PubMed Health⌕ Search

Biomedical subjects

Errol Lobo

Publications and source records attributed to Errol Lobo.

5 recordsLinked to original sources
PubMed2006

Laparoscopic fundoplication in elderly patients with gastroesophageal reflux disease.

HYPOTHESIS: It is unclear if age should be considered a factor in the choice of treatment for gastroesophageal reflux disease (GERD) and if fundoplication in elderly patients is as safe and effective as it is in younger patients. We hypothesized that the outcome of laparoscopic antireflux operations in patients younger than 65 years is similar to that of patients 65 years and older. DESIGN: Retrospective review of findings from a prospectively acquired database. SETTING: University-based tertiary care center. PATIENTS: Three hundred four consecutive patients underwent laparoscopic fundoplication for GERD. Two hundred forty-one patients were younger than 65 years (group A; median age, 46 years), and 63 patients were 65 years or older (group B; median age, 69 years). MAIN OUTCOME MEASURES: Presence, duration, and severity of GERD symptoms; presence of a hiatal hernia or esophageal stricture; duration of operation; incidence of complications; and length of hospital stay. RESULTS: Elderly patients more often had regurgitation and respiratory symptoms in addition to heartburn. Hiatal hernias were more common among elderly patients (77% vs 51%). The duration of the operation was similar for the 2 groups. The incidence of intraoperative and postoperative complications was low and similar in the 2 groups. The median hospital stay was 24 hours for each group. Heartburn resolved in approximately 90% of patients in each group. CONCLUSIONS: Elderly patients more often had hiatal hernias and respiratory symptoms. Laparoscopic antireflux surgery was as safe in elderly patients as it was in younger patients, and clinical outcomes were as good.

Adolescent↗
PubMed2005

Effect of alpha2B-adrenoceptor polymorphism on peripheral vasoconstriction in healthy volunteers.

BACKGROUND: Alpha-2B adrenoceptor is the vasoconstrictive subtype in the mouse. Human alpha2B-AR deletion (D) allele has been associated with loss of short-term agonist-promoted receptor desensitization, which may lead to increased vasoconstriction on alpha2 activation. The goal of this study was to test the hypothesis that alpha2B-adrenoceptor activation induces enhanced vasoconstriction in carriers of the DD genotype, compared with carriers of the insertion/insertion (II) genotype. METHODS: The authors administered increasing doses of dexmedetomidine (targeting plasma concentrations of 0.15, 0.3, 0.6, and 1.2 ng/ml) to 16 healthy young volunteers (8 carrying the alpha2B DD genotype, 8 carrying the II genotype) in whom sympatholytic effects of the drug were attenuated by general anesthesia. Measurements were made of finger blood volume (an indicator of vasoconstriction) by photoplethysmographic determination of light transmitted through a finger, finger blood flow by venous occlusion plethysmography, and hemodynamic variables. RESULTS: All concentration of dexmedetomidine increased light transmitted through the finger (vasoconstriction) and systolic blood pressure and decreased heart rate in both groups (P < 0.001 for all). Dexmedetomidine reduced finger arterial inflow only in the DD group (P < 0.001). Dexmedetomidine had no effect on finger venous outflow or venous capacitance. There were no significant differences between the II and DD groups in any of the variables. CONCLUSIONS: The results of this study confirm the alpha2 agonist induced vasomotor and hemodynamic effects in peripheral vasculature. However, the results do not support the hypothesis that alpha2B-adrenoceptor polymorphism has an effect on peripheral vasoconstriction in humans.

Adrenergic alpha-Agonists↗
PubMed2005

Alpha-2B adrenoceptor polymorphism and peripheral vasoconstriction.

OBJECTIVES: Alpha-2B adrenoceptors (AR) mediate vasoconstriction in the mice. A human alpha-2B AR deletion (D) variant has been associated with loss of short-term agonist-promoted receptor desensitization, which may lead to increased vasoconstriction upon alpha-2 AR activation. This study tested the hypothesis that alpha-2 AR activation will induce enhanced vasoconstriction in carriers of the alpha-2B AR DD genotype, compared to carriers of the II or the DI genotypes. METHODS: We administered 1 microg/kg dexmedetomidine (an alpha-2 agonist) intravenously to 80 surgical patients in whom sympatholytic effects of the drug were attenuated by general anesthesia. Measurements were made of finger blood volume (an indicator of vasoconstriction) by photoplethysmographic determination of light transmission through a finger (LTF) and of hemodynamic variables. RESULTS: Dexmedetomidine increased LTF (vasoconstriction), induced an initial increase in systolic blood pressure and decreased heart rate in all genotype groups (P<0.0001 for all). Three min after the start of dexmedetomidine infusion, the increase in LTF was more pronounced (P=0.014) in the DD group compared to the DI and II groups. There were no significant differences in LTF values between the groups at the end of or 5 min after dexmedetomidine infusion. There were no differences in systolic blood pressure or heart rate values between the groups during or after the dexmedetomidine infusion. CONCLUSIONS: The results of this study confirm that the alpha-2 agonist dexmedetomidine induced marked peripheral vasoconstriction. Subjects with the alpha 2B DD genotype had an enhanced vasoconstrictive response at the beginning of dexmedetomidine infusion. However, this enhanced vasoconstrictive response was not sustained throughout or after the 15-min dexmedetomidine infusion.

Adrenergic alpha-2 Receptor Agonists↗
PubMed2003

Systemically administered alpha2-agonist-induced peripheral vasoconstriction in humans.

BACKGROUND: alpha(2)-Adrenoceptors mediate both sympatholytic and vasoconstrictive hemodynamic effects. The goal of this study was to profile the peripheral vasoconstrictive effects of a selective alpha(2)-adrenoceptor agonist in isolation from the sympatholytic effects it also induces. METHODS: The authors administered increasing plasma target concentrations of dexmedetomidine (0.075, 0.15, 0.3, and 0.6 ng/mL) or saline placebo to healthy young volunteers in whom the sympatholytic effects of the drug were attenuated in one of two ways: general anesthesia (propofol-alfentanil-nitrous oxide) or axillary brachial plexus block. Measurements were made of finger blood volume (an indicator of vasoconstriction) by photoplethysmographic determination of light transmitted through a finger (LTF) and hemodynamic variables. Measurements made before and during the four steps of infusion were compared by repeated-measures ANOVA. RESULTS: In anesthetized volunteers, all concentrations of dexmedetomidine increased LTF (vasoconstriction) and systolic blood pressure (P < 0.001 for both), whereas placebo did not. In awake volunteers, all concentrations decreased systolic blood pressure (P < 0.001). Concentrations of 0.15, 0.3, and 0.6 ng/mL decreased LTF (vasodilation) in the neurally intact hand; in contrast, the same concentrations increased LTF (vasoconstriction) in the sympathectomized hand (P < 0.001 for both). CONCLUSIONS: The results of this study are the first to characterize the lower end of the dose-response curve for vasoconstriction induced by dexmedetomidine. By denervating the vascular bed of interest or by decreasing sympathetic nervous system activity, the authors were able to observe vasoconstriction induced by a systemically administered alpha(2)-agonist with minimal interference from the sympatholytic effects of the drug.

Adrenergic alpha-2 Receptor Agonists↗