Treatment of Ureteral Colic with Intravenous Indomethacin

Holmlund, D; Sjödin, Jan-Gunnar

doi:10.1016/s0022-5347(17)57325-5

Cited by 96 publications

(23 citation statements)

References 6 publications

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“…The drug may interrupt the trans port of urine from the kidney to the bladder, and may thus have an adverse effect on the urologic tract. On the other hand, this inhibitory effect may be useful for treat ment of pain induced by renal colic, since it is reported that non-steroid anti-inflammatory drugs reduce the con tractility of ureteral and renal pelvic smooth muscle and the effects contribute to the pain relief in the patient (6,9,23,24).…”

Section: Effects Of Drugs On Ureteral Peristaltic Functionmentioning

confidence: 99%

Neuroprotective Activity of Fructose-1,6-Bisphosphate Following Transient Forebrain Ischemia in the Mongolian Gerbil

Kontani

Masumi

Sakai

1993

Japanese Journal of Pharmacology

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ABSTRACT-In supine anesthetized rats, two cannulae were inserted into a unilateral ureter near the kidney and urinary bladder, respectively. Fluid from a reservoir placed approximately 27 cm above the rat was infused into the ureter lumen through the cannula near the kidney, and the resulting peristaltic pressure signals were measured from the cannula near the bladder. When drugs acting on ion channels were applied from the ureter lumen and their effects on the peristaltic pressure signals were studied, the K+ channel opener BRL 38227 (1 x 10-4 M and 1 x 10-3 M) was found to decrease the frequency dose-dependently. However, the K+ channel blockers glibenclamide and 4-aminopyridine at 1 X 10-3 M did not affect peristaltic movement. Nifedipine (1 x 10-5 M and 1 x 10-4 M) decreased the frequency of peristalsis, but the effect was weaker than that of BRL 38227. Lidocaine at very high concentration (1.5 x 10-2 and 1.5 x 10-' M) decreased the amplitude and increased the frequency of the peristaltic signals. These results indicate that the K+ channel opener has the most inhibitory effect on ureteral peristaltic function.

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Section: Effects Of Drugs On Ureteral Peristaltic Functionmentioning

confidence: 99%

Neuroprotective Activity of Fructose-1,6-Bisphosphate Following Transient Forebrain Ischemia in the Mongolian Gerbil

Kontani

Masumi

Sakai

1993

Japanese Journal of Pharmacology

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“…In postulated in the upper urinary tract but the picture emergthe urinary bladder, prostanoids are produced during bladder ing from the available data is far from clear (see below). The distension at cystometry and exert both a direct myotropic tissue is of clinical relevance because of the increasing action on detrusor muscle and a sensitizing activity on blad-evidence that COX inhibitors produce pain relief during renal der afferents which set the gain for the activation of the colic (Holmlund & Sjodin, 1978;Lundstrom et al, 1982;Oosterlink et al, 1990). …”

Section: Introductionmentioning

confidence: 99%

Modulation by stereoselective inhibition of cyclo‐oxygenase of electromechanical coupling in the guinea‐pig isolated renal pelvis

Santicioli

Carganico²,

Meini

et al. 1995

British J Pharmacology

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1 The effects of the (S)-and (R)-enantiomers of the cyclo-oxygenase (COX) inhibitor, ketoprofen, have been investigated on the spontaneous activity of the guinea-pig isolated renal pelvis and on electrical field stimulation-(EFS) induced contractions of the guinea-pig ureter in comparison with the effects of the achiral COX inhibitor, indomethacin. 2 (S)-ketoprofen (O.1-1I00 LM) produced a concentration-and time-dependent inhibition of the spontaneous myogenic activity of the renal pelvis. The maximal inhibitory effect (% inhibition of motility index) averaged 29, 42, 47 and 56% inhibition of control values at 0.1, 1, 10 and 100Mm. The (R)-enantiomer was ineffective up to 10pM.3 Indomethacin (0.1-100lgM) likewise produced a concentration-and time-dependent inhibition of spontaneous motility of the isolated renal pelvis: its maximal inhibitory effect was larger than that produced by (S)-ketoprofen and averaged 21, 40, 69 and 95% inhibition of motility index at 0.1, 1, 10 and 100 MM respectively. In the presence of a maximally effective (100 iM) concentration of (S)-ketoprofen, 100 IM indomethacin produced >90% inhibition of residual motility. 4 In the guinea-pig isolated ureter, phasic contractions were induced by EFS (5 ms pulse width, 60 V):(S)-ketoprofen (100-500 1IM) had no effect on the EFS-evoked contractions. Indomethacin (100-500IM) produced a concentration-dependent inhibition and/or suppression of the EFS-evoked contractions. When contraction of the ureter was evoked by 80 mM KCI, indomethacin produced about 30 and 80% inhibition at 100 and 300 jaM, respectively, while (S)-ketoprofen (300 JiM) was ineffective. 5 The effect of (S)-ketoprofen or indomethacin (10 MM each) on the propagation of myogenic impulses along the ureter was determined by use of a three chamber organ bath. The renal end of the ureter was electrically stimulated while recording the mechanical activity of the renal and bladder ends of the ureter: addition of either (S)-ketoprofen or indomethacin (10 tiM) did not effect propagation of impulses from the renal to the bladder end of the ureter, while nifedipine (10 MM) promptly blocked the propagated contractions.6 In sucrose gap experiments, (S)-ketoprofen (10-100IM) produced a time-dependent shortening of spontaneous action potentials of the guinea-pig renal pelvis and reduced the amplitude and duration of the accompanying phasic contractions. Indomethacin (10 IM) produced comparable effects on the same parameters and significantly reduced the maximal amplitude of depolarization of the pacemaker potential. In the presence of 100 MM (S)-ketoprofen, 100pM indomethacin promptly suppressed the residual pacemaker potential and contraction. 7 Neither (S)-ketoprofen nor indomethacin (10 MM each for 60 min) affected the parameters of action potential and contraction of the guinea-pig ureter evoked by EFS. Both drugs produced a sustained membrane depolarization.8 The present findings demonstrate that stereoselective COX inhibition affects pacemaker potentials and contractility (electromechanic...

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“…The use of synthetic prostaglandin inhibitors, such as nonsteroidal anti-inflammatory drugs (NSAIDs), is considered nowadays the best and most effective way of treating patients who suffer from renal colics [4,6,7]. Nevertheless, NSAIDs exert undesirable side effects on the excretory tract: Perlmutter et al [8] demonstrated that the use of NSAIDs in subjects with acute obstruction of the excretory tract greatly reduces PRF, which remains low for a long period of time.…”

Section: Introductionmentioning

confidence: 99%

Evaluation of the Effects of Desmopressin in Acute Ureteral Obstruction

et al. 1999

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Objective: To evaluate the effects of desmopressin on pressure values inside the pelvis and ureter of the rat following acute obstruction. Materials and Methods: By means of a microsurgical technique, 24 male Wistar rats were submitted to ureteral obstruction; pressure inside the ureter was recorded using a cannula and a micrometric glass column. In the treatment group (14 animals) 6 mg/kg of desmopressin were administered 30 min before the beginning of the experiment. Results: Rats pretreated with desmopressin showed a statistically significant reduction in mean intraureteral pressure following acute obstruction (p = 0.05). Conclusions: In Wistar rats desmopressin demonstrated a powerful antidiuretic effect, reducing the intraureteral pressure. The experimental model is useful for a better understanding of physiopathology of renal colic and acute obstruction.

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Treatment of Ureteral Colic with Intravenous Indomethacin

Cited by 96 publications

References 6 publications

Neuroprotective Activity of Fructose-1,6-Bisphosphate Following Transient Forebrain Ischemia in the Mongolian Gerbil

Neuroprotective Activity of Fructose-1,6-Bisphosphate Following Transient Forebrain Ischemia in the Mongolian Gerbil

Modulation by stereoselective inhibition of cyclo‐oxygenase of electromechanical coupling in the guinea‐pig isolated renal pelvis

Evaluation of the Effects of Desmopressin in Acute Ureteral Obstruction

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