Biomedical subjects

A F Sved

Publications and source records attributed to A F Sved.

At least 91 records · Page 5Linked to original sources

PubMed1992

Pharmacological characterization of serotonin receptor subtypes involved in vasopressin and plasma renin activity responses to serotonin agonists.

Serotonergic drugs with 5-HT2 receptor agonist properties have been suggested to increase plasma vasopressin concentration, blood pressure (BP) and plasma renin activity (PRA). To study whether these actions are mediated by the same or different receptors, we used three potent 5-HT agonists with different structures and receptor binding profiles. All drugs were administered i.v. to conscious, unrestrained rats. The selective agonist, 1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane (DOI), which has high affinity for 5-HT2 receptors, caused marked increases in BP and PRA but no change in plasma vasopressin concentrations. The 5-HT1C agonist, m-chlorophenylpiperazine (m-CPP), which also binds to other 5-HT receptors, caused moderate increases in BP and PRA and significantly elevated plasma vasopressin concentrations. The 5-HT1A agonist, 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT), did not increase any of these parameters. BP and PRA elevations paralleled each other after all drugs, while vasopressin responses were clearly different. Vasopressin responses to m-CPP were entirely antagonised by the 5-HT1/5-HT2 antagonist metergoline, partially by the 5-HT2/5-HT1C antagonists ritanserin and LY 53857, but not by the 5-HT2 antagonist ketanserin. Ritanserin, LY53857 and ketanserin all very effectively blocked BP responses to m-CPP. These findings suggest that BP and PRA but not vasopressin responses are mediated by 5-HT2 receptors. Vasopressin secretion is mediated by 5-HT1 receptors, most likely by 5-HT1C receptors.

8-Hydroxy-2-(di-n-propylamino)tetralin↗

PubMed1992

Cholecystokinin induces c-fos expression in hypothalamic oxytocinergic neurons projecting to the dorsal vagal complex.

Systemic administration of cholecystokinin (CCK) decreases gastric motility and stimulates pituitary secretion of oxytocin (OT). Although peripheral OT does not affect gastric function, increasing evidence suggests that central OT secretion acting within the dorsal vagal complex (DVC) can alter gastric motility. To evaluate whether systemically administered CCK is capable of activating oxytocinergic neurons projecting to the DVC, we utilized fluorogold retrograde labeling from the DVC in combination with c-fos and OT immunocytochemical staining to quantitatively analyze paraventricular nucleus (PVN) neurons of rats following injection of CCK at a dose known to cause maximal pituitary OT secretion (100 micrograms/kg i.p.). Our results showed that 2320 +/- 63 PVN neurons were retrogradely labeled from the DVC; 146 +/- 21 (6.3%) of these contained OT, and these cells were predominantly located in the medial parvocellular subdivision of the PVN. Of all retrogradely labeled cells, 671 +/- 112 (28.9%) expressed c-fos after CCK stimulation, and 68 +/- 14 of these (10.1%) contained OT. Approximately 50% of the OT-containing neurons retrogradely labeled from the DVC stained positively for c-fos. Many magnocellular OT neurons in the PVN that were not retrogradely labeled from the DVC also expressed c-fos after CCK stimulation. These results demonstrate that parvocellular OT neurons projecting to the DVC are co-activated along with magnocellular OT neurons projecting to the pituitary following administration of a large dose of CCK, and lend support to a possible functional role for OT as a central neurotransmitter that modulates vagal efferent traffic to the gastrointestinal tract.

Animals↗

PubMed1992

Nucleus tractus solitarius and control of blood pressure in chronic sinoaortic denervated rats.

To determine the role of the nucleus tractus solitarius (NTS) in the tonic maintenance of arterial pressure (AP) following chronic baroreceptor denervation, the present study examined the effect of inhibition of the NTS on AP in chronic sinoaortic denervated (SAD) and control rats. One to two weeks after complete SAD (no residual arterial baroreceptor reflexes) mean AP was not significantly different from that of control rats. Bilateral microinjections of muscimol and lidocaine into the NTS markedly increased AP in alpha-chloralose-anesthetized control rats. However, microinjections of these neuroinhibitory drugs had no effect on AP in SAD rats. Similarly, 1 h after bilateral destruction of the NTS conscious control rats were hypertensive, while AP in SAD rats was not changed. Plasma levels of vasopressin (VP), which were also elevated in control rats 1 h after NTS lesions, were not significantly altered in SAD rats. These results demonstrate that inhibition of the NTS has no effect on AP or plasma levels of VP in chronic SAD rats. This suggests neither the NTS nor afferents to the NTS supply a tonic inhibitory influence on AP after chronic baroreceptor denervation.

Animals↗

PubMed1991

Effect of suckling on gastric motility in lactating rats.

Recent reports indicate that in male rats dehydration, LiCl, and cholecystokinin (CCK) each stimulate pituitary oxytocin (OT) secretion and also decrease gastric emptying and motility. In contrast, the present experiments demonstrate that nipple attachment and sucking by pups, a well-known stimulus for neurohypophysial secretion of OT, did not decrease gastric motility in lactating rats. Moreover, systemic injection of naloxone, which is known to potentiate the inhibitory effects of LiCl and CCK on gastric motility in male rats, had no effect on gastric motility of lactating rats while nursing. These data indicate that pituitary OT secretion from magnocellular neurons is not invariably linked to decreased gastric motility in rats. As such, our results support previous findings that inhibition of gastric motility is not secondary to the pituitary secretion of OT but allow a possible role for parvocellular oxytocinergic neurons that project from the hypothalamic paraventricular nucleus to the brain stem in the control of gastric function.

Analysis of Variance↗

PubMed1991

Prior exposure to chronic stress results in enhanced synthesis and release of hippocampal norepinephrine in response to a novel stressor.

The release and synthesis of norepinephrine (NE) in hippocampus were measured in naive and chronically cold-stressed rats in response to acute tail-shock stress. Using in vivo microdialysis, it was determined that the basal extracellular concentrations of NE and 3,4-dihydroxyphenylacetic acid (DOPAC) in hippocampus were the same in the two groups. However, 30 min of intermittent tail shock produced a greater elevation of extracellular NE and 3,4-dihydroxyphenylacetic acid in the chronically cold-stressed rats than in the native controls. In hippocampus, the extracellular concentration of DOPAC may reflect NE biosynthesis, and thus the enhanced DOPAC response in the chronically stressed rats suggests an increase in NE synthesis. In order to investigate this possibility, two further methods of assessing NE biosynthesis were employed. Tyrosine hydroxylase (TH) activity was assayed in vitro in the presence of saturating concentrations of cofactor. No change in maximal TH activity could be detected in hippocampus of chronically cold-stressed rats. In addition, the in vivo rate of tyrosine hydroxylation in cold-stressed rats was measured by the accumulation of 3,4-dihydroxyphenylalanine in tissue following inhibition of aromatic amino acid decarboxylase. It was found that, whereas basal synthesis was the same in both groups of rats, synthesis accompanying a novel stressor was increased to a greater extent in the chronically stressed rats.

3,4-Dihydroxyphenylacetic Acid↗

PubMed1990

Endogenous GABA acts on GABAB receptors in nucleus tractus solitarius to increase blood pressure.

Previous studies found that injection of the GABA uptake inhibitor nipecotic acid into the nucleus tractus solitarius (NTS) increases arterial pressure. This effect of nipecotic acid was not antagonized by the selective GABAA receptor blocking agent bicuculline, suggesting that the action of nipecotic acid was mediated through an action of GABA on GABAB receptors in the NTS. The present studies examined this issue using a newly described GABAB antagonist, phaclofen. Injection of phaclofen (4 nmol in 100 nl artificial CSF) into the NTS of chloralose-anesthetized rats produced a slight decrease in arterial pressure (-8 +/- 2 mmHg) lasting less than 1 min. Smaller doses had no effect. Phaclofen antagonized in a dose-dependent (0.5-4 nmol) manner the increase in arterial pressure produced by injection into the NTS of the GABAB agonist baclofen (5-100 pmol). In contrast, phaclofen had no effect on the pressor response elicited by injection into the NTS of the GABAA agonist muscimol. Phaclofen (4 nmol) injected into the NTS totally reversed the increase in blood pressure elicited by injection into the NTS of a maximally effective dose of nipecotic acid (10 nmol). Phaclofen also inhibited the pressor response elicited by injection into the NTS of another indirectly acting GABA agonist, gamma-vinylGABA (GVG). Although GVG is an effective inhibitor of GABA transaminase, the enzyme involved in the metabolism of GABA, the time course of inhibition of GABA transaminase evoked by GVG was not consistent with the pressor response being produced by this mechanism. However, the pressor response elicited by GVG is consistent with its reported ability to inhibit GABA uptake.(ABSTRACT TRUNCATED AT 250 WORDS)

4-Aminobutyrate Transaminase↗

PubMed1990

Effect of monoamine oxidase inhibition on catecholamine levels: evidence for synthesis but not storage of epinephrine in rat spinal cord.

Epinephrine levels in the intermediolateral cell group in the rat spinal cord are very low, although there is a dense projection to this region from cells containing all the enzymes required for epinephrine biosynthesis. One explanation for this finding is that epinephrine in the nerve terminals is degraded as soon as it is synthesized, so that no epinephrine is actually stored in synaptic vesicles. To test this hypothesis, epinephrine levels were measured in spinal cord of rats pretreated with an inhibitor of monoamine oxidase, the major enzyme involved in epinephrine degradation. Selected other tissues (i.e. brainstem, hypothalamus, adrenal gland, superior cervical ganglion) were examined for comparison. Pargyline treatment (75 mg/kg i.p., 4 h prior to sacrifice) increased catecholamine levels in spinal cord, hypothalamus, and brainstem. However, the percent increase in epinephrine in the spinal cord and brainstem was much larger than that for dopamine and norepinephrine in the 3 central nervous system regions studied, as well as larger than that for epinephrine in the hypothalamus. These results suggest that phenylethanolamine N-methyltransferase (PNMT)-containing terminals in the rat spinal cord can synthesize epinephrine, but that little if any epinephrine is stored in synaptic vesicles due to the rapid metabolism of cytoplasmic catecholamines by monoamine oxidase. In contrast, pargyline pretreatment had no effect on catechol levels in the adrenal gland, suggesting that little metabolism of catecholamines takes place in those epinephrine-synthesizing cells. Furthermore, since pargyline pretreatment increased norepinephrine levels but decreased dopamine levels in the superior cervical ganglion, it is suggested that most of the dopamine in that sympathetic ganglion is present as a precursor to norepinephrine in noradrenergic postganglionic sympathetic neurons.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1990

Plasma epinephrine modulates the cerebrovasodilation evoked by electrical stimulation of dorsal medulla.

We examined whether plasma epinephrine contributes to the increase in regional cerebral blood flow (rCBF) evoked by electrical stimulation of the dorsal medullary reticular formation (DMRF). Rats were anesthetized (alpha-chloralose, 30 mg/kg, s.c.), paralyzed and artificially ventilated. The DMRF was electrically stimulated through microelectrodes stereotaxically implanted. During stimulation, blood gases and arterial pressure were monitored and maintained within normal range. rCBF was determined in 11 dissected brain regions using the [14C]iodoantipyrine technique. Plasma epinephrine and norepinephrine were measured radioenzymatically in rats with intact adrenals or adrenalectomy, and with or without infusion of epinephrine. DMRF stimulation induced widespread increases in rCBF associated with a 50-fold increase in plasma epinephrine and a 20-fold increase in norepinephrine without changes in the electroencephalogram. In contrast, stimulation of the adjacent medial longitudinal fasciculus had no effect upon rCBF or plasma catecholamines. Acute bilateral adrenalectomy produced regionally selective reductions in the stimulation-coupled increases in rCBF throughout brain (P less than 0.05). Infusion of epinephrine in adrenalectomized rats to levels comparable to those observed in intact animals during DMRF stimulation did not by itself modify rCBF. However, when infused in conjunction with stimulation of the DMRF, but not medial longitudinal fasciculus, epinephrine fully restored the stimulus-related increases in rCBF in all brain regions to levels comparable to those observed in intact rats. We conclude that stimulation of the DMRF elevates rCBF through two mechanisms; by a neurally-mediated increase in local metabolism and thereby flow (adrenal independent secondary vasodilation) and by releasing epinephrine from adrenal medulla which secondarily acts to increase rCBF by an action on brain.

Animals↗

PubMed1990

Quipazine increases renin release by a peripheral hemodynamic mechanism.

Systemically administered serotonin (5-HT) agonists have been suggested to act centrally to increase plasma renin activity (PRA) and arterial pressure (AP). To test this hypothesis, hemodynamic responses were determined in conscious male rats after intracerebroventricular (i.c.v.) or intravenous (i.v.) administration of the direct 5-HT agonist quipazine. When administered i.v., quipazine increased AP and PRA, and decreased renal blood flow (RBF); doses of quipazine i.c.v. that increased AP to a similar degree failed to increase PRA. The increase in PRA elicited by i.v. quipazine was not blocked by propranolol, suggesting non-neural mechanisms. The increase in AP and decrease in RBF elicited by i.v. quipazine were not eliminated by prazosin, enalapril, or a V1-vasopressin antagonist administered alone or in combination. LY 53857, a 5-HT2 antagonist that enters the central nervous system (CNS), blocked all responses to i.v. quipazine. In contrast, the peripheral 5-HT2 antagonist xylamidine blocked the renin and RBF responses, but only attenuated the pressor response to quipazine. These data suggest that quipazine can act in the CNS to increase AP, but when administered systemically quipazine also activates vascular 5-HT2 receptors to increase AP further and to decrease RBF. The increase in PRA caused by i.v. quipazine is secondary to renal hemodynamics and is unrelated to CNS actions of this drug.

Angiotensin II↗

PubMed1990

Hyponatremia and hypouricemia: differentiation from SIADH.

Hypouricemia in coexistence with hyponatremia often differentiates the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) from most other causes of hyponatremia. We report clearance studies in 5 cases of hyponatremia and hypouricemia that were not due to SIADH. One had metastatic pancreatic carcinoma with ascites, edema, hypoalbuminemia and hypophosphatemia. Two had adenocarcinoma of the lung with metastasis to the brain in 1, 1 had disseminated cryptococcus and 1 had Hodgkin's disease. None received radiation or known nephrotoxins at least 4 months prior to study. None had serum creatinine greater than 106.1 mumol/l (1.2 mg/dl). Two had postural hypotension and hyponatremia that responded to saline therapy. Fluid restriction corrected the hyponatremia in all patients, but the hypouricemia, high fractional excretion (FE) of urate, and high urine sodium concentration persisted. In 2 patients studied, ADH was appropriately suppressed after volume repletion but there was a defect in free water clearance due to high renal solute excretion. In contrast to patients with SIADH who correct their defect in renal urate transport with correction of hyponatremia by water restriction, our patients appear to have a persistent renal urate transport defect and abnormality in sodium conservation. Elevated FE urate of greater than 10% after correction of hyponatremia can thus differentiate these patients from SIADH. The diametrically opposing goals of fluid therapy emphasize the importance of differentiating one group from the other.

Adult↗

PubMed1989

PNMT-containing catecholaminergic neurons are not necessarily adrenergic.

The intermediolateral cell column (IML) in the spinal cord is densely innervated by the phenylethanolamine-N-methyltransferase (PNMT)-containing neurons of the ventrolateral medulla (C1 cell group). The present study used a sensitive HPLC-EC assay for catecholamines to quantitate epinephrine levels in the region of the spinal cord containing the IML. In dissections of thoracic cord enriched in IML, as well as total thoracic cord, epinephrine levels were below the limit of sensitivity of the assay, indicating that epinephrine levels were less than 0.2 pg/mg tissue. In the region of the IML, epinephrine levels were less than 0.05% of the norepinephrine content. Thus, no epinephrine could be detected in the IML even though the IML contains a dense network of nerve terminals that stain immunohistochemically for PNMT and the other enzymes required for epinephrine biosynthesis. These results suggest that nerve terminals that contain all the enzymes required for epinephrine biosynthesis are not necessarily adrenergic.

Adrenergic Fibers↗

PubMed1989

Cardiovascular responses elicited by gamma-aminobutyric acid in the nucleus tractus solitarius: evidence for action at the GABAB receptor.

Previous studies in this laboratory have shown that GABAergic neurotransmission in the nucleus tractus solitarius contributes to the maintenance of blood pressure. Increasing the synaptic action of GABA in the nucleus tractus solitarius by injection of the blocker of the uptake of GABA, nipecotic acid elevated blood pressure. The current studies examined the subtype of GABA receptor involved in mediating this response. Bilateral injections of (-)baclofen into the nucleus tractus solitarius (1-100 pmol in 100 nl) of chloralose-anesthetized, paralyzed, ventilated Sprague-Dawley rats increased blood pressure without significantly altering heart rate. This pressor response was neither attenuated nor blocked by the selective GABAA receptor antagonist bicuculline. Similarly, the pressor response elicited by the injection of nipecotic acid into the nucleus tractus solitarius was totally unaffected by the GABAA receptor blockade with bicuculline. Since nipecotic acid acts by potentiating the action of synaptic GABA, and the GABA present presumably can interact with both GABAA and GABAB receptors, the observation that bicuculline did not block or attenuate the pressor response to nipecotic acid suggests that the pressor response to the enhanced synaptic action of GABA in the nucleus tractus solitarius can be produced independently of the involvement of GABAA receptors, and presumably is mediated through an action on GABAB receptors.

Animals↗

PubMed1988

Enhanced pressor response to GABA in the nucleus tractus solitarii of the spontaneously hypertensive rat.

A previous study from this laboratory demonstrated that ongoing GABAergic neurotransmission in the nucleus tractus solitarii (NTS) functions to maintain baseline arterial pressure (AP). In that study, bilateral microinjection of nipecotic acid into the NTS was observed to elevate AP. Since nipecotic acid is a selective GABA uptake blocker, changes in GABA release should be reflected by changes in the response to nipecotic acid. The present study utilized this approach to assess endogenous GABA activity within the NTS of the spontaneously hypertensive rat (SHR). Male SHR, 16-20 weeks of age, were anesthetized with chloralose, paralyzed and ventilated. Age-matched Wistar-Kyoto (WKY) rats were studied as controls. Bilateral microinjection of nipecotic acid (10 nmol in 100 nl; a maximally effective dose) into the NTS elicited a pressor response which was significantly greater in the SHR than the response observed in the WKY rats. Similarly, direct stimulation of GABAB receptors in the NTS with (-)-baclofen 40 pmol, a maximally effective dose) elicited an increase in AP which was significantly greater in the SHR. In contrast, bilateral microinjection of the direct acting GABAA agonist muscimol (160 pmol, a maximally effective dose) resulted in a similar elevation of AP in both the SHR and WKY rats. These results suggest that the enhanced pressor response caused by endogenous GABA in the NTS of the SHR is due to a greater response evoked by stimulation of GABAB receptors. Thus, enhanced GABAB receptor-mediated neural transmission in the NTS may contribute to the expression or maintenance of hypertension in this genetic model of hypertension.

Animals↗

PubMed1988

Lesions of the AV3V region attenuate sympathetic activation but not the hypertension elicited by destruction of the nucleus tractus solitarius.

Previous studies have implicated a functionally defined area of the forebrain, the anteroventral third ventricle (AV3V) region as being involved in the regulation of blood pressure and required for the expression of neurogenic hypertension. The present study re-examined the effect of AV3V lesion on hypertension caused by the destruction of the nucleus tractus solitarius (NTS), focussing on whether ablation of the AV3V region altered either the sympathoadrenal or vasopressin (VP) components of NTS hypertension. Bilateral electrolytic lesions of the NTS elicited acute severe hypertension in conscious, freely moving rats whether or not the animals had received AV3V or Sham lesions 14 days previously. Mean arterial pressure (MAP) measured 45 min following NTS lesion was 157 +/- 6 mm Hg in AV3V + NTS lesioned rats and 161 +/- 7 mm Hg in SHAM + NTS lesioned rats. Plasma VP levels were similarly elevated in the two groups of NTS lesioned animals, and the contribution of VP to the hypertensive response (as assessed by the decrease in arterial pressure in response to a VP pressor antagonist) was the same in both groups. In contrast, NTS lesion appeared to produce a lesser degree of sympathetic nervous system activation in AV3V lesioned rats, as evidenced by a substantially smaller increase in plasma norepinephrine (NE) levels. These results demonstrate that AV3V lesions do not attenuate or prevent NTS hypertension. However, AV3V lesions do appear to attenuate the sympathoadrenal activation caused by NTS lesions.

Animals↗

PubMed1987

Stimulation of the locus coeruleus decreases arterial pressure.

Unilateral microinjection of L-glutamate (L-Glu, 0.5-5 nmol) into the locus coeruleus (LC) of rats anesthetized with chloralose elicited decreases in blood pressure and heart rate. The maximal depressor response elicited by injection of L-Glu into the LC was approximately 30 mmHg, and the maximal bradycardic response was approximately 35 bpm. Microinjections into the LC of DL-homocysteic acid (1 nmol) and carbachol (1 nmol), agents which (like L-Glu) stimulate neurons within the LC, also produced depressor and bradycardic responses. Vagal blockade with methyl atropine eliminated the bradycardic response, but had no effect on the decrease in arterial pressure elicited by stimulation of neurons within the LC. Destruction of the noradrenergic neurons of the LC by local administration of 6-hydroxydopamine eliminated the cardiovascular responses elicited by injection of L-Glu or carbachol into the LC. These results are in direct contrast to the pressor response elicited by electrical stimulation of the region containing the LC. Destruction of the LC with 6-hydroxydopamine, which totally eliminated the depressor response to L-Glu, slightly potentiated the pressor response elicited by electrical stimulation of this region. Electrical stimulation of the region containing the LC has also been reported to increase plasma vasopressin levels; this response could not be reproduced by by stimulation of the LC by microinjection of L-Glu. These results indicate that stimulation of the noradrenergic neurons of the rat LC decreases arterial pressure and heart rate. Furthermore, these results suggest that the pressor response elicited by electrical stimulation of this region is not due to stimulation of neurons of the LC.

Animals↗

PubMed1987

GABAergic mechanisms in nucleus tractus solitarius alter blood pressure and vasopressin release.

GABAergic agents microinjected into the nucleus tractus solitarius (NTS) influence blood pressure (BP) and plasma vasopressin (VP) levels. The direct-acting GABAergic agonist muscimol (3.75-160 pmol) microinjected bilaterally into the NTS of chloralose-anesthetized, paralyzed, ventilated rats increased BP without significantly altering heart rate. Similar results were obtained using the indirect GABA agonist nipecotic acid (10 nmol), a GABA uptake blocker. In contrast, blocking the action of GABA with bicuculline (5 pmol) elicited a small but consistent decrease in BP. Injections of the vehicle (artificial cerebrospinal fluid) into the NTS or GABAergic agents in an area lateral to the NTS did not alter BP. Unilateral injection of muscimol into the NTS did not elicit immediate pressor responses as did bilateral injections; unilateral muscimol injections following destruction of the contralateral NTS produced a pressor response similar to that seen following bilateral muscimol administration. Stimulation of GABA receptors within the NTS by either muscimol or nipecotic acid resulted in an increase in plasma VP levels. The elevated levels of plasma VP contributed to the pressor response elicited by stimulation of GABAergic receptors as evidenced by the decrease in BP observed following the intravenous administration of a VP pressor antagonist during the pressor response. These studies indicate that tonically active GABAergic mechanisms within the NTS influence BP and VP release, and provide further evidence that VP can be involved in cardiovascular responses elicited from the NTS.

Animals↗

PubMed1987

Vaginocervical probing elevates blood pressure and induces analgesia by separate mechanisms.

Vaginocervical stimulation (VS) applied as a calibrated mechanical probe force against the cervix produced an increase in blood pressure (BP) of greater than 50 mmHg and an increase in heart rate (HR) of greater than 80 beats per minute (bpm). This response was immediate and reached maximum levels within 5-10 seconds. The magnitude of the response was proportional to the force of the VS over a range of 50-600 grams (g). Administration of propranolol (1 mg/kg, IV), a beta-adrenergic receptor antagonist, attenuated the acceleration of HR in response to VS. Administration of chlorisondamine (5 mg/kg, IV), which eliminates both sympathetic and parasympathetic influences, abolished the increase in BP and HR in response to VS, indicating that VS stimulates autonomic activity involved in the control of these two processes and that the tachycardia resulted from vagal withdrawal as well as sympathetic activation. The analgesic effect of VS, as measured by the VS-produced increase in tail flick latency (TFL), was unaffected by any of the drug treatments that abolished the HR and BP elevating effects of VS. Furthermore, elevation of BP by administration of phenylephrine (5 micrograms/kg, IV), to a level comparable to that produced by VS, did not produce analgesia. These results demonstrate that VS produces a profound increase in BP and HR due primarily to an increase in sympathetic activity. In addition, the increase in HR in response to VS appears to be partly due to a decrease in parasympathetic activity. The analgesia produced by VS is independent of the elevation in BP produced by VS.

Analgesia↗

PubMed1987

Functional integration of fetal cortical grafts into the afferent pathway of the rat somatosensory cortex (SmI).

The somatosensory area of fetal (E15-16) Sprague-Dawley rat neocortex was implanted into the barrel receptor area of adult first somatosensory cortex (SmI) to determine if it could be integrated into the host vibrissa-cortical pathway. Functional integration was tested 3-6 months later using the 2-deoxyglucose [44,45] (2-dg) method for estimation of glucose utilization. A variety of control grafts (cerebellum in SmI cortex, neocortex outside the host SmI cortex and appropriately placed neocortex in non-stimulated hosts) all had uniform 2-dg uptake (70 +/- 10 mumol/100 g/min) throughout each graft which averaged 42% less than non-stimulated host SmI cortex (121 +/- 6 mumol/100 g/min; p less than 0.001) but was 3-fold greater than white matter (24.8 +/- 3.1 mumol/100 g/min; p less than 0.001). In appropriately placed neocortical grafts, vibrissal stimulation produced 125% greater average 2-dg uptake (157 +/- 19 mumol/100 g/min) than control grafts (p less than 0.01). Such appropriately placed and stimulated neocortical grafts also contained focal areas of increased 2-dg uptake which were 43% greater than average graft uptake. These data suggest that fetal neocortical grafts were functionally integrated into the physiologically relevant afferent pathways of adult host brains.

Afferent Pathways↗