We explored the possible mechanisms of hypotension during the administration of sedation-analgesia doses of remifentanil in young (ASA physical status I) volunteers (n = 24). Cardiorespiratory and sympathetic variables were collected at baseline and at plasma concentrations of remifentanil (2 and 4 ng/mL). Monitoring included electrocardiogram, heart rate (HR), direct blood pressure, muscle sympathetic nerve activity, and forearm blood flow (FBF). A cold pressor test (1-min hand immersion in ice water) quantified analgesia effectiveness (visual analog scale, 0-100). Visual analog scale to the cold pressor test (62 at baseline) decreased to 27 and 18 during remifentanil infusions. Respiratory rate decreased and end-tidal carbon dioxide (ETCO(2)) increased with increasing doses of remifentanil; HR, direct blood pressure, muscle sympathetic nerve activity, SpO(2) remained unchanged, but FBF increased compared with placebo. In a second study (n = 7), timed respiration was used to maintain ETCO(2) during remifentanil, but FBF still increased. In a third study (n = 11), direct effects of remifentanil on vascular tone were determined with progressive infusions from 1 to 100 micro g/h into the brachial artery; FBF increased significantly from 3.5 to 4.3 mL/min per 100 mL of tissue (approximately 13%-18% increase). Sedative doses of remifentanil resulted in analgesia but no changes in neurocirculatory end-points except FBF. Direct effects of remifentanil on regional vascular tone may play a role in promoting hypotension. IMPLICATIONS: Remifentanil occasionally has been associated with hypotension, the mechanism of which is unclear. This study found that remifentanil directly causes the forearm arterial vasculature to dilate. 相似文献
BACKGROUND: An understanding of demographic differences in injury types among the elderly will help in targeting interventions. METHODS: Rates were calculated from the 1997 to 1999 National Hospital Ambulatory Medical Care Surveys by dividing the estimated number of visits by census population estimates. Age-adjusted standardized morbidity ratios were calculated to facilitate comparison between genders and between races. RESULTS: Although men had fewer fractures than expected on the basis of the rate for women (standardized morbidity ratio = 0.57), they had more open wounds (standardized morbidity ratio = 1.785, p < 0.001). Blacks had fewer fractures than expected, based on the rates for whites (standardized morbidity ratio = 0.601, p = 0.004) but had higher visit rates than expected for less severe injuries such as contusions, strains, and sprains. CONCLUSION: The trends noted in the present analysis suggest interventions for improved machinery safety targeted at elderly men and a continuing focus on access to primary care for minority elderly. 相似文献
Patients with pseudocholinesterase (BChE) variants may exhibit markedly prolonged paralysis after the administration of succinylcholine or mivacurium. We sought to evaluate to what extent molecular biology may contribute to the biological assessment of such patients. We conducted a prospective cohort study in patients referred to our center between 1995 and 1999 for prolonged neuromuscular blockade after mivacurium or succinylcholine. For each patient, phenotyping was performed with a conventional biochemical technique and molecular biology for the detection of the atypical mutation (A variant). Among the 36 patients referred, 31 had low BChE activity, 26 had received mivacurium (BChE activity, 2.1 U/mL; 0.3-4.3 U/mL), and 5 had received succinylcholine (BChE activity, 1.9 U/mL; 1.1-3.2 U/mL) (mean; extreme values). The mean clinical duration of paralysis was 90 min (40-140 min) after succinylcholine and 301 min (120-720 min) after mivacurium. Thirty-two patients had a BChE deficiency of genetic origin: 20 were homozygous (AA), 10 were heterozygous (UA) for the A variant, and 2 did not have the A mutation (UU). One heterozygous UA patient had normal BChE activity. Nine among the heterozygous UA and the two homozygous UU patients probably carried a not-screened variant. In most cases, biochemical diagnosis was sufficient to confirm the existence of constitutional deficiency; molecular biology improved the accuracy of diagnosis in 11 patients (30%) but had few or no clinical implications for the patient him- or herself. IMPLICATIONS: Systematic screening for the pseudocholinesterase atypical variant by biochemical and DNA analysis after a prolonged neuromuscular blocking effect of succinylcholine or mivacurium shows that molecular biology could improve the diagnosis in approximately one third of patients, but with few clinical implications, compared with biochemical testing. 相似文献
Compared with equi-minimum alveolar anesthetic concentration (MAC) isoflurane, desflurane is associated with greater levels of sympathetic nerve activity in humans but similar reductions in blood pressure. To explore these divergent effects, we evaluated vascular alpha(1)-adrenoceptor responses in the human forearm during isoflurane and desflurane anesthesia to determine if alpha(1)-adrenoceptor responses were more substantially attenuated during desflurane administration. Bilateral forearm venous occlusion plethysmography was used to examine arterial blood flow and to determine changes in forearm vascular resistance during brachial artery infusions of saline and phenylephrine (0.2, 0.4, 0.8, and 1.6 microg/min) in 22 conscious subjects and during anesthesia with 0.65 and 1.3 MAC isoflurane or desflurane. Infusion of phenylephrine into the brachial artery increased the forearm vascular resistance in a dose-dependent manner. The arterial response to phenylephrine was significantly attenuated by 0.65 and 1.3 MAC desflurane and similarly attenuated during 1.3 MAC isoflurane (P < 0.05). Impaired arterial alpha(1)-adrenoceptor responsiveness occurred during desflurane. However, this effect was statistically similar (P > 0.05) to the impaired responses during isoflurane. Blood pressure decreases during volatile anesthesia may be, in part, caused by decreased alpha(1)-adrenoceptor responsiveness. IMPLICATIONS: alpha-receptors on blood vessels regulate constriction and dilation and therefore modulate blood pressure. This research indicates that vasoconstriction via the alpha(1)-receptor vascular response is impaired during isoflurane and desflurane anesthesia. 相似文献
Background: Bronchospasm is a potential complication in anyone undergoing general anesthesia. Because volatile anesthetics relax bronchial smooth muscle, the effects of two newer volatile anesthetics, desflurane and sevoflurane, on respiratory resistance were evaluated. The authors hypothesized that desflurane would have greater bronchodilating effects because of its ability to increase sympathetic nervous system activity.
Methods: Informed consent was obtained from patients undergoing elective surgery with general anesthesia. We recorded airway flow and pressure after thiopental induction and tracheal intubation (baseline) and for 10 min after beginning volatile anesthesia (~ 1 minimum alveolar concentration inspired). Respiratory system resistance was determined using the isovolume technique.
Results: Fifty subjects were randomized to receive sevoflurane (n = 20), desflurane (n = 20), or thiopental infusion (n = 10, 0.25 mg [middle dot] kg-1 [middle dot] h-1). There were no differences between groups for age, height, weight, smoking history, and American Society of Anesthesiologists physical class. On average, sevoflurane reduced respiratory resistance 15% below baseline, whereas both desflurane (+5%) and thiopental (+10%) did not decrease respiratory resistance. The respiratory resistance changes did not differ in patients with and without a history of smoking during sevoflurane or thiopental. In contrast, administration of desflurane to smokers resulted in the greatest increase in respiratory resistance. 相似文献
Haim-Munk syndrome is an extremely rare autosomal recessive disorder of keratinization characterized clinically by palmoplantar hyperkeratosis, severe early onset periodontitis, onychogryphosis, pes planus, arachnodactyly, and acro-osteolysis. Recently, germline mutations in the lysosomal protease cathepsin C gene have been identified as the underlying genetic defect in Haim-Munk syndrome and in the clinically related disorders, Papillon-Lefèvre syndrome and prepubertal periodontitis. 相似文献