28: Chronic Infusion Catheters: An Oncologist's Perspective

2000 ◽  
Keyword(s):  
Chronic Infusion

An Investigation Into the Effects of Chronic Infusion of Corticotrophin-Releasing Factor on Hind Paw Inflammation in Adjuvant-Induced Arthritis

Stress ◽  
1996 ◽  
Vol 1 (2) ◽  
pp. 105-111 ◽  
Author(s):  
M. S. Harbuz ◽  
H. S. Chowdrey ◽  
S. L. Lightman ◽  
E. T. Wei ◽  
D. S. Jessop
Keyword(s):  
Adjuvant Induced Arthritis ◽  
Corticotrophin Releasing Factor ◽  
Chronic Infusion

A critical role for central vasopressin in regulation of fever during bacterial infection

1992 ◽  
Vol 263 (6) ◽  
pp. R1235-R1240
Author(s):  
R. A. Cridland ◽  
N. W. Kasting
Keyword(s):  
Body Temperature ◽  
Arginine Vasopressin ◽  
Continuous Measurement ◽  
Critical Role ◽  
Experimental Models ◽  
Bacterial Endotoxins ◽  
Chronic Infusion ◽  
Live Bacteria ◽  
The Brain

Previous investigations on the antipyretic properties of arginine vasopressin have used bacterial endotoxins or pyrogens to induce fever. Because these experimental models of fever fail to mimic all aspects of the responses to infection, we felt it was important to examine the role of endogenously released vasopressin as a neuromodulator in febrile thermoregulation during infection. Therefore the present study examines the effects of chronic infusion of a V1-receptor antagonist or saline (via osmotic minipumps into the ventral septal area of the brain) on a fever induced by injection of live bacteria. Telemetry was used for continuous measurement of body temperature in the awake unhandled rat. Animals infused with the V1-antagonist exhibited fevers that were greater in duration compared with those of saline-infused animals. These results support the hypothesis that vasopressin functions as an antipyretic agent or fever-reducing agent in brain. Importantly, they suggest that endogenously released vasopressin may play a role as a neuromodulator in natural fever.

Ouabain- and central sodium-induced hypertension depend on the ventral anteroventral third ventricle region

1999 ◽  
Vol 276 (1) ◽  
pp. H63-H70 ◽  
Author(s):  
Shereeni J. Veerasingham ◽  
Frans H. H. Leenen
Keyword(s):  
Hypertonic Saline ◽  
Wistar Rats ◽  
Third Ventricle ◽  
Cardiovascular Responses ◽  
Ibotenic Acid ◽  
Air Jet ◽  
Artificial Cerebrospinal Fluid ◽  
Induced Hypertension ◽  
Chronic Infusion

To examine the role of the ventral anteroventral third ventricle (vAV3V) in the hypertension induced by chronic subcutaneous ouabain and intracerebroventricular hypertonic saline, neurons in this area were destroyed by microinjection of an excitotoxin, ibotenic acid. Sham-operated or lesioned Wistar rats were administered ouabain (50 μg/day) or placebo for 3 wk from subcutaneously implanted controlled release pellets or artificial cerebrospinal fluid (CSF) or CSF containing 0.8 mol/l NaCl (5 μl/h) infused intracerebroventricularly for 2 wk. At the end of the experiment, mean arterial pressure (MAP) and heart rate at rest and in response to ganglionic blockade by intravenous hexamethonium (30 mg/kg) were assessed. In rats infused with hypertonic saline, responses to air jet stress were also assessed. Baseline MAP in sham-operated rats receiving intracerebroventricular hypertonic saline or subcutaneous ouabain was significantly higher than in control rats (115 ± 1 vs. 97 ± 3 and 121 ± 3 vs. 103 ± 3 mmHg, respectively). vAV3V lesions abolished the increase in MAP elicited by chronic infusion of hypertonic saline or administration of ouabain. Sham-operated rats treated with hypertonic saline or ouabain exhibited significantly enhanced decreases in MAP to hexamethonium, but lesioned rats did not. Rats infused with hypertonic saline demonstrated enhanced responses to air jet stress that were similar in sham-operated and lesioned rats. These results demonstrate that neurons in the vAV3V are essential for the hypertension induced by intracerebroventricular hypertonic saline and subcutaneous ouabain, possibly by increasing sympathetic tone. Cardiovascular responses to air jet stress appear not to be mediated by the vAV3V.

Placement of Intrathecal Needle and Catheter for Chronic Infusion

2016 ◽  
pp. 253-261
Author(s):  
Timothy R. Deer ◽  
Michael H. Verdolin ◽  
Jason E. Pope
Keyword(s):  
Chronic Infusion

Chronic infusion of islet amyloid polypeptide causes anorexia in rats

1996 ◽  
Vol 271 (6) ◽  
pp. R1654-R1659 ◽  
Author(s):  
U. Arnelo ◽  
J. Permert ◽  
T. E. Adrian ◽  
J. Larsson ◽  
P. Westermark ◽  
...  
Keyword(s):  
Food Intake ◽  
Body Weight Gain ◽  
Islet Amyloid Polypeptide ◽  
Reduce Food Intake ◽  
Islet Amyloid ◽  
Minimal Effective Dose ◽  
Subcutaneous Infusion ◽  
Pathophysiological Role ◽  
Chronic Infusion ◽  
High Doses

Islet amyloid polypeptide (IAPP) is a hormonal peptide that at high doses has been shown to reduce food intake. In the present study, the dose-response effects of subcutaneous infusion of IAPP (0, 2, 7, and 25 pmol.kg-1.min-1) for 8 days on food intake and meal patterns in rats were investigated. At the end of the experiment, plasma was obtained and levels of IAPP were measured by radioimmunoassay. IAPP dose-dependently and transiently inhibited food intake. The minimal effective dose (2 pmol.kg-1.min-1) caused a small but significant (up to 14%, P < 0.01) inhibition of food intake that lasted 5 days. The highest dose administered (25 pmol.kg-1.min-1) had the greatest effect (up to 44%, P < 0.001), which lasted throughout the 8-day period. Reductions in feeding during light and dark phases occurred through a decrease in number of meals consumed rather than meal size or meal duration. IAPP also decreased body weight gain and water intake dose dependently. IAPP infusion of 2, 7, and 25 pmol.kg-1.min-1 increased plasma IAPP concentrations from a basal level of 10.3 +/- 0.7 pM to 35.1 +/- 5.4, 78.1 +/- 11.2, and 236.6 +/- 23.6 pM, respectively, values that are likely to be close to physiological and within the pathophysiological ranges. Thus IAPP may play an important physiological or pathophysiological role in control of food intake.

scholarly journals Renal release of N-acetyl-seryl-aspartyl-lysyl-proline is part of an antifibrotic peptidergic system in the kidney

2019 ◽  
Vol 316 (1) ◽  
pp. F195-F203 ◽  
Author(s):  
Cesar A. Romero ◽  
Nitin Kumar ◽  
Pablo Nakagawa ◽  
Morel E. Worou ◽  
Tang-Dong Liao ◽  
...  
Keyword(s):  
De Novo ◽  
Renal Medulla ◽  
Distal Portion ◽  
Distal Nephron ◽  
Sprague Dawley ◽  
Nephron Segments ◽  
Long Term Effect ◽  
Chronic Infusion ◽  
A Minor ◽  
Stop Flow

The antifibrotic peptide N-acetyl-seryl-aspartyl-lysyl-proline (Ac-SDKP) is released from thymosin-β4 (Tβ4) by the meprin-α and prolyl oligopeptidase (POP) enzymes and is hydrolyzed by angiotensin-converting enzyme (ACE). Ac-SDKP is present in urine; however, it is not clear whether de novo tubular release occurs or if glomerular filtration is the main source. We hypothesized that Ac-SDKP is released into the lumen of the nephrons and that it exerts an antifibrotic effect. We determined the presence of Tβ4, meprin-α, and POP in the kidneys of Sprague-Dawley rats. The stop-flow technique was used to evaluate Ac-SDKP formation in different nephron segments. Finally, we decreased Ac-SDKP formation by inhibiting the POP enzyme and evaluated the long-term effect in renal fibrosis. The Tβ4 precursor and the releasing enzymes meprin-α and POP were expressed in the kidneys. POP enzyme activity was almost double that in the renal medulla compared with the renal cortex. With the use of the stop-flow technique, we detected the highest Ac-SDKP concentrations in the distal nephron. The infusion of a POP inhibitor into the kidney decreased the amount of Ac-SDKP in distal nephron segments and in the proximal nephron to a minor extent. An ACE inhibitor increased the Ac-SDKP content in all nephron segments, but the increase was highest in the distal portion. The chronic infusion of a POP inhibitor increased kidney medullary fibrosis, which was prevented by Ac-SDKP. We conclude that Ac-SDKP is released by the nephron and is part of an important antifibrotic system in the kidney.

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