Simple flow-thru swivel for infusions into unrestrained animals

Brown, Zavie W.; Amit, Zalman; Weeks, James R.

doi:10.1016/0091-3057(76)90090-3

Cited by 98 publications

(28 citation statements)

References 1 publication

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“…Drug infusions were given at the rate of 0.15 ml min'; infusion of saline at this rate had no cardiovascular effects. Throughout the experiment, when cardiovascular variables were not being recorded, the arterial catheter was connected to a fluid-filled swivel (Brown et al, 1976) through which saline was infused (10 u m'l heparin at 0.3 mlh-') to keep the catheter patent.…”

Section: Methodsmentioning

confidence: 99%

Effects of chronic treatment with nitric oxide synthase inhibitors on regional haemodynamic responses to vasodilators in conscious Brattleboro rats

Gardiner

Kemp

Bennett

1993

British J Pharmacology

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1 The effects of acute inhibition of nitric oxide (NO) synthase on cardiovascular responses to vasodilator challenges have already been described. We now report the responses to vasodilators during and after chronic NO synthase inhibition. 2 In conscious Brattleboro rats, the regional haemodynamic effects of 3 min infusions of acetylcholine (4 g min-'), sodium nitroprusside (15 fg min ') or adrenaline (0.2 ig min-') were assessed (from areas under or over curves (AUC, AOC)) under control conditions, 6 and 72 h after the addition of the NO synthase inhibitor, N0-monomethyl-L-arginine (L-NMMA) to the drinking water (1 mg ml-'), and 6, 24and 48 h after the withdrawal of L-NMMA. In a separate group of Brattleboro rats, responses to acetylcholine, sodium nitroprusside and adrenaline were assessed before and 6 h after the onset of oral ingestion of the more potent nitric oxide synthase inhibitor, N0-nitro-L-arginine methyl ester (L-NAME; 0.05 mg ml-1). 3 Acetylcholine caused renal vasodilatation (87 ± 11 units) and mesenteric vasoconstriction (-31 ± 5 units), sodium nitroprusside caused vasodilatation in renal (96 ± 12 units), mesenteric (222 ± 13 units) and hindquarters (49 ± 15 units) vascular beds, whereas adrenaline caused hindquarters vasodilatation (92 ± 8 units). Seventy two h after the onset of oral ingestion of L-NMMA, acetylcholine had a decreased renal vasodilator (59 ± 9 units) effect, sodium nitroprusside had an increased renal vasodilator (142 ± 23 units) action, while adrenaline had a decreased hindquarters vasodilator (55 ± 6 units) influence. Twenty four h after withdrawal of L-NMMA, the renal vasodilator effect of acetylcholine was greater than the control response (106 ± 14 units), but the regional haemodynamic effects of sodium nitroprusside and adrenaline were not different from those under control conditions. Hence, the increased renal vasodilator response to acetylcholine was probably due to changes in muscarinic receptor-mediated mechanisms rather than to any increase in guanylyl cyclase or its sensitivity to NO.

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Section: Methodsmentioning

confidence: 99%

Effects of chronic treatment with nitric oxide synthase inhibitors on regional haemodynamic responses to vasodilators in conscious Brattleboro rats

Gardiner

Kemp

Bennett

1993

British J Pharmacology

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“…The catheters ran through a flexible spring connected to a harness worn by the rat and the linking cable to the flow probes was taped to the spring. The venous catheter that was to be used to monitor central venous pressure was connected to a slow infusion pump (SRI) through a fluidfilled swivel (Brown et al, 1976). Isotonic saline (NaCl 157 mmol l-') was infused (0.3 ml h -) through this catheter to ensure it remained patent until recordings were started (Gardiner et al, 1990c).…”

Section: Methodsmentioning

confidence: 99%

Differential effects of (±)‐dobutamine and human α‐CGRP on cardiac and on regional haemodynamics in conscious Long Evans rats

Gardiner

Compton

Kemp

et al. 1991

British J Pharmacology

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1 Comparisons were made of the full haemodynamic profiles of the known cardiostimulant, (± )-dobutamine, and the putative inotropic peptide, human a-calcitonin gene-related peptide (human a-CGRP), in conscious, chronically-instrumented Long Evans rats. Both substances were administered continuously i.v. for 60min at two doses ((±)-dobutamine, 2 and lOpmolkgr'h-i; human a-CGRP, 0.15 and 1.5 nmol kg1 h 1). 2 In spite of their similar (small) effects on mean arterial blood pressure, the low doses of (±)-dobutamine and human a-CGRP influenced cardiac haemodynamics differently. Thus, (±)-dobutamine caused an increase in cardiac index (due to a tachycardia), accompanied by rises in peak aortic flow, maximum rate of rise of aortic flow (dF/dtmai) and total peripheral conductance. However, the latter waned during the infusion, and after the infusion there was a significant systemic vasoconstriction and reductions in peak aortic flow, dF/dtmax and stroke index. Such 'off' effects following dobutamine infusion have not been described previously. The infusion of the lower dose of human cx-CGRP caused only a transient fall in central venous pressure.3 The rise in total peripheral conductance during infusion of the lower dose of (±)-dobutamine was associated with increases in hindquarters and common and internal carotid vascular conductances. The fall in total peripheral conductance after infusion was associated with renal vasoconstriction. Although there was no significant change in total peripheral conductance during the infusion of the lower dose of human a-CGRP there were hindquarters and carotid vasodilatations together with mesenteric vasoconstriction. 4 Infusion of the higher dose of ( )-dobutamine had greater effects than the lower dose on all cardiac haemodynamic variables and additionally, increased stroke index. However, the negative cardiac haemodynamic effects following the offset of infusion were also enhanced in association with marked renal and mesenteric vasoconstrictions. While infusion of the higher dose of human a-CGRP increased cardiac index, peak aortic flow, dF/dtmax and total peripheral conductance, stroke index fell together with central venous pressure. 5 (±)-Dobutamine caused greater cardiostimulation and increases in hindquarters blood flow than did human a-CGRP. However, the latter at the higher dose caused substantially greater common and internal carotid hyperaemia than did (±)-dobutamine, possibly indicating a selective and additional effect of human a-CGRP on cranial blood flow. Furthermore, there were no adverse cardiovascular effects following infusion of human a-CGRP.

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“…The harness provided a point of attachment for the catheter to a needle-tubing leash that passed out the top of the animal chamber. A leak proof swivel (Brown et al, 1976) was used to attach the leash to the tubing leading to the infusion pump so that the animals had almost complete freedom of movement. The rats were allowed to recover for 7 days before the initiation of experimental procedures with programmed infusions (0.2 ml delivered over 6.2 s) of heparinized saline (1.7 U/ ml) administered at hourly intervals in the home cage to maintain functional catheters.…”

Section: Surgical Techniquesmentioning

confidence: 99%

Self-Administered Heroin and Cocaine Combinations in the Rat: Additive Reinforcing Effects—Supra-Additive Effects on Nucleus Accumbens Extracellular Dopamine

Smith

Coller

et al. 2005

Neuropsychopharmacol

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The concurrent use of cocaine and opiate combinations (speedball) has increased since the 1970s and now represents a growing subset of intravenous drug abusers. An isobolographic analysis was applied to the ascending limb of the dose-effect curves for rat selfadministration of cocaine, heroin, and their combination to determine the nature of the interaction. The addition of heroin to cocaine shifted the dose-effect curve for self-administration to the left, and the modulation in reinforcing efficacy of the combination of cocaine and heroin was found to be additive. A second experiment used microdialysis to determine the effects of this drug combination on nucleus accumbens (NAc) extracellular levels of dopamine ([DA] e ) in rats self-administering low doses of cocaine, heroin, or cocaine/ heroin combinations. These doses of cocaine and cocaine/heroin combinations significantly increased NAc [DA] e , while heroin alone did not. The ratio of the % baseline of [DA] e (or the dialysate concentrations of DA) to cocaine in the dialysate was higher during selfadministration of cocaine/heroin combinations than with cocaine alone. These data indicate that although the interaction between cocaine and heroin in maintaining self-administration is additive, a potentiation of NAc dopaminergic neurotransmission is present, suggesting that NAc [DA] e may not be a direct measure of reinforcing efficacy and/or it is not central to the mediation of the selfadministration of this drug combination.

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Simple flow-thru swivel for infusions into unrestrained animals

Cited by 98 publications

References 1 publication

Effects of chronic treatment with nitric oxide synthase inhibitors on regional haemodynamic responses to vasodilators in conscious Brattleboro rats

Effects of chronic treatment with nitric oxide synthase inhibitors on regional haemodynamic responses to vasodilators in conscious Brattleboro rats

Differential effects of (±)‐dobutamine and human α‐CGRP on cardiac and on regional haemodynamics in conscious Long Evans rats

Self-Administered Heroin and Cocaine Combinations in the Rat: Additive Reinforcing Effects—Supra-Additive Effects on Nucleus Accumbens Extracellular Dopamine

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