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To determine the effect of halothane on cerebral blood flow velocity measured by transcranial Doppler, 23 healthy young children were studied during surgery. Anaesthesia was induced with thiopental, fentanyl and vecuronium, and maintained with halothane in 70% nitrous oxide in oxygen. A continuous epidural anaesthesia with 0. 25% bupivacaine was performed. End-tidal carbon dioxide pressure, temperature, heart rate and systolic blood pressure were kept constant. Three minimal alveolar concentrations (MAC; 0.5, 1.0 and 1. 5) of halothane were administered in stepwise increases. The cerebral blood flow velocity increased significantly at 1.0 (p < 0. 01) and 1.5 MAC (p < 0.001) compared with the value at 0.5 MAC. No further change in cerebral blood flow velocity was seen between 1.0 and 1.5 MAC. These data show that maximal changes in cerebral blood flow velocity are obtained at 1.0 MAC and that further increases in halothane concentration do not modify the cerebral circulation. It is suggested that young children differ from adults in that the maximal effect of halothane occurs at lower concentrations.

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To determine whether the incidence of masseter muscle rigidity is affected by the anaesthetic induction sequence, we prospectively studied for ten months the anaesthetic course in 5,641 infants and children who received muscle relaxation to facilitate tracheal intubation. The anaesthetic induction sequence consisted of intravenous sodium thiopentone (STP) 5 mg.kg-1 alone, halothane induction alone 1-4%, or halothane followed by STP. Inhalational inductions with halothane included nitrous oxide and oxygen. Tracheal intubation was facilitated by either intravenous succinylcholine (Sch) at least 1.5 mg.kg-1 or by a non-depolarizing muscle relaxant. The induction sequence and all episodes of MMR were recorded. Ninety percent of the patients received Sch and 10% received a non-depolarising agent. Of those who received Sch, 88% (5,064 patients) were anaesthetised with STP and 12% (607 patients) were anaesthetised with halothane alone or halothane followed by STP. Masseter muscle rigidity was defined clinically by the transient inability to distract the mandible from the maxilla such that the mouth could not be opened or could only be opened with force. No children anaesthetised with STP followed by Sch developed MMR. One child (0.9%) developed MMR after halothane and Sch and two developed MMR after halothane, STP and Sch (0.4%). The incidence of MMR after Sch was less with STP than with halothane alone or with halothane and STP (P < 0.025). The peak CPK values in the three children who developed MMR were 17,580 IU.L-1 after halothane and Sch, and 7,280 IU.-1 and 3,273 IU.-1 after halothane, STP and Sch. There was no evidence of MH reactions in these patients.(ABSTRACT TRUNCATED AT 250 WORDS)

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The purpose of this study was to evaluate the stability of the arterial PCO2 (PaCO2) to end-tidal PCO2 (PETCO2) partial pressure difference (Pa-ETCO2) during surgery using PETCO2 monitoring, in children with congenital heart disease (CHD). Forty children with CHD were studied: ten children with no interchamber communication and normal pulmonary blood flow (PBF) (normal group); ten acyanotic children with increased PBF (acyanotic-shunting group); ten cyanotic children with mixing type lesions and normal or increased PBF (mixing group), and ten cyanotic children with right-to-left intracardiac shunts demonstrating decreased and variable PBF (cyanotic-shunting group). Simultaneous PaCO2 recordings and PETCO2 measurements were obtained for each patient during five intraoperative events: (1) control time, arterial line placement under anaesthesia; (2) time 1, patient preparation; (3) time 2, immediately after sternotomy; (4) time 3, after heparin administration; and (5) time 4, immediately after aortic cannulation. Initially, cyanotic children demonstrated a greater Pa-ETCO2 compared with acyanotic children (P less than 0.05). There was no difference in the Pa-ETCO2 over time in the control, acyanotic-shunting, or mixing groups. The Pa-ETCO2 in the children with cyanotic-shunting lesions at times 2 and 3 was greater (P less than 0.05) than at their control times. We conclude that the Pa-ETCO2 of children with acyanotic-shunting and mixing congenital heart lesions is stable intraoperatively, although patients with mixing congenital heart lesions may demonstrate large individual variations. In children with cyanotic-shunting congenital heart lesions, the Pa-ETCO2 is not stable. The PETCO2 cannot be used during surgery to estimate reliably the PaCO2 in children with cyanotic CHD.

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The beneficial effect of dopamine in circulatory shock induced by tricyclic antidepressants (TCA) overdose may be decreased due to compromise of the endogenous stores of norepinephrine caused by TCA. The successful outcome of two cases of TCA overdose complicated by hypotension, unresponsive to an initial treatment with physostigmine fluid challenge and dopamine (greater than 15 micrograms/kg/min) but subsequently responsive to an infusion of norepinephrine is reported.

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Symptoms of hyperphosphatemia usually relate to the associated hypocalcemia. In a 33-year-old patient accidental infusion of a bolus of potassium phosphate (5 ml intravenously) was immediately followed by cardiac arrest. During CPR, clinically important hypocalcemia or hyperkalemia was not detected, but serum phosphorus was significantly increased. Because acute phosphate load can precipitate life-threatening cardiac arrhythmias, familiarity with doses and rate of infusion of phosphate is extremely important.

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Secretory IgA antibody may be important in protection against respiratory viral infections, and the concept of a common mucosal immune system offers the theoretical basis for the convenient stimulation of this antibody. Therefore, the oral route was compared with intramuscular injection in a double-blind, placebo-controlled study in young healthy volunteers. A killed influenza vaccine, given in enteric-coated capsules (total of 98 ug hemagglutinin of A/Bangkok) led to significant salivary and nasal IgA antibody rises in a 4-week period. The preimmunization titers in secretions were inversely correlated with the antibody rise after immunization. The orally administered vaccine was associated with no more side effects than placebo, in contradistinction to reactions following the intramuscular route. The latter route also was without significant effect in regard to a stimulation of secretory antibodies. The observed simultaneous induction of antibodies in saliva and nasal secretions following oral administration of killed vaccine gives further evidence of a common mucosal immune system and its possible clinical use.

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By ingestion of subunit-killed influenza virus vaccine in the form of enteric-coated capsules, local synthesis of secretory IgA (sIgA) antibody was stimulated in human nasal secretions. A fairly equal antibody response initiated by oral and intramuscular administration was demonstrated in the nasal secretions, although a systemic immune response was not elicited from ingestion of the vaccine. If the secretory antibody response resulted from absorption of antigen and transport to the respiratory mucosa, systemic (serum) antibody would be expected. Therefore these findings support the hypothesis that specialized collections of lymphoid cells in the small intestines have IgA precursor cells which circulate and populate distant mucosal sites. A number of studies have suggested that protection against mucosal infection by a variety of respiratory viruses correlates better with the presence and level of sIgA antibody than with serum antibody. The orally administered vaccine was associated with no more side effects than placebo, in contradistinction to the intramuscular route. Thus, the oral method of influenza vaccination could prove to be superior in providing for immunological protection due to equal secretory antibody stimulation, improved convenience and less toxicity.

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In the past three decades significant strides have been made in attempts at nonparenteral immunization. Appreciation of the importance of secretory immunity led to attempts to stimulate antibody production locally. The vaccines developed against respiratory pathogens as a result of this new knowledge have many practical limitations, such as the need for highly trained personnel, expensive equipment, very cooperative recipients for intranasal or aerosol administration, and a vaccine that is both adequately attenuated, immunogenic, and stable during storage. With recognition of the presence of a common mucosal defense system, new approaches to vaccine development have become possible. Oral immunization, by stimulating GALT, presents a promising approach for protecting many secretory surfaces against a variety of infectious agents. Recently, emphasis has been placed on developing an oral vaccine against S. mutans. McGhee et al. have demonstrated antibody to S. mutans in saliva and tears following oral ingestion of that antigen, without a rise in serum antibody, in both humans and rats. The rats were afforded protection from caries after rechallenge with both the original and cross-reacting serotypes of S. mutans. Similar results have recently been seen with viral antigens. Mice have been shown to have significant protection against influenza infection following oral immunization. And in a pilot study with human volunteers, the secretory antibody response in nasal washes was similar following either oral or parenteral vaccination. Oral immunization may prove to be far superior to parenteral vaccination against a variety of pathogens, because of fewer side effects and greater ease in vaccine preparation and administration.

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Immunobiological properties of guinea pig and human peritoneal macrophages were studied at temperatures ranging from 25 degrees C to 37 degrees C. Glass adherence, random migration, response to MIF and killing of Salmonella typhimurium and Saccharomyces cerevesiae by guinea pig macrophages were decreased with temperatures below 37 degrees C. Killing of Sacch. cerevesiae by human macrophages was also reduced at temperatures less than 37 degrees C. Acid phosphatase and beta-N-acetylglucosaminidase (NAG) activity assayed at 37 degrees C did not change when the cells were preincubated for 1 and 5 hours at various temperatures. Impaired macrophage function with subnormal temperatures may contribute to enhanced susceptibility to infection of patients with chronic diseases such as renal failure and cirrhosis.

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