Given a passage, construct a question on the basis of the information present in the passage. Construct the question in such a way that (i) it is unambiguous, (ii) it is answerable from the passage, (iii) its answer is unique (iv) it answer uses text phrases from the passage. Avoid creating questions that (i) can't be answered correctly without actually understanding the passage and (ii) uses the same words or phrases given in the passage.

Q: The local anesthetic properties of tetrodotoxin, a potent naturally occurring sodium channel blocker, have been recently reexamined. It was found that sciatic nerve block duration could be greatly increased and systemic toxicity greatly decreased if epinephrine was injected with tetrodotoxin. The mechanism that underlies epinephrine-mediated prolongation of tetrodotoxin nerve blocks is not known, but indirect evidence suggests that epinephrine may slow the clearance of tetrodotoxin from the site of injection. The authors hypothesized that tetrodotoxin causes vasodilatation at its injection site, which accelerates its systemic uptake, and that this vasodilatation is attenuated by coinjected epinephrine.', 'The radiolabeled microsphere technique was used to measure tissue blood flow in anesthetized rats before and after perisciatic injection of tetrodotoxin alone and in combination with epinephrine.', 'Tetrodotoxin, in a dose of 0.1 ml of a 60 microM solution, significantly increased blood flow in perisciatic muscle at the injected side compared with simultaneous contralateral control and ipsilateral preinjection baseline. Tetrodotoxin did not increase blood flow in the sciatic nerve. Coinjection of epinephrine with tetrodotoxin prevented tetrodotoxin-induced increases in perisciatic muscle blood flow over time and did not alter sciatic nerve blood flow. Arterial blood pressure was maintained with this dose of tetrodotoxin, although brain blood flow decreased. Coinjection of epinephrine with tetrodotoxin prevented decreases in brain blood flow. Higher doses of tetrodotoxin produced hypotension.

A: Does epinephrine prevent muscle blood flow increases after perineural injection of tetrodotoxin?
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Q: Repeated hypoglycemia is associated with hypoglycemia-associated autonomic failure (HAAF), a syndrome of defective counterregulation.', 'HAAF increases the risk of severe hypoglycemia in diabetes, although its mechanism remains unresolved. Because beta-endorphin influences the autonomic response to hypoglycemia via opioid receptor activation, we hypothesized that it is also involved in the pathogenesis of HAAF.', 'We asked whether opioid receptor blockade during antecedent hypoglycemia (60 mg/dl) on d 1 would prevent development of HAAF on d 2 in eight nondiabetic subjects (five males, 3 females; age, 28 +/- 3.5 yr; body mass index, 24.2 +/- 2.1 kg/m(2)). On four occasions, d 1 was: 1) two 90-min hypoglycemic clamps (N-); 2) two 90-min hypoglycemic clamps plus naloxone (N+); 3) two euglycemic 90-min clamps (C); or 4) two euglycemic 90-min clamps plus naloxone (C+).', 'Day 1 hypoglycemia caused marked deterioration of d 2 hormonal responses to hypoglycemia, consistent with HAAF-i.e. decreased plasma epinephrine, norepinephrine, and glucagon compared to control (C) (374 +/- 71 vs. 810 +/- 94, 307 +/- 65 vs. 686 +/- 98, and 71 +/- 9 vs. 93 +/- 4 pg/ml, respectively, P < 0.01), as well as in endogenous glucose production (24 vs. 163%; P < 0.01). In contrast, naloxone on d 1 completely prevented the defective counterregulatory responses; epinephrine, norepinephrine, and glucagon (852 +/- 82, 769 +/- 77, and 98 +/- 7 pg/ml) and endogenous glucose production recovery (167%) were identical to those after d 1 euglycemia (P < NS for all). Infusion of naloxone alone during euglycemia on d 1 (C+) had no effect on d 2 responses.

A: Is hypoglycemia-associated autonomic failure prevented by opioid receptor blockade?
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Q: We evaluate the frequency of empiric acyclovir administration to patients in the emergency department (ED) who are ultimately diagnosed with encephalitis.', "We conducted an explicit retrospective medical record review of consecutive patients discharged with a final diagnosis of herpes simplex encephalitis or viral encephalitis not otherwise specified for the period 1993 to 2003. The frequency of ED administration of empiric acyclovir was measured for patients who met the inclusion criteria of fever, neuropsychiatric abnormality, and cerebrospinal fluid pleocytosis with a negative Gram's stain result in the ED.", "Of the 90 patients reviewed, 24 (27%) met the inclusion criteria of fever, neuropsychiatric abnormality, and cerebrospinal fluid pleocytosis with a negative Gram's stain result in the ED. Of these 24 patients, 7 (29%) received empiric acyclovir in the ED, 6 (86%) patients after cerebrospinal fluid results were available, with a median time to administration of 1.5 hours (95% confidence interval [CI] 0 to 3.1 hours). The remaining 17 (71%) patients did not receive acyclovir in the ED, with median times of 16 hours (95% CI 7.5 to 44 hours) before initiation of acyclovir in inpatient settings.

A:
Is empiric acyclovir infrequently initiated in the emergency department to patients ultimately diagnosed with encephalitis?
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