General anesthesia in pigs.

Conventional swine weighing 20-45 kg were anesthetized for surgical procedures. After fasting for 24 hours, ketamine hydrochloride and xylazine were administered intramuscularly. Following tracheal intubation, sodium thiopental was administered via the aural or femoral vein.     

General anesthesia in Eisenmenger's syndrome.

The anesthetic management of a woman with Eisenmenger''s syndrome undergoing abdominal hysterectomy with general anesthesia is described. Proper anesthetic management of patients with this syndrome depends on a knowledge of the pathophysiologic process and associated complications. The potential problems of systemic hypotension, pulmonary embolism and infective endocarditis are outlined. Sudden death is a common and pregnancy is a major hazard.     

Polyamine metabolism in enterocytes isolated from newborn pigs.

In the pig, the growth of intestinal mucosa is very intense after birth. Since the polyamines are key elements affecting cell proliferation and differentiation, the present work was undertaken in order to know whether this hypertrophy is associated with an adaptation of polyamine metabolism. Villus enterocytes isolated from pig immediately after birth or 2 days later were found to contain similar amounts of putrescine, spermidine and spermine, i.e., 0.23; 0.41 and 1.24 nmol/10(6) cells, respectively. At birth, despite a relatively high ODC activity, putrescine synthesis from 1 mM L-arginine or 2 mM L-glutamine was very low in isolated enterocytes (6.4 +/- 3.8 pmol/10(6) cells per 30 min), while spermidine and spermine production were not detectable. This could be explained by a very low L-ornithine generation from both amino acids and to an inhibitory effect of polyamines on ODC activity. Two days later, polyamine synthesis from L-arginine remained undetectable despite a higher L-ornithine generation. This was concomitant with a dramatic fall in ODC activity. At both stages, enterocytes were able to take up polyamines from the extracellular medium in a temperature-dependent manner. It is concluded that de-novo synthesis of polyamines from L-arginine or L-glutamine does not play a significant role in the control of polyamine content of pig enterocytes during the postnatal period. In contrast, polyamine uptake by enterocytes would contribute to maintain a steady-state polyamine content during this period.     

Asphyxia-induced release of alpha-melanocyte-stimulating hormone in newborn pigs.

Asphyxia and reperfusion induced changes in the plasma and cerebrospinal fluid (CSF) concentrations of alpha-melanocyte-stimulating hormone (alpha-MSH) were studied in newborn pigs using a specific radioimmunoassay technique. Cardiovascular and metabolic failure induced by neonatal asphyxia resulted in a 3-fold, significant (P < 0.05) increase in plasma alpha-MSH levels, whereas the hormone concentration in CSF was significantly (P < 0.05) reduced by 50% during postasphyxial reperfusion. Our data indicate an asphyxia-induced release of alpha-MSH, and suggest a discordant regulation of plasma and CSF concentrations in newborn pigs.     

General anesthesia of infant mice by isoflurane inhalation for medium-duration surgery.

In this report we describe a means of general anesthesia for medium-duration (i.e., 20 to 60 min) surgery of infant mice. We tested isoflurane inhalation (2.0% isoflurane in air or oxygen during induction, and 1.5% after surgical anesthesia) anesthesia of 6-to 10-day-old C57BL/6JJcl mice and obtained safe, effective, and reproducible results.     

Inspiratory timing regulation of PGF2 alpha in newborn pigs.

In intact and vagotomized anesthetized, spontaneously breathing piglets, we investigated the regulation of inspiratory timing evoked by i.v. administration of prostaglandin (PG) F2 alpha. The inspiratory time was evaluated from the flow trace as an index of mechanical inspiratory time (Ti) and from costal and crural diaphragmatic EMG (TiEMG) as an index of neural inspiratory time. Our results under control conditions showed that TiEMG was shorter than Ti. Vagotomy abolished the difference, inducing a change in the power spectrum without modifying the centroid frequency (Cf). PGF2 alpha lengthened TiEMG, causing a postinspiratory diaphragmatic discharge to appear, while mechanical inspiratory time decreased significantly. Postvagotomy i.v. administration of PGF2 alpha did not cause any significant changes in inspiratory time and did not evoke the postinspiratory discharge. The i.v. administration of PGF2 alpha before and after vagotomy did not change the centroid frequency in spite of recruitment of new motor units synchronized with those that are active under control conditions.     

General anesthesia and hepatic circulation

This article describes hepatic circulatory disturbances associated with anesthesia and surgical intervention. The material is presented in three parts: part 1 describes the effects of general anesthetics on the hepatic circulation; part 2 deals with different factors related to surgical procedures and anesthesia; and part 3 analyzes the role of hepatic circulatory disturbances and hepatic oxygen deprivation in anesthesia-induced hepatotoxicity. The analysis of available data suggests that general anesthesia affects the splanchnic and hepatic circulation in various directions and to different degrees. The majority of anesthetics decreases portal blood flow in association with a decrease in cardiac output. However, hepatic arterial blood flow can be preserved, decreased, or increased. The increase in hepatic arterial blood flow, when it occurs, is usually not enough to compensate for a decrease in portal blood flow and therefore total hepatic blood flow is usually decreased during anesthesia. This decrease in total hepatic blood flow has certain pharmacokinetic implications, namely a decrease in clearance of endogenous and exogenous substances with a high hepatic extraction ratio. On the other hand, a reduction in the hepatic oxygen supply might play a certain role in liver dysfunction occurring perioperatively. Surgical procedures-preparations combined with anesthesia have a very complex effect on the splanchnic and hepatic circulation. Within this complex, the surgical procedure-preparation plays the main role in developing circulatory disturbances, while anesthesia plays only a modifying role. Hepatic oxygen deprivation may play an important role in anesthesia-induced hepatotoxicity in different experimental models.     

Central and peripheral adrenergic mechanisms in endotoxin fever and newborn guinea pigs.

In 0--3 day-old guinea pigs cerebroventricular pretreatment with alpha-methyl-p-tyrosine failed to modify the course of fever induced by E. coli endotoxin administration into the cerebral ventricles. Central or intraperitoneal administration of phentolamine or central administration of propranolol were also ineffective. Intraperitoneal propranolol, however, prevented both the first and the second temperature rise after endotoxin, while the transient fall in temperature that usually occurs between them still ensued. Central noradrenergic mechanisms seem to play, at most, a minor role in the mediation of endotoxin fever, while the integrity of peripheral beta adrenergic receptors is indispensable for the febrile response to occur.     

Endotoxin and prostaglandin fever of newborn guinea pigs at different ambient temperatures.

At an ambient temperature (Ta) of 30 degrees C, injection of 0.2 micrograms E. coli endotoxin into the lateral cerebral ventricle (icv) of three-day-old or younger guinea pigs was followed by a biphasic febrile rise in body temperature (Tc) and oxygen consumption (VO2), interrupted by a transient fall. At Ta 20 degrees C the change in Tc and VO2 was still biphasic, the first rise was similar as that seen at Ta 30 degrees C, but the subsequent fall was more pronounced. Thus, Tc became lower than before endotoxin and remained below the pre-injection level during and after the second rise. Injection of 10 ng PGE1 icv caused sustained monophasic hyperthermia at both Ta-s. Icv injection of 0.9% NaCl did not affect Tc and VO2 at either Ta. Accordingly, prostaglandins might contribute to, but cannot account for, the whole febrile response to endotoxin.     

Cerebral and intestinal perfusion and metabolism in normocythemic hyperviscous hypoxic newborn pigs.

We studied the effects of hypoxia on cerebral cortical and intestinal perfusion and metabolism in normocythemic hyperviscous newborn pigs. Seven pigs were made hyperviscous by an injection of cryoprecipitate, increasing viscosity from 5.8 +/- 0.9 to 9.0 +/- 1. 2 (SD) cycles/s. Six normoviscous pigs received 0.9% NaCl. Reducing the inspired O(2) decreased the arterial O(2) content (Ca(O(2))) from 9.5 +/- 1.6 to 3.6 +/- 1.3 ml O(2)/100 ml. Increases in brain and decreases in gastrointestinal blood flow at the lower Ca(O(2)) values were similar between the groups. During hypoxia, blood flow to stomach, distal intestinal mucosa, and large intestines was lower (-50, -23, and -28%, respectively) in the hyperviscous than normoviscous group. At the lower Ca(O(2)) values, cerebral cortical vascular resistance decreased in both groups and intestinal vascular resistance increased (+257%) in the hyperviscous but not in the normoviscous group. During hypoxia, systemic oxygen delivery decreased, extraction increased, and uptake did not change; cerebral cortical O(2) delivery, extraction, and uptake did not change; and intestinal O(2) delivery decreased, extraction increased, and uptake did not change in both groups. Our study demonstrated that 1) during hypoxia, increases in systemic O(2) extraction compensated for decreases in delivery and systemic uptake did not change; vasodilation sustained cerebral cortical O(2) delivery and preserved metabolism; increases in intestinal oxygen extraction offset decreases in delivery and uptake was preserved; and 2) nonpolycythemic hyperviscosity did not have a major influence on cardiovascular or metabolic responses to hypoxia, except for modest effects on intestinal resistance and perfusion to certain gastrointestinal regions. We conclude that, under normocythemic conditions, a moderate increase in viscosity does not have a major impact on hemodynamic or metabolic adjustments to hypoxia in newborn pigs.     

Evidence for a putative second receptor for porcine transmissible gastroenteritis virus on the villous enterocytes of newborn pigs.

Aminopeptidase-N (APN) has been identified [B. Delmas, J. Gelfi, R. L'Haridon, L. K. Vogel, H. Sjostrom, O. Noren, and H. Laude, Nature (London) 357:417-420, 1992] as a major receptor for porcine transmissible gastroenteritis virus (TGEV). Binding of TGEV to villous enterocytes from the jejuna of newborn pigs is saturable and at a higher level than that of binding of virus to newborn cryptal enterocytes or to enterocytes from older piglets (H. M. Weingartl and J. B. Derbyshire, Vet. Microbiol. 35:23-32, 1993). The distribution of APN in enterocytes in the jejuna of neonatal and 3 week-old-piglets, as determined by the measurement of enzymatic activity and by labeling of the cells with an anti-APN monoclonal antibody, did not correspond with the reported distribution of saturable binding sites on enterocytes. Monoclonal antibodies, which were prepared against plasma membranes derived from enterocytes harvested from the upper villi of newborn pigs, blocked the replication of TGEV, but not the porcine respiratory coronavirus, in ST cells and immunoprecipitated a 200-kDa protein in ST cell lysates. This protein was demonstrated by immunohistochemistry and by fluorescence-activated cell scanning to be present on the villous enterocytes of newborn pigs but to be lacking on the cryptal enterocytes of newborn pigs and on the villous and cryptal enterocytes of 3-week-old piglets. Since this distribution of the protein corresponds to the previously demonstrated distribution of saturable binding sites, we conclude that the 200-kDa protein may be an additional receptor for TGEV which is restricted to the villous enterocytes of newborn pigs and which contributes to the age sensitivity of these animals to the virus.     

Cholinergic component of histamine-induced bronchoconstriction in newborn guinea pigs

The magnitude of parasympathetic reflex-mediated bronchoconstriction during histamine infusion was compared in anesthetized paralyzed newborn and adult guinea pigs. The animals were ventilated using a constant-flow ventilator, and the conductance and compliance of the respiratory system were continuously monitored. We found that reactivity to histamine infusion was less in newborns than in adults, because newborns required a larger dose of histamine than adults (300 vs. 125 ng.kg-1.s-1) to produce an equivalent decrease in conductance (42 +/- 13 vs. 42 +/- 15%). Vagal interruption by bilateral cervical vagotomy or muscarinic blockade with atropine (3 mg/kg) significantly reduced the bronchoconstrictor response to histamine in adults. By contrast, neither vagotomy nor atropine significantly changed this response in the newborns. These results indicate the lack of a vagal component in the bronchoconstriction that histamine induced in the newborns. Their relative unresponsiveness to histamine might partly be related to the fact that, in the newborn, histamine mainly acts directly via its airway receptors.     

PGF2 alpha and breathing pattern in newborn pigs

The effect of PGF2 alpha has been evaluated in 11 unanaesthetized unrestrained piglets and in 3 anaesthetized piglets (2-3 days old) using a barometric-plethysmographic technique. PGF2 alpha (mg 0.25/pig) was administered as aerosol for 5 min. In 3 of the unanaesthetized newborn pigs the effect of PGF2 alpha aerosol has been evaluated after indomethacin (mg 1/Kg i.v.). The vagal dependent activity of the prostaglandin was also evaluated after atropine (mg 0.08/Kg i.m.). Our results show that PGF2 alpha in newborn pigs causes hypoventilation due to a decrease in respiratory rate and to a lengthening in TE. The changes in TE are due to an increase in the incidence and duration of apneic events characterizing the respiratory activity at birth. After indomethacin PGF2 alpha does not change the breathing pattern. Atropine only partially reduces the effects of PGF2 alpha while, after anaesthesia, prostaglandin does not change the breathing pattern. Consequently our results show that PGF2 alpha in newborn animals similar to other prostaglandins acts as a depressant of respiratory activity.