1,720,972 research outputs found
PCB congener 126-induced ultrastructural alterations in the rat liver: a stereological study
No full textHepatocyte cytoplasmic alterations were morphometrically determined in male and female Sprague-Dawley rats fed PCB congener 126 (3,3',4,4',5-pentachlorobiphenyl) in concentrations of 0.1, 1.0, 10, 100 ppb or corn oil in diets for 13 weeks. A dose-dependent increase (P < 0.05) in the volume fraction of smooth endoplasmic reticulum (SER) and mitochondria was measured in the hepatocytes of the females. However, these cells of the male rats contained a significantly greater baseline volume fraction of SER compared to that in the females. Statistical differences were not detected in the volume fractions of rough endoplasmic reticulum, peroxisomes or lipid droplets of the hepatocytes in either the males or females. We conclude the increase in mitochondrial volume was a necessary cellular adaptation to meet the heightened energy demands by the SER to produce the necessary enzymes to detoxify the PCB. Morphometric analysis rather than a descriptive methodology allowed for a more accurate determination of the liver pathology induced by PCB 126. (C) 1999 Elsevier Science Ireland Ltd. All rights reserved.PT: J; CR: AHLBORG UG, 1994, CHEMOSPHERE, V28, P1049 BANDIERA S, 1982, CHEM-BIOL INTERACT, V39, P259 CHU I, 1994, FUND APPL TOXICOL, V22, P457 CLARKE DW, 1984, CAN J PHYSIOL PHARM, V62, P1253 DEVITO MJ, 1993, FUND APPL TOXICOL, V20, P125 GHADIALLY FN, 1988, ULTRASTRUCT PATHOL, V2, P767 GILLETTE DM, 1987, FUND APPL TOXICOL, V8, P4 GILROY C, 1998, TOXICOLOGY, V127, P179 HANSELL MM, 1974, TOXICOL APPL PHARM, V28, P418 HARRIS C, 1984, ARCH ENVIRON CON TOX, V13, P715 HONG CS, 1992, ECOTOX ENVIRON SAFE, V23, P118 KANNAN N, 1989, ARCH ENVIRON CON TOX, V18, P850 KASZA L, 1978, J ENVIRON PATHOL TOX, V1, P241 KIMBROUGH RD, 1972, ARCH ENVIRON HEALTH, V25, P354 LEECE B, 1985, J TOXICOL ENV HEALTH, V16, P379 LIN FS, 1979, ARCH ENV CONTAM TOXI, V88, P321 MACLELLAN K, 1994, HISTOL HISTOPATHOL, V9, P453 MACLELLAN K, 1994, HISTOL HISTOPATHOL, V9, P461 MACLELLAN K, 1994, J SUBMICR CYTOL PATH, V26, P279 MARTUCCI CP, 1993, PHARMACOL THERAPEUT, V57, P237 OKEY AB, 1990, PHARMACOL THERAPEUT, V45, P241 PARKINSON A, 1980, CHEM-BIOL INTERACT, V30, P217 PATTERSON DG, 1994, ENVIRON HEALTH PERSP, V102, P195 PENG J, 1997, TOXICOLOGY, V120, P171 POLAND A, 1977, MOL PHARMACOL, V13, P924 SAFE S, 1990, CRIT REV TOXICOL, V21, P51 SAFE SH, 1994, CRIT REV TOXICOL, V24, P87 SATO T, 1968, J ELECTRON MICROSC, V17, P158 SCHECTER A, 1984, BANBURY REPORT, V18, P177 SHAPIRO BH, 1995, INT J BIOCHEM CELL B, V27, P9 SINGH A, 1981, PATHOLOGY, V13, P487 SINGH A, 1996, ULTRASTRUCT PATHOL, V20, P275 SINGH A, 1997, ULTRASTRUCT PATHOL, V21, P143 SMITH LM, 1990, CHEMOSPHERE, V21, P1063 TANABE S, 1987, ENVIRON POLLUT, V47, P147 TEHSEEN WM, 1992, B ENVIRON CONTAM TOX, V48, P101 VANBIRGELEN APJM, 1994, TOXICOL APPL PHARM, V127, P209 VOS JG, 1972, TOXICOL APPL PHARM, V23, P563 WASSERMANN D, 1979, TOXICOL EUR RES, V1, P159 WEIBEL ER, 1969, J CELL BIOL, V42, P68 WEISS L, 1988, CELL TISSUE BIOL TXB, P1; NR: 41; TC: 4; J9: TOXICOLOGY; PG: 9; GA: 240XASource type: Electronic(1
Modulation of the cardiac baroreflex following reversible blockade of the parabrachial nucleus in the rat
No full textThe parabrachial nucleus (PBN) has a prominent anatomical connection with the nucleus of the solitary tract as well as other central baroreflex centres which suggests a role for the PBN in the regulation of this cardiovascular reflex. This study examined the effects of a reversible, bilateral blockade of the PBN on the cardiac baroreflex. Male Sprague-Dawley rats were anesthetized with sodium butabarbitol and instrumented to monitor blood pressure and heart rate and for the intravenous administration of drugs. The cardiac baroreflex was evoked using bolus intravenous injections of phenylephrine (PE) and sodium nitroprusside (NaNp) at various doses and a graph of baroreflex sensitivity was constructed. Bilateral microinjections of the reversible anesthetic, lidocaine (5%, 300 nl), into the PBN did not significantly change baseline blood pressure or heart rate when compared to microinjections of saline (0.9%, 300 nl) into the PBN. The pressor or depressor responses evoked by bolus injections of PE or NaNp, respectively, were not significantly affected by the bilateral pretreatment of the PBN with lidocaine when compared to saline controls. However, approximately 30 min following lidocaine injection, the amplitudes of both the evoked-reflex bradycardia and reflex tachycardia were significantly increased by approximately 98%. The cardiovascular responses to various doses of PE and NaNp were graphed and baroreflex sensitivity curves were constructed. This graph showed an increased slope of the baroreflex sensitivity curve following lesions of the PBN. Reflex changes in heart rate returned to pre-lidocaine injection levels after approximately 2 h. The results of the present investigation suggest that the PBN participates in the modulation of the cardiac baroreflex which in turn suggests a role for this nucleus in the central integration of cardiovascular reflex function.LR: 20061115; PUBM: Print; JID: 0045503; 0 (Anesthetics, Local); 137-58-6 (Lidocaine); ppublishSource type: Electronic(1
Role of the insular cortex in the modulation of baroreflex sensitivity
No full textCervical vagal stimulation for 2 h results in a depressed baroreflex sensitivity produced by an enhanced sympathetic output, as indicated by increased plasma norepinephrine levels. The current study examined the role of the insular cortex in modulating the vagal stimulation-induced changes in baroreflex sensitivity. Male Sprague-Dawley rats were anesthetized with thiobutabarbitol sodium and instrumented for recording blood pressure, heart rate, intravenous drug administration, and vagal afferent nerve stimulation. Stereotaxic microinjections (300 nl) of either 5% lidocaine or 0.9% saline were made bilaterally into the insula. Thirty minutes after 2 h of vagal stimulation, the baroreflex was significantly depressed and plasma norepinephrine levels were significantly elevated in both groups. The baroreflex was also significantly depressed after bilateral lidocaine injections into the insula, independent of vagal stimulation. However, no significant change in plasma norepinephrine was observed, suggesting that an attenuated parasympathetic output contributed to the altered baroreflex. Taken together, the results suggest that the insular cortex modulates the cardiac baroreflex through a modulation of parasympathetic output.LR: 20061115; PUBM: Print; JID: 0370511; 0 (Anesthetics, Local); 137-58-6 (Lidocaine); ppublishSource type: Electronic(1
17beta-estradiol modulates baroreflex sensitivity and autonomic tone of female rats
No full textThe following experiments examine the role of estrogen as a central modulator of autonomic tone and baroreflex sensitivity in the female rat. Female Sprague-Dawley rats were ovariectomized and then supplemented daily for 7 days with a fixed dose of estrogen (5 microg/kg; sc) to produce a stable level of estrogen similar to that present at proestrous (17 pg/ml). The rats were then anaesthetized with sodium thiobutabarbital (100 mg/kg) and instrumented to record blood pressure, heart rate and both vagal and renal efferent nerve activities. The sensitivity of the cardiac baroreflex was tested using intravenous injection of multiple doses of either phenylephrine hydrochloride or sodium nitroprusside. Estrogen-supplemented female rats exhibited a significantly enhanced BRS as compared to male rats from a previous study (0.78 vs. 0.5). Furthermore, bolus injection of estrogen (1x10(-2) mg/kg; iv) in estrogen-supplemented female rats produced a significant increase in vagal nerve activity and a significant decrease in renal nerve activity which together resulted in a further enhancement of the BRS (0.78 vs. 2.4). Injection of the selective estrogen receptor antagonist, ICI 182,780, into nucleus ambiguus and the intrathecal space of the spinal cord blocked the respective changes in parasympathetic and sympathetic nerve activities indicating that intravenously administered estrogen modulates baseline autonomic tone via the activation of central estrogen receptors.LR: 20061115; PUBM: Print; JID: 8003419; 0 (Vasoconstrictor Agents); 0 (Vasodilator Agents); 15078-28-1 (Nitroprusside); 50-28-2 (Estradiol); 59-42-7 (Phenylephrine); ppublishSource type: Electronic(1
The parabrachial nucleus mediates the decreased cardiac baroreflex sensitivity observed following short-term visceral afferent activation
No full textPrevious investigations have provided evidence demonstrating that the extracellular release of glutamate into the parabrachial nucleus was significantly enhanced following visceral afferent activation. This period of enhanced glutamate release into the parabrachial nucleus corresponded to a time during which the pressor response to a bolus phenylephrine injection was significantly enhanced, and the reflex bradycardia was attenuated. This decrease in the sensitivity of the baroreflex is suggestive of an enhanced sympathetic tone as a result of the vagal stimulation. The present investigation was done to determine if the decreased baroreflex sensitivity observed following short-term vagal stimulation is mediated by an increase in sympathetic activity and was dependent on the parabrachial synapse. Male Sprague-Dawley rats were anaesthetized with sodium thiobutabarbitol and instrumented to monitor blood pressure and heart rate and for the placement of a stimulating electrode on the left cervical vagus nerve. Femoral arterial blood samples were taken before, during and after 2 h of vagal stimulation which were later assayed for plasma catecholamines. The results showed that plasma norepinephrine levels decreased during, and were significantly elevated immediately following termination of the vagal stimulation, indicative of an increase in sympathetic tone. To determine if the parabrachial nucleus is involved in mediating an enhanced sympathetic activity following vagal stimulation, a second group of animals underwent an identical surgical preparation, vagal stimulation and blood sampling protocol with the addition of bilateral microinjections of either the reversible anaesthetic, lidocaine, or saline into the parabrachial nucleus. The results showed that reversible blockade of the parabrachial nucleus prior to the onset of the vagal stimulation was effective in blocking both the elevation in plasma norepinephrine levels and the depressed baroreflex sensitivity previously observed following 2 h of vagal stimulation. These results suggest that the parabrachial nucleus mediated the sympathoexcitation and consequent depression in baroreflex sensitivity observed following visceral afferent activation.LR: 20061115; PUBM: Print; JID: 7605074; 0 (Anesthetics, Local); 0 (Catecholamines); 137-58-6 (Lidocaine); ppublishSource type: Electronic(1
Role of 17beta-estradiol in the modulation of baroreflex sensitivity in male rats
No full textFemale mammals have an enhanced baroreflex sensitivity compared with their male counterparts, leading researchers to speculate that estrogen modulates autonomic tone. Therefore, this study tests the hypothesis that exogenous estrogen can enhance the baroreflex sensitivity of male rats. Male Sprague-Dawley rats anesthetized with thiobutabarbitol sodium (50 mg/kg) were instrumented to measure blood pressure and heart rate and for the intravenous injection of drugs. The baroreflex was tested using intravenous injections of phenylephrine (0.025, 0.05, and 0.1 mg/kg), and the cardiovascular responses were plotted to obtain a measure of the sensitivity of the cardiac baroreflex. Intravenous injection of estrogen produced dose-related increases in the baroreflex sensitivity due to an increase in the magnitude of the reflex bradycardia. In a separate group of animals, stimulation of the vagus nerve for 2 h resulted in a decrease in baroreflex sensitivity. This effect was blocked when estrogen (1 x 10(-2) mg/kg) was administered immediately before the end of stimulation. In conclusion, intravenous injection of estrogen in male rats significantly enhanced baroreflex sensitivity and blocked the attenuation in the baroreflex sensitivity observed after vagal stimulation.LR: 20061115; PUBM: Print; JID: 0370511; 0 (Estrogen Antagonists); 0 (Vasoconstrictor Agents); 129453-61-8 (fulvestrant); 481-96-9 (estradiol-3-sulfate); 50-28-2 (Estradiol); 59-42-7 (Phenylephrine); ppublishSource type: Electronic(1
Centrally mediated effect of 17beta-estradiol on parasympathetic tone in male rats
No full textThe following experiments were conducted to determine if peripherally administered estrogen has an effect on central autonomic tone and whether this change in tone results in an alteration in cardiovascular reflex control. Male Sprague-Dawley rats were anesthetized with thiobutabarbitol sodium (50 mg/kg) and instrumented to record blood pressure, heart rate, and vagal parasympathetic or renal sympathetic efferent nerve activity. Additional rats were instrumented to test the sensitivity of the cardiac baroreflex using intravenous injections of phenylephrine hydrochloride (0.025, 0.05, 0.1 mg/kg) or sodium nitroprusside (0. 0025, 0.005, 0.01 mg/kg) and plotting the cardiovascular responses. Intravenous injection of estrogen (10(-4), 10(-2), and 10(-1) mg/kg) produced a significant increase in vagal efferent activity and in baroreflex sensitivity. The bilateral microinjection of an estrogen receptor antagonist, ICI-182,780 (1 pM, 50 nl/side) into the nucleus ambiguus blocked both the estrogen-induced increase in vagal efferent activity and baroreflex sensitivity. These results demonstrate that in male rats estrogen acts centrally to enhance baroreflex sensitivity by increasing parasympathetic efferent tone.LR: 20061115; PUBM: Print; JID: 0370511; 0 (Estrogen Antagonists); 129453-61-8 (fulvestrant); 50-28-2 (Estradiol); ppublishSource type: Electronic(1
Central nuclei mediating estrogen-induced changes in autonomic tone and baroreceptor reflex in male rats
No full textThe current investigation examines the significance of estrogen in central cardiovascular regulatory nuclei in modulating autonomic tone and baroreceptor reflex function. Experiments were done in anaesthetized male Sprague-Dawley rats. Changes in autonomic tone were assessed by monitoring vagal and renal efferent nerve activities before and following bilateral injection of estrogen into select central autonomic nuclei. In the first study, selective blockade of neurotransmission through the central nucleus of the amygdala (CNA), lateral hypothalamic area (LHA) and ventral posteromedial thalamic nucleus (VPM) using the local anaesthetic lidocaine was done to determine which nuclei were involved in mediating the autonomic changes observed following bilateral injections of estrogen into the insular cortex (IC). In the second study, the role of the parabrachial nucleus (PBN) in mediating the autonomic changes observed following bilateral estrogen injections into the CNA, LHA, VPM and IC was determined by blocking neurotransmission through the PBN using lidocaine.Injections of estrogen into the IC produced a significant increase in renal sympathetic nerve activity (RSNA; from 10+/-2 to 24+/-4 microV/sec; p0.05). Injection of estrogen into the CNA resulted in a significant decrease in RSNA (48+/-5%; p<0.05) whereas estrogen injection into the LHA resulted in a significant increase (28+/-4%; p<0.05) in RSNA. Pre-injection of lidocaine into the PBN resulted in complete blockade of the autonomic changes observed following estrogen injection into the CNA but did not affect the changes observed following estrogen injection into the LHA. These results suggest that estrogen acting in forebrain and midbrain cardiovascular nuclei activated efferent pathways which synapse in the LHA, CNA and/or PBN prior to projecting to autonomic preganglionic nuclei to affect autonomic tone. These nuclei may therefore provide an added level of processing and/or integration of the autonomic response(s) following activation by local or systemic estrogen.LR: 20031114; PUBM: Print; JID: 0045503; 0 (Estrogens); 0 (Sodium Channel Blockers); 137-58-6 (Lidocaine); ppublishSource type: Electronic(1
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