, bilateral injections (0.1 microliter/site) of DAME caused a dose-related (2.5-500.0 ng) increase in blood pressure and heart rate, as well as exaggeration of the response to occlusion of the carotid. The effects of DAME on blood pressure were completely abolished by alpha-adrenergic blockade (phentolamine, 2 mg/kg, i.v.) and all effects of DAME were reversed by the administration of naloxone HCl (1 mg/kg, i.v.). Naloxone reversal was accompanied by an unexpected "rebound" hypertension. Saline had no significant effects when injected, or administered intravenously, in the absence or presence of DAME. It was concluded that stimulation of opiate receptors in the ventrolateral vasodepressor areas activated sympathetic outflow. An enkephalinergic system in this area of the brain stem may serve to modulate blood pressure, heart rate and cardiovascular reflexes.

Animals↗
PubMed1984

Cardiac vagolytic action of some neuromuscular blockers.

Cardiac vagolytic effect of four commonly used neuromuscular blockers, (viz. D-tubocurarine, decamethonium, pancuronium and gallamine) was compared in midcollicular decerebrate rats. The intravenous doses of neuromuscular blockers used (d-tubocurarine: 0.1 mg/kg; decamethonium: 2 mg/kg; pancuronium: 0.1 mg/kg; gallamine: 20 mg/kg) were sufficient to produce the paralysis of respiratory muscles. Bradycardia was induced by electrical stimulation of the vagus or by injecting dimethyl-phenyl-piperazinium (DMPP; a ganglionic stimulant). It was observed that d-tubocurarine and decamethonium were devoid of cardiac vagolytic action. On the other hand, pancuronium and gallamine inhibited significantly the bradycardia induced by electrical stimulation of the vagus or injection of DMPP; gallamine was found to have greater vagolytic action. The pressor responses to DMPP were not attenuated by pancuronium and gallamine indicating that in the dose administered, these agents did not block the ganglia. Bradycardia induced by the administration of acetylcholine in the left atrium was also attenuated by pancuronium and gallamine suggesting that the drugs produce cardiac vagolytic action by acting on the post-synaptic cholinergic receptors of the heart.

Acetylcholine↗
PubMed1984

Endogenous GABAergic mechanisms in the medulla and the regulation of blood pressure.

In the present study, the gamma-aminobutyric acid receptor antagonist, bicuculline methiodide (BMI), was used to explore the role of endogenous medullary GABAergic mechanisms in the neural control of circulation. In urethane-anesthetized rats, microinjections of the neuroexcitatory amino acid, L-glutamate (150-300 ng/site) were used to functionally identify rostral ventrolateral vasopressor neuron pools (VLPA) and caudal ventrolateral vasodepressor neuron pools (VLDA). The bilateral microinjection of BMI into the ventrolateral vasodepressor neuron pool caused a dose-related (0.1-100.0 ng/site) decrease in blood pressure (BP), pulse pressure and heart rate (HR). Maximum decreases in BP and HR were 51 +/- 2 mm Hg and 245 +/- 9 beats/min, respectively. In the VLPA, BMI caused a dose-related (0.1-100.0 ng/site) increase in BP, HR and pulse pressure. Maximum increases in BP and HR were 88 +/- 3 mm Hg and 73 +/- 4 beats/min, respectively. In the VLPA, BMI also caused a 40% increase in the carotid artery occlusion response and a 48% reduction in the aortic depressor nerve response. It seems plausible that GABAergic mechanisms in both the caudal and rostral ventrolateral medulla are tonically involved with the maintenance and reflex regulation of vasomotor activity. Medullary gamma-aminobutyric acid may provide a reciprocal inhibition between rostral vasopressor and caudal vasodepressor neuron pools.

Animals↗
PubMed1984

Cardiovascular control by cholinergic mechanisms in the rostral ventrolateral medulla.

The cardiovascular effects associated with the microinjection (100 nl) of carbachol, physostigmine and atropine into the pressor area in the ventrolateral medulla (VLPA) were studied. In urethane anesthetized rats, VLPAs were functionally identified bilaterally by microinjection of the neuroexcitatory amino acid L-glutamate (300 ng/site). L-Glutamate microinjections into the VLPA cause a transient rise in blood pressure (BP) and heart rate (HR). The bilateral microinjection of carbachol into the VLPA caused a prolonged dose-related increase in BP and HR in the dose range of 0.8 to 400.0 ng/site. At higher doses (1-10 micrograms), carbachol caused a decrease in BP and HR; indicative of depolarization blockade. Acetylcholine esterase inhibition by physostigmine microinjections in the VLPA caused cardiovascular effects similar to those observed with carbachol. The hypertensive responses evoked by muscarinic receptor stimulation in the VLPA were mediated by increasing sympathetic outflow. The pathway by which cholinergic receptor stimulation in the VLPA activates vasomotor outflow appears to be entirely descending as coronal knife cuts at the level of the trapezoid body failed to alter the hypertensive responses. Pressor responses elicited by both physostigmine and carbachol were reversed completely by the i.v. administration of atropine sulfate (0.5-3 mg/kg i.v.). Muscarinic receptor blockade in the VLPA after atropine sulfate microinjection caused a dose-related (0.4-15.0 micrograms/site) fall in the BP and HR suggesting that cholinergic mechanisms in the VLPA are tonically active.

Adrenergic alpha-Antagonists↗
PubMed1983

Pulmonary resistance and compliance changes evoked by pulmonary opiate receptor stimulation.

The administration of [D-Ala2,Met5]enkephalinamide (DAME, 10-250 micrograms/kg) or morphine sulfate (MS, 2 mg/kg) into the right atrium (RA) of spontaneously breathing decerebrate rats caused an increase in lung resistance (RL) and a decrease in dynamic compliance (Cdyn). The maximal percentage increase in RL for DAME (250 micrograms/kg) and MS (2 mg/kg) was 120 +/- 21 and 160 +/- 40%, respectively, occurring during the first 30 s following an initial period of apnea, and subsiding within 1.5-2.0 min. The fall in Cdyn (DAME = -31 +/- 8%; MS = -35 +/- 4%) followed a more prolonged time course returning to control within 4-5 min. These responses were completely abolished by pretreatment with naloxone HCl (100 micrograms/kg i.v.), as well as bilateral cervical vagotomy. Pretreatment with antihistaminic, antiserotinergic, and antimuscarinic agents had no effect on the opioid induced changes in RL and Cdyn. Further studies carried out in ventilated animals showed blockade of the mechanical responses following the administration of neuromuscular blockers, C7 spinal cord transection, and ventral midline opening and retraction of the chest. Electromyograms obtained from intercostal muscles showed excitation of expiratory motor units and inhibition of inspiratory motor units following the administration of opioids. Similar results were obtained with phenyldiguanide (PDG), a known stimulant of pulmonary J-receptors. However, PDG effects were not blocked by naloxone. It was concluded that changes in RL resulted from a decrease in thoracic volume and resultant decrease in the radial traction of the airways. Changes in Cdyn were caused by spasm of expiratory muscles of the chest wall.

Animals↗
PubMed1983

Involvement of central dopamine receptors in the hypotensive action of pergolide.

The involvement of central dopamine receptors in the hypotensive action of the dopaminergic ergoline, pergolide was determined in anesthetized rats. Intravenous (i.v.) or intracerebroventricular (i.v.t.) administration of pergolide (12.5, 25 and 50 micrograms/kg) produced dose-dependent decreases in blood pressure. The magnitude of hypotension seen following either i.v. or i.v.t. administration of pergolide was similar. However, while both sulpiride (1 mg/kg, i.v.) as well as phentolamine (1 mg/kg, i.v.) antagonized the hypotensive action of i.v. pergolide, only sulpiride (1 mg/kg, i.v.t.) was able to antagonize the hypotension seen following i.v.t. administration of pergolide. Phentolamine (1 mg/kg, i.v.t.) did not alter the central hypotensive action of pergolide. In a separate group of rats, clonidine (25 micrograms/kg, i.v.t.) also produced a decrease in blood pressure. While phentolamine (i.v.t.) antagonized the central hypotensive action of clonidine, sulpiride (i.v.t.) did not have any effect on the action of clonidine. These results show that selective activation of central dopamine receptors was responsible for the hypotensive action of centrally-administered pergolide. In a separate group of rats greater splanchnic sympathetic nerve activity was measured. Intravenous pergolide produced similar hypotensive response as seen in previous groups, and this was accompanied by a concomitant decrease in the sympathetic nerve activity. The maximum fall in blood pressure (26 +/- 6 mm Hg) was correlated with a 40% reduction in sympathetic nerve activity. The return of blood pressure to control levels occurred after 60-70 min and was also associated with the return of sympathetic nerve activity to control levels.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗