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Health care workers with frequent blood contact are at high risk of infection with hepatitis B virus. We surveyed 154 physician anesthesiologists (MD) and certified registered nurse anesthetists (CRNA) at four university-affiliated medical centers to determine the prevalence of serologic markers of hepatitis B virus (HBV). Questionnaires were used to ascertain historical and demographic information, nonoccupational risk factors, and characteristics of the participants' anesthesia practice. The overall prevalence of seropositivity was 18.8% (range 10.2-30.3%), and there were no statistically significant differences among the four centers, MD and CRNA groups, or males and females. In contrast to other studies, the prevalence of seropositive markers did not increase with an increase in the participants' age or length of time in the specialty. For the groups sampled in this study, geographic location or type of practice did not influence the increased prevalence of HBV seropositivity in anesthesia personnel. The current methods of HBV infection control were not associated with a decreased prevalence of serum markers. The majority of the susceptible anesthesia personnel at these four institutions did not plan to receive the hepatitis B vaccine when surveyed at the time of this study.

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Vagal reflexes are generally recognized as a possible cause of cardiac arrest during anaesthesia. Studies were performed to determine whether hypoxia, respiratory acidosis or deep halothane anaesthesia modify the cardiovascular effect of vagal stimulation (VS) in dogs. The animals were anaesthetized with intravenous urethane and chloralose, and paralysed with metocurine. Normal temperature and arterial blood gas variables were maintained and supramaximal VS was applied to the distal end of both vagus nerves for 5 min. No differences were found in any of the variables measured among the time periods when VS was repeated five times in six control dogs receiving urethane-chloralose basal narcosis only to determine the effects of time. VS resulted in 15 +/- 3 s (mean +/- s.e. mean) of asystole. Heart rate, cardiac output (CO) and mean arterial pressure (MAP) were still significantly decreased (P less than 0.001) and central venous pressure, right atrial pressure, pulmonary capillary wedge pressure (PCW), systemic (SVR) and pulmonary vascular resistance significantly increased (P less than 0.01--P less than 0.001) at the end of stimulation when compared to values before VS in all 24 dogs. Neither hypoxia [PaO2 5.3 kPa (40 mmHg)] nor respiratory acidosis [pH 7.00, PaCO2 10.6 kPa (80 mmHg)] modified these effects of VS. VS during halothane anaesthesia (1.6% end-tidal concentration) resulted in further significant decreases (P less than 0.05--P less than 0.001) in CO, MAP, mean pulmonary arterial pressure, PCW and SVR when compared to VS under basal narcosis. VS under halothane anaesthesia combined with hypoxia or respiratory acidosis did not decrease the cardiovascular parameters as much as VS under halothane anaesthesia alone. VS alone, or in combination with hypoxia or respiratory acidosis, failed to cause persistent asystole.

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Halothane-induced changes in renal function have generally been attributed to alterations in systemic hemodynamics, sympathetic tone, and various hormones. Studies were performed to determine whether halothane directly affects the kidney. Twenty-one canine kidneys were perfused in vitro utilizing hemodilution, pulsatile flow, and membrane oxygenation. Temperature and arterial blood-gas variables were controlled and mean and pulse pressures were maintained. Four experimental periods (I-IV)(each consisting of two 10-min sample collection periods) were conducted, with a 20-min "rest" period between succeeding experimental periods (elapsed time = 140 min). Responsiveness was assured by obtaining a normal response to furosemide, acetylcholine, or epinephrine after Period IV. In eight additional kidney preparations halothane was administered to achieve either a "low" (17 +/- 3 mg/100 ml) or "high" (35 +/- 5 mg/100 ml) concentration in Period II, the sequence reversed for Period III, and halothane eliminated by Period IV. Halothane produced marked increases in blood flow (21-26 per cent), total (203-267 per cent) and fractional (173-179 per cent) sodium excretion, osmolal clearance (62-111 per cent) and urinary volume (130-161 per cent). These changes were associated with a shift of microspheres from outer to inner cortex, and were completely reversible by eliminating the halothane. In the absence of external influences, halothane produces renal vasodilation and natriuresis. Direct tubular depression cannot be ruled out.

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Renal blood flow, when not affected by humoral or neural influences, remains relatively constant over a wide range of renal arterial perfusion pressures. This phenomenon, referred to as "autoregulation," is an important mechanism allowing kidneys to maintain homeostasis of the internal milieu over a wide range of arterial pressures. The present study showed that 0.9 per cent halothane had no effect on autoregulation in an isolated, perfused dog kidney as renal arterial perfusion pressure was varied between 75 and 125 torr.

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The effects of four commonly used halogenated anesthetic agents (methoxyflurane, halothane, enflurane and fluroxene) on rho-aminohippurate (PAH) uptake by rabbit renal cortical slices were examined. All agents depressed PAH uptake in a linear dose-dependent manner after 60 minutes of incubation and the effect was reversible. When the data were normalized for anesthetic potency, all agents exhibited a parallel dose-response curve. Since these agents do not share a common metabolite, it is concluded that the depression of PAH transport is mediated primarily by a direct effect of the agents acting through a common pathway. Exposure of kidney slices to perithreshold concentrations of halothane and enflurane for 180 minutes did not result in a cumulative inhibitory effect on PAH transport. A slight time-dependent effect was seen with methoxyflurane. It is suggested that with prolonged exposure metabolic conversion of methoxyflurane may occur leading to further inhibition of PAH uptake.

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Nonrecollection end-proximal tubule micropuncture technique and the microsphere method for estimating fractional distribution of renal cortical blood flow were applied to further define the mechanism of the natriuresis in the isolated dog kidney in response to volume expansion with equilibrated blood. Following volume expansion sodium excretion increased +79 plus or minus 24 muEq/min (P less than 0.01) in the face of significant decreases in inulin clearance (C IN) and renal blood flow (RBF) and in the absence of changes in renal perfusion pressure, plasma protein concentration or packed cell volume. (TF/P)IN of end-proximal tubular fluid decreased from 1.65 plus or minus 0.03 to 1.53 plus or minus 0.04, P less than 0.025, and proximal tubule absolute reabsorption decreased from 36 plus or minus 3 to 29 plus or minus 2 nl/min, P less than 0.05. The decrease in absolute reabsorption, however, was balanced by a decrease in single nephron GFR (SNGFR) so that no increase in distal delivery of fluid (V TF) out of the proximal tubule was detected. SNGFR/C-IN remained constant. No change in fractional distribution of RBF was detected. The data indicate that volume expansion with equilibrated blood depresses proximal tubule fractional and absolute reabsorptive rates in the isolated kidney but since V-TF did not increase, they imply that the natriuresis derives from a decrease in sodium transport along more distal nephron segments.

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