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R Segstro

Publications and source records attributed to R Segstro.

5 recordsLinked to original sources

Indomethacin as a postoperative analgesic for total hip arthroplasty.

This prospective, randomized, double-blind trial evaluated the efficacy of rectal indomethacin as an adjunct to morphine for controlling postoperative pain. Fifty healthy patients undergoing elective hip arthroplasty were investigated. Group 1 (n = 25) received placebo suppositories, Group 2(n = 25) received indomethacin suppositories, 100 mg q8hr for five doses, starting at the end of the procedure. Both groups received morphine via a PCA pump, which recorded the amount of morphine delivered each hour. After a standardized general anaesthetic, PCA was begun in the recovery room. Pain was measured with a standard 100 mm VAS at 2, 6, 20, 28, 42 hr after surgery and the morphine consumption recorded. Over the 42-hr study period, patients in Group 2 required less morphine than those in Group 1 (34.8 +/- 21.8 mg vs 89.6 +/- 43.7, P less than 0.01). Pain scores were lower in Group 2 at 20, 28, 42 hr postoperatively. The incidence of side-effects did not differ between groups and no patient had excessive postoperative bleeding. The combination of indomethacin and morphine provided superior pain relief to morphine alone even though the control group had liberal access to morphine. This synergistic effect would make indomethacin a useful adjunct to intramuscular or epidural narcotics.

Administration, Rectal

Nasal sensor attachment.

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Blood Gas Monitoring, Transcutaneous

Effects of nifedipine on hepatic blood volume in cats: indirect venoconstriction and absence of inhibition of postsynaptic alpha 2-adrenoceptor responses.

Intravenous administration of hypotensive doses (30-200 micrograms/kg) of nifedipine to cats anesthetized with pentobarbital caused an increase in cardiac output accompanied by hepatic venoconstriction. The hepatic venoconstriction and the increase in cardiac output were abolished in animals in which the hepatic sympathetic nerves were cut, the adrenal glands were excluded, and the kidneys were removed. This contrasts with the indirect hepatic venoconstrictor action of isoproterenol which was shown previously not to be abolished by these procedures. Further experiments showed that the hepatic venoconstrictor effect of nifedipine was blocked by removal of the kidneys, but not by removal of the hepatic sympathetic nerves and adrenals. These results support the hypothesis that venoconstriction plays an important role when drugs produce increased cardiac output. In nephrectomized animals, nifedipine had no direct effects on hepatic blood volume and it did not alter the effects of infusions of norepinephrine on hepatic blood volume, which have previously been shown to be mediated through alpha 2-adrenoceptors. However, it did reduce the hepatic venous responses to hepatic sympathetic nerve stimulation by 30%.

Animals

Alpha adrenoceptor subtype mediating sympathetic mobilization of blood from the hepatic venous system in anesthetized cats.

Previous studies have suggested that sympathetic effects on hepatic blood volume may be mediated through alpha-2 adrenoceptors in anesthetized cats as prazosin did not block whereas phentolamine and phenoxybenzamine impaired these responses markedly. In this study we have shown that yohimbine blocks hepatic volume responses to both nerve stimulation and norepinephrine infusions. In comparison with norepinephrine, phenylephrine had much weaker effects on hepatic blood volume than on arterial and portal pressures. Clonidine produced a slow weak contraction of the hepatic venous bed which was blocked by yohimbine but not by prazosin. alpha-Methylnorepinephrine produced a norepinephrine-like contraction of the hepatic venous bed which was blocked by yohimbine but not by prazosin. Taken together, these data suggest that hepatic blood volume responses to both sympathetic nerve stimulation and infusions of catecholamines are mediated through alpha-2 adrenoceptors, whereas portal pressure responses are mediated through both alpha-1 and alpha-2 adrenoceptors.

Anesthesia