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PubMed2003

In vitro relaxation of vascular smooth muscle by atropine: involvement of K+ channels and endothelium.

Cumulative addition of atropine to the organ bath containing endothelium-intact (+E) rat aorta, which was precontracted with phenylephrine (PE, 1 microM) and subsequently relaxed with carbachol (1 microM), caused biphasic changes in the vascular contractility of +E rat aortic rings. Low concentrations of atropine (10 nM-1.0 microM) caused progressive restoration of contraction to PE; whereas at higher concentrations (1-100 microM), atropine caused progressive relaxation. Atropine-induced aortic relaxation was significantly inhibited upon endothelium removal by either rubbing or saponin treatment, but considerable relaxation still persisted in the range of 30-100 microM atropine. Similar findings were also obtained when the nitric oxide (NO) generation was inhibited with 300 microM NO synthase inhibitor, L-NAME. Atropine-induced relaxation was also observed when 5-hydroxytryptamine (5-HT) was used as the agonist and the atropine-relaxation was more potent at lower concentrations of PE and 5-HT. However, atropine had no effect on the contraction elicited by KCl or prostaglandin F(2 alpha). Also, atropine-induced relaxation was not affected by indomethacin (1-10 microM), nicotine (10-100 microM) or hexamethonium (30 microM). Pretreatment of +E aorta with tetraethylammonia (TEA, 3-10 mM) or 4-aminopyridine (4-AP, 1-3 mM) showed prominent inhibitory effect on atropine-induced relaxation; on the other hand, preincubation with glibenclamide (1-10 microM), BaCl(2) (1-30 microM) or 2 microM charybdotoxin and apamin, had little effect on the relaxation induced by atropine. When added to tissues after relaxation to atropine, TEA and 4-AP concentration-dependently reversed the relaxation in -E aorta, whereas in +E aorta, TEA up to 30 mM and 4-AP up to 10 mM only partially affected atropine-induced relaxation. Although TEA and 4-AP potentiated the PE-contraction, such potentiation is unlikely to contribute to the change in sensitivity to atropine-induced relaxation, since in the presence of 15 mM KCl, which also potentiated PE-contraction to a comparable extent, the atropine-relaxation remains unchanged. Scopolamine also acts like atropine, except that the effect of scopolamine was smaller than that of atropine and is primarily endothelium-dependent. Atropine-induced relaxation also occurs in medium artery (renal artery) and small muscular artery (mesenteric artery). In conclusion, atropine-relaxation is mediated in part via voltage-dependent K(+) channels in both smooth muscle and endothelium and forms the mechanistic basis for the observed vasodilation, reduced blood pressure and facial flushing following atropine overdose.

Animals↗
PubMed2004

Pediatric rapid sequence intubation: incidence of reflex bradycardia and effects of pretreatment with atropine.

BACKGROUND: The American College of Emergency Physicians (ACEP) recommends atropine as adjunctive therapy to prevent reflex bradycardia prior to laryngoscopy/tracheal intubation (L/TI) in pediatric patients. OBJECTIVE: To describe the incidence of reflex bradycardia and its relationship to the administration of atropine during L/TI in a Pediatric Emergency Department. DESIGN/METHODS: A retrospective cohort study was designed through review of records of all patients who received L/TI in the ED at an urban children's hospital from January 1997 to March 2001. Patients meeting inclusion criteria were placed into cohorts defined by whether they had received atropine prior to L/TI or not. RESULTS: One hundred sixty-three patients received L/TI during the study period. One hundred forty-three patients met inclusion criteria. Sixty-eight patients received atropine (atropine group) prior to L/TI. Seventy-two percent of atropine group patients met ACEP criteria for atropine pretreatment. Seventy-five patients did not receive atropine pretreatment (no-atropine group). Forty-three percent of no-atropine group patients met ACEP criteria for pretreatment with atropine. The atropine group was younger [mean 22.5 vs. 36.4 months, P = 0.003, 95% CI (-28.5, 0.70)], averaged the same number of intubation attempts [1.6 vs. 1.5, P = 0.941, 95% CI 0.1 (-0.3,0.4)], and had normal or elevated HR for age prior to L/TI (mean 159 bpm). Hypoxia occurred more often in the atropine group [28% vs. 16%, P = 0.046, 95% CI for difference (0.3, 27.1)]. Bradycardia was noted in 6 patients during L/TI; 3 in the atropine group and 3 in the no-atropine group. CONCLUSION: Atropine is not routinely administered prior to L/TI in this pediatric ED. Pretreatment with atropine did not prevent bradycardia in all cases. These data suggest that use of atropine prior to L/TI may not be required for all pediatric patients. Some patients will experience bradycardia regardless of atropine pretreatment.

Adolescent↗
PubMed2000

The use of intravenous atropine after a saline infusion in the prevention of spinal anesthesia-induced hypotension in elderly patients.

UNLABELLED: We investigated the efficacy of IV atropine for preventing spinal anesthesia-induced hypotension in elderly patients. Seventy-five patients undergoing transurethral prostate or bladder surgery were randomized to receive either placebo (n = 25), atropine 5 microg/kg (small-dose atropine, n = 25) or atropine 10 microg/kg (large-dose atropine, n = 25) after the induction of spinal anesthesia. All the patients received an IV infusion of 10 mL/kg 0.9% normal saline over 10 min before the induction of anesthesia. The systolic blood pressure decreased in all three groups after spinal anesthesia. There was a significant increase in the mean heart rate in both atropine groups as compared to the placebo group (placebo group: 78 bpm, 95% confidence interval [CI]: 76.6-78.5; small-dose atropine group: 86 bpm, 95% CI 83.9-88.8; large-dose atropine group: 97 bpm, 95% CI 94.5-100.3; P: = 0.001). There was a significant decrease in the incidence of hypotension in patients who received atropine (placebo group: 76%, small-dose atropine group: 52%, large-dose atropine group: 40%, P: = 0.03). The mean dose of ephedrine required was significantly decreased in the atropine groups (placebo group: 12.2 mg [SD= 10.5], small-dose atropine group: 7.4 mg [SD= 10.0], large-dose atropine group: 5.4 mg [SD= 8.7 mg], P: = 0.048). The total amount of IV fluid and number of patients requiring metaraminol in addition to 30 mg of ephedrine were not significantly different among the three groups. Significant side effects, such as confusion, ST segment changes or angina were not detected in any of the patients. We conclude that IV atropine may be a useful supplement to the existing methods in preventing hypotension induced by spinal anesthesia. IMPLICATIONS: IV atropine increases heart rate in a dose-dependent manner in elderly patients undergoing spinal anesthesia. It reduces the incidence of hypotension and the dose of ephedrine required. Small-dose atropine may be a useful supplement in preventing spinal anesthesia-induced hypotension in elderly patients.

Aged↗