Pulmonary chemoreflex sensitivity is enhanced by prostaglandin E2 in anesthetized rats

1995 ◽  
Vol 79 (5) ◽  
pp. 1679-1686 ◽  
Author(s):  
L. Y. Lee ◽  
R. F. Morton
Keyword(s):  
Prostaglandin E2 ◽  
Constant Infusion ◽  
Electrophysiological Recording ◽  
Sprague Dawley ◽  
C Fibers ◽  
Sprague Dawley Rats ◽  
Organ Systems ◽  
C Fiber ◽  
Cardiovascular Depression ◽  
Chemical Irritants

Stimulation of vagal pulmonary C-fiber afferents by chemical irritants is believed to be responsible for eliciting the pulmonary chemoreflex (apnea, bradycardia, and hypotension). This study was carried out in anesthetized Sprague-Dawley rats to determine whether the pulmonary chemoreflex was altered by prostaglandin E2 (PGE2), which is one of the major inflammatory mediators in the lungs and is known to enhance the sensitivity of C-fiber afferents in several other organ systems. Capsaicin injected at a dose just above the stimulation threshold (0.25 or 0.5 microgram/kg i.v.) elicited a very mild respiratory and cardiovascular depression. In sharp contrast, during a constant infusion of PGE2 (1.5 micrograms.kg-1.min-1 i.v.), the same dose of capsaicin triggered a long apnea, with the expiratory duration reaching 843% of the baseline expiratory duration, accompanied by intense bradycardia and hypotension. Similarly, the pulmonary chemoreflex response elicited by a bolus injection of phenyl biguanide (1 or 2 micrograms/kg i.v.) was also greatly augmented by PGE2. These enhanced responses were completely abolished, by a perineural capsaicin treatment of both cervical vagi to selectively block the conduction of C fibers, suggesting the involvement of these afferents. Electrophysiological recording of pulmonary C-fiber afferent activity further supported our conclusion that the sensitivity of these sensory endings to capsaicin challenge was potentiated by PGE2.

Rapid determination of glomerular filtration rate by single-bolus inulin: a comparison of estimation analyses

1998 ◽  
Vol 84 (6) ◽  
pp. 2154-2162 ◽  
Author(s):  
Cord Sturgeon ◽  
Albert D. Sam ◽  
William R. Law
Keyword(s):  
Mathematical Model ◽  
Glomerular Filtration Rate ◽  
Mathematical Models ◽  
Glomerular Filtration ◽  
Filtration Rate ◽  
Rapid Determination ◽  
Constant Infusion ◽  
Sprague Dawley ◽  
Single Bolus ◽  
Sprague Dawley Rats

Rapid measurement of glomerular filtration rate (GFR) by an inulin single-bolus technique would be useful, but its accuracy has been questioned. We hypothesized that reported inaccuracies reflect the use of inappropriate mathematical models. GFR was measured in 14 intact and 5 unilaterally nephrectomized conscious male Sprague-Dawley rats (mean weight 368 ± 12 g) by both single-bolus (25 mg/kg) and constant-infusion techniques (0.693 mg ⋅ kg−1 ⋅ min−1). The temporal decline in plasma inulin concentration was analyzed through biexponential curve fitting, which accounted for renal inulin loss before complete vascular and interstitial mixing. We compared our mathematical model based on empirical rationale with those of other investigators whose studies suggest inaccuracy of single-bolus methods. Our mathematical model yielded GFR values by single bolus that agreed with those obtained by constant infusion [slope = 0.94 ± 0.16 (SE); y intercept = 0.23 ± 0.64; r = 0.82]. In comparison to the data obtained by constant inulin infusion, this method yielded a very small bias of −0.0041 ± 0.19 ml/min. Two previously reported models yielded unsatisfactory values (slope = 1.46 ± 0.34, y intercept = 0.47 ± 1.5, r = 0.72; and slope = 0.17 ± 1.26, y intercept = 17.15 ± 5.14, r = 0.03). The biases obtained by using these methods were −2.21 ± 0.42 and −13.90 ± 1.44 ml/min, respectively. The data indicate that when appropriate mathematical models are used, inulin clearance after single-bolus delivery can be used to measure GFR equivalent to that obtained by constant infusion of inulin. Attempts to use methods of analysis for simplicity or expediency can result in unacceptable measurements relative to the clinical range of values seen.

Endogenous CCK disrupts the MMC pattern via capsaicin-sensitive vagal afferent fibers in the rat

1997 ◽  
Vol 272 (1) ◽  
pp. G100-G105 ◽  
Author(s):  
A. Rodriguez-Membrilla ◽  
P. Vergara
Keyword(s):  
Intravenous Infusion ◽  
Sprague Dawley ◽  
Rat Intestine ◽  
Intracerebroventricular Infusion ◽  
C Fibers ◽  
Afferent Fibers ◽  
Sprague Dawley Rats ◽  
Vagal Afferent ◽  
Endogenous Release ◽  
Stimulation Of

A meal disrupts migrating motor complexes (MMC) in the rat intestine through stimulation of peripheral cholecystokinin (CCK)-B and central CCK-A receptors. The aim of this study was to determine pathways implicated in postprandial disruption of the MMC mediated by CCK. Sprague-Dawley rats were prepared with electrodes for electromyography in the small intestine, and ablation of vagal afferent C-fibers by capsaicin was carried out. Endogenous release of CCK was induced by oral administration of soybean trypsin inhibitor (SBTI). In control rats SBTI disrupted MMC and generated an irregular spiking activity that lasted longer than 3 h. Intravenous infusion of L-365,260 (2 x 10(-7) mol/kg) but not of L-364,718 (3 x 10(-9) mol/kg) restored the MMC pattern. In capsaicin-treated rats, SBTI did not modify fasting activity. Infusion of CCK octapeptide (CCK-8) at 3 x 10(-9) mol.kg-1.h-1 disrupted the MMC, although the response was quantitatively and qualitatively different from SBTI. The effect was reversed by intravenous infusion of L-364,718 or L-365,260 and intracerebroventricular infusion of L-364,718. In capsaicin-treated rats, the intracerebroventricular or intravenous infusion of L-364,718 inhibited CCK-8 effects. However, the intravenous infusion of L-365,260 did not reverse the MMC pattern. These results suggest that the disruption of the MMC mediated by CCK is due to stimulation of peripheral CCK-B receptors located in vagal afferent fibers. This initiates a reflex including stimulation of central CCK-A receptors. Exogenous CCK also stimulates peripheral CCK-A receptors not located in capsaicin-sensitive vagal afferent fibers.

scholarly journals Mechanism of dopamine inhibition of renal phosphate transport.

1992 ◽  
Vol 2 (11) ◽  
pp. 1601-1607
Author(s):  
J Isaac ◽  
R P Glahn ◽  
M M Appel ◽  
M Onsgard ◽  
T P Dousa ◽  
...  
Keyword(s):  
Parathyroid Hormone ◽  
Brush Border Membrane ◽  
Phosphate Transport ◽  
Constant Infusion ◽  
Saline Control ◽  
Control Group ◽  
Sprague Dawley ◽  
Pi Transport ◽  
Sprague Dawley Rats ◽  
Dependent Transport

Dopamine (DA) is natriuretic and phosphaturic. However, whether the effect of DA on Pi reabsorption is a consequence of its effect on sodium transport is not known. Therefore, this study was performed to determine the effect of DA on the maximal transport of phosphate (TmPi), and upon the capacity of renal proximal brush border membrane (BBM) for (Naextra-vesicular greater than Naintravesicular)-gradient-dependent transport of Pi, as compared with the transport of other solutes. Graded infusions of Pi (0, 1, 2, and 3 mumols/min) were given to thyroparathyroidectomized male Sprague-Dawley rats in the presence of vehicle (0.9% NaCl; N = 5), DA 15 micrograms/kg/min; N = 6), or parathyroid hormone ((PTH); 1 U/kg/min; N = 5). The TmPi for rats infused with DA (3.3 +/- 0.3 mumol/mL) was significantly less than the TmPi for saline control rats (4.4 +/- 0.2 mumol/mL). Rats infused with PTH exhibited the lowest TmPi (1.8 +/- 0.3 mumol/mL). No differences in sodium excretion were observed among any of the groups. Na-dependent Pi transport was studied in BBM vesicles (BBMV) prepared from rats fed a low-phosphate diet for 2 days that were anesthetized, acutely thyroparathyroidectomized, and systemically infused with DA (350 micrograms bolus, plus 35 micrograms/kg/min; N = 8), PTH (33 U/kg bolus, followed by a continuous infusion of 1 U/kg/min; N = 6), or vehicle (1 mL/kg bolus, plus 2 mL/h constant infusion of 0.9% NaCl; N = 8) for 90 min. DA significantly inhibited the Na cotransport of Pi by 22.4 +/- 4.1% (P less than 0.01) as compared with the control group.(ABSTRACT TRUNCATED AT 250 WORDS)

Mechanism of prostaglandin E2-induced increase of proximal sodium reabsorption in the rat

1990 ◽  
Vol 258 (1) ◽  
pp. R82-R86 ◽  
Author(s):  
Y. Kinoshita ◽  
F. G. Knox
Keyword(s):  
Angiotensin Ii ◽  
Prostaglandin E2 ◽  
Rat Kidney ◽  
Sodium Reabsorption ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Convoluted Tubules ◽  
Stimulation Of ◽  
Interstitial Infusion

Prostaglandin E2, when infused directly into the renal interstitium, enhances sodium reabsorption by the superficial proximal convoluted tubules of anesthetized Sprague-Dawley rats. The present study was designed to investigate the role of angiotensin II in the prostaglandin E2-induced stimulation of proximal sodium reabsorption. Micropuncture at the superficial late proximal tubule demonstrated a significant increase in the fractional reabsorption of sodium from 39.9 +/- 2.3% in control conditions to 51.8 +/- 3.0% (n = 9, P less than 0.01) during the renal interstitial infusion of prostaglandin E2. The stimulatory effect of prostaglandin E2 on proximal sodium reabsorption was markedly attenuated by pretreatment with saralasin. During intravenous saralasin infusion, prostaglandin E2 did not significantly change the fractional reabsorption of sodium from 42.2 +/- 5.8 to 45.4 +/- 6.0% (n = 7, NS). In summary, the stimulatory effect of renal interstitial infusion of prostaglandin E2 on proximal sodium reabsorption was attenuated by pretreatment with saralasin. Therefore renal interstitial infusion of prostaglandin E2 may enhance proximal sodium reabsorption, at least in part, through stimulation of angiotensin II production in the rat kidney.

Effects of TRH on thyrotroph function and number in rat pituitaries transplanted to renal capsule

1986 ◽  
Vol 251 (5) ◽  
pp. E563-E568
Author(s):  
S. Amr ◽  
S. S. Lippman ◽  
B. D. Weintraub
Keyword(s):  
Biologically Active ◽  
Constant Infusion ◽  
Control Group ◽  
Mrna Levels ◽  
Renal Capsule ◽  
Sprague Dawley ◽  
Subunit Mrna ◽  
Sprague Dawley Rats ◽  
Hypophysectomized Rats ◽  
Hypothalamic Influence

We investigated the function of thyrotrophs in rat pituitaries that were transplanted under the renal capsule of 3-wk-old male Sprague-Dawley rats, which were either intact or hypophysectomized. Groups of 12 animals were implanted with osmotic minipumps that delivered a constant infusion of either thyrotropin-releasing hormone (TRH; 1 mg X kg-1 X day-1) or normal saline for 1 wk. In hypophysectomized rats, TRH infusion led to the appearance of substantial amounts of biologically active serum TSH and prevented the hypothyroidism that occurred in the control group. However, TRH did not change the transplant contents of DNA, immunoactive TSH, and mRNA levels for TSH subunits. Comparison of sellar and renal pituitary tissues, obtained from intact rats after 1 wk of either saline or TRH infusion, showed that removal of the pituitary from hypothalamic influence resulted in a 90% depletion of the thyrotroph TSH content. TRH infusion depleted only 63% of the TSH content of sellar thyrotrophs. The mRNA levels for TSH beta-subunit were similar in sellar and transplanted pituitaries and did not significantly change after TRH infusion. When immunocytochemically stained using rat TSH antiserum, the thyrotrophs in pituitary transplants were morphologically and numerically indistinguishable from the thyrotrophs in sellar pituitaries, in the presence or absence of TRH. These data indicate that in transplanted pituitary, for up to 1 wk of a constant infusion, TRH does not significantly affect either the number of thyrotrophs or their ability to synthesize TSH subunit mRNA. However, it is required to maintain released TSH in circulation, since TSH levels were low in the absence of TRH.(ABSTRACT TRUNCATED AT 250 WORDS)

Protective and defensive airway reflexes evoked by nasal exposure to wood smoke in anesthetized rats

2000 ◽  
Vol 88 (3) ◽  
pp. 863-870 ◽  
Author(s):  
C.-Y. Ho ◽  
Y. R. Kou
Keyword(s):  
Hydroxyl Radical ◽  
The Other ◽  
Wood Smoke ◽  
Radical Scavenger ◽  
Sprague Dawley ◽  
C Fibers ◽  
Sprague Dawley Rats ◽  
Nasal Application ◽  
Airway Responses ◽  
Saline Vehicle

We investigated the airway responses evoked by nasal wood smoke in anesthetized Sprague-Dawley rats. Wood smoke (5 ml, 1.4 ml/s) was delivered into an isolated nasal cavity while animals breathed spontaneously. In study 1, nasal wood smoke triggered either an apneic response ( n = 26) or a sniff-like response ( n = 16) within 1 s after smoke exposure in 42 normal rats. Both airway responses were abolished by trigeminal nerve denervation and by nasal application of a local anesthetic or a hydroxyl radical scavenger, but they were not significantly affected by removal of smoke particulates or nasal application of a saline vehicle. In study 2, nasal wood smoke only triggered a mild apneic response in two rats neonatally treated with capsaicin and had no effect on breathing in the other six; the treatment is known to chronically ablate C fibers and some Aδ fibers. In contrast, nasal wood smoke evoked an apneic response in six rats neonatally treated with the vehicle of capsaicin and elicited a sniff-like response in the other two. These results suggest that the apneic and sniff-like responses evoked by nasal wood smoke result from the stimulation of trigeminal nasal C-fiber and Aδ-fiber afferents by the gas-phase smoke and that hydroxyl radical is the triggering chemical factor.

scholarly journals Neoplasms in Rats Ingesting Acrylonitrile for Two Years

1988 ◽  
Vol 7 (5) ◽  
pp. 603-615 ◽  
Author(s):  
G.T. Gallagher ◽  
E.A. Maull ◽  
K. Kovacs ◽  
S. Szabo
Keyword(s):  
Drinking Water ◽  
Weight Gain ◽  
Pituitary Adenomas ◽  
Early Death ◽  
Early Mortality ◽  
Low Doses ◽  
Sprague Dawley ◽  
Exposure Age ◽  
Sprague Dawley Rats ◽  
Organ Systems

Male Sprague-Dawley rats ingested 0, 20 ppm, or 500 ppm of acrylonitrile in drinking water for 2 years. Rats receiving 500 ppm of acrylonitrile exhibited early mortality and retarded weight gain. Tumors of Zymbal's gland were associated in dose-response fashion with acrylonitrile exposure. Age-associated incidence of pituitary adenomas containing immunoreactive prolactin was decreased in acrylonitrile-treated rats. A decrease in pituitary tumor incidence also was observed in rats treated with low doses of acrylonitrile, suggesting that reduction in this tumor frequency was not because of early death. No increases were found in tumors of other organ systems, but a trend toward development of forestomach papillomas was noted in rats receiving the highest concentration of acrylonitrile.

Phosphaturic effect of L-NMMA in the presence of parathyroid hormone

1996 ◽  
Vol 271 (6) ◽  
pp. R1477-R1480
Author(s):  
M. J. Onsgard-Meyer ◽  
R. J. Kerrigan ◽  
M. Collins ◽  
A. A. Khraibi ◽  
F. G. Knox
Keyword(s):  
Parathyroid Hormone ◽  
Fractional Excretion ◽  
Parathyroid Glands ◽  
Constant Infusion ◽  
Sprague Dawley ◽  
Phosphate Excretion ◽  
Sprague Dawley Rats ◽  
Additional Group ◽  
Renal Clearances ◽  
Intact Rats

The objective of this study was to examine the effect of NG-monomethyl-L-arginine (L-NMMA) on phosphate excretion in the presence and absence of parathyroid hormone (PTH). Renal clearances were obtained before and during infusion of L-NMMA (15 mg/kg bolus and 500 micrograms.kg-1.min-1 infusion) in Sprague-Dawley rats with intact parathyroid glands (n = 6), in thyroparathyroidectomized (TPTX) rats receiving a constant infusion of PTH-(1-34) (0.01-0.03 U.kg-1.min-1) (n = 11) throughout the experiment, or in TPTX rats, that received an acute infusion of PTH-(1-34) (33 U/kg bolus and 1 U.kg-1.min-1 infusion) after L-NMMA infusion alone (n = 7). In rats with intact parathyroid glands, L-NMMA increased the fractional excretions of phosphate (FEPi) and sodium (FENa) and mean arterial pressure (MAP) (delta 8.6 +/- 1.5%, delta 0.62 +/- 0.1%, and delta 26.7 +/- 4.9 mmHg, respectively; P < 0.05). In TPTX rats receiving a constant infusion of PTH, L-NMMA again increased FEPi, FENa, and MAP (delta 9.5 +/- 3.6%, delta 1.1 +/- 0.4%, and delta 28.4 +/- 4.5 mmHg, respectively; P < 0.05). However, in TPTX rats, L-NMMA alone did not increase FEPi (delta 0.9 +/- 0.3%), whereas the subsequent infusion of PTH with L-NMMA increased FEPi (delta 15.6 +/- 3.1%; P < 0.05). In an additional group of intact and TPTX rats, the fractional excretion of lithium (FELi) was measured as an index of proximal reabsorption. L-NMMA increased FELi in intact rats (delta 13.2 +/- 2.6%; P < 0.05), but not in TPTX rats (delta 4.2 +/- 3.3%). In conclusion, L-NMMA increases phosphate excretion in association with increases in MAP and FENa, and this phosphaturic effect is dependent on the presence of PTH.

Blood pressure vulnerability to volume contraction: regulation by adrenal cortical hormones

1977 ◽  
Vol 233 (5) ◽  
pp. R239-R242 ◽  
Author(s):  
T. Waldinger ◽  
J. F. Seaton ◽  
T. S. Harrison
Keyword(s):  
Blood Pressure ◽  
Mean Arterial Pressure ◽  
Constant Infusion ◽  
Intravenous Bolus ◽  
Sprague Dawley ◽  
Bleeding Volume ◽  
Sprague Dawley Rats ◽  
Volume Sensitivity ◽  
Contraction Regulation ◽  
Adrenalectomized Rats

Although the unique sensitivity of blood pressure to hemorrhage after adrenalectomy can be overcome by adrenocortical hormones the specificity of this steroid effect is not known. Under pentobarbital anesthesia five groups of six adult male Sprague-Dawley rats were bled into a 0.9% saline-primed pressure-balanced reservoir. A mean arterial pressure of 50 Torr was maintained for 3 h. When compared to normal rats, those with adrenalectomy showed significantly lowered bleeding volume (P less than 0.05 to less than 0.001). In untreated adrenalectomized rats 120 min following hemorrhage, saline was consistently taken up from the reservoir to maintain blood pressure at 50 Torr. Deoxycorticosterone-cortisol (intravenous bolus coupled with infusion) restored bleeding volume to normal in adrenalectomized rats. Aldosterone (constant infusion) also protected bleeding volume after adrenalectomy, P less than 0.05 to less than 0.01, but this effect was significantly less striking than that of cortisol 180 min after the onset of bleeding, P less than 0.001. Sham adrenalectomy did not affect bleeding volume. Aldosterone appears to be effective in restoring normal bleeding volume sensitivity after adrenalectomy but this effect of aldosterone is less sustained than that seen with cortisol.

Toxic effects of subchronic oral acetamiprid exposure in rats

2019 ◽  
Vol 35 (11-12) ◽  
pp. 679-687 ◽  
Author(s):  
Bahar Ulus Karaca ◽  
Yağmur Emre Arican ◽  
Tugce Boran ◽  
Sevgi Binay ◽  
Alper Okyar ◽  
...  
Keyword(s):  
Oxidative Damage ◽  
Nicotinic Acetylcholine Receptors ◽  
Acetylcholine Receptors ◽  
Male Rats ◽  
Sprague Dawley ◽  
Tissue Samples ◽  
Plasma Urea ◽  
Sprague Dawley Rats ◽  
Organ Systems ◽  
Liver And Kidney

Acetamiprid, a selective agonist of type-2 nicotinic acetylcholine receptors, is one of the most widely used neonicotinoids. The hepato- and nephrotoxic potential of acetamiprid has not been clarified although it is known to be toxic to other several organ systems, including the nervous, respiratory and immune systems. The present study aimed to investigate acetamiprid liver and kidney toxicity in male rats after a 90-day subchronic exposure to 12.5, 25 and 35 mg/kg. The biochemical and oxidative damage parameters were determined in the plasma and tissue samples as well as histopathological evaluation in the liver and kidney tissues. Acetamiprid caused oxidative damage and affected the liver, denoted by injury markers including the levels of cholesterol, and alanine aminotransferase and aspartate aminotransferase enzymes. There was also a decrease in plasma urea, uric acid and creatinine levels, all of which might result from liver injury. Additionally, acetamiprid was more toxic to the liver than the kidney according to the histopathological examinations. In conclusion, acetamiprid exhibited hepatotoxic potential at all treatment doses on male Sprague Dawley rats.

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