D. R. McCaffree

Evaluation of right-heart catheterization in the critically ill patient without acute myocardial infarction

FLOW-directed right-heart catheterization is used extensively to monitor the hemodynamic status of critically ill patients. After acute myocardial infarction, measurements of the cardiac index and pulmonary capillary wedge pressure are useful in several ways: they allow accurate assessment of short-term and long-term prognosis,1 help in directing immediate and subsequent therapy,2 3 4 and correlate well with the clinical assessment of the hemodynamic status.5 Although there is no evidence that right-heart catheterization reduces the mortality of patients with acute myocardial infarction,6 the information it yields is sufficiently useful in assessing prognosis and directing therapy that the risks associated with catheterization7 , 8 are thought to .xa0.xa0.

Effects on breathing of putative neurotransmitters in the rostral hypothalamus of the rat

The putative neurotransmitters norepinephrine (NE) and thyrotropin releasing hormone (TRH) are normally present in the rostral hypothalamic region (RHT) of the rat, and our aim was to evaluate possible effects of these agents on ventilatory regulations associated with this region. Using haloperidol-tranquilized Sprague-Dawley rats, microinfusions of both NE and TRH into the RHT resulted in an increase in rate, but not depth, of breathing. Control infusions and control infusion sites, mainly in the posterior hypothalamus, yielded no significant effect on breathing rate. Since NE and TRH can inhibit the discharge of some cells in the RHT, it was possible that the observed effects on breathing were due to depression of an inhibitory neural pathway. This idea was further tested by performing microinfusions using lidocaine. Evidence suggests that lidocaine can inhibit discharge in the central nervous system and that inhibitory pathways may be preferentially affected. Lidocaine produced effects on breathing comparable to NE and TRH, thereby supporting the proposition that inhibition of neural pathways in the RHT can stimulate breathing.

Lidocaine in the Rat Rostral Hypothalamus: Effect on Arterial Carbon Dioxide

Abstract Lidocaine hydrochloride causes an increase in respiratory frequency (f) when infused into the rostral hypothalamus of the rat. The purpose of our study was to determine whether this increased f was primarily due to: (i) a direct increase in neural respiratory drive; (ii) a change in metabolism, mediated by the hypothalamus, causing increased carbon dioxide production and secondary hyperpnea; or (iii) a combination of these phenomena. Arterial carbon dioxide tension (P aCO2),f, and tidal volume (V t) were measured in awake, unrestrained, tranquilized rats before and after the infusion of either lidocaine or hypertonic saline into the rostral hypothalamus. At peak increase in f, approximately 2 min after lidocaine infusion, f had increased 26.5 breaths/min (28.3%), P aCO2 had decreased 3.5 mm Hg (10.3%), and V t was unchanged. There was no change inf, V t, or P aCO2 2 min after saline infusion. Since an increase in carbon dioxide production typically causes increased ventilation with a stable P aCO2, the increasedf and hypocapnia seen following infusion of the local anesthetic lidocaine are best explained by a depression of inhibitory neural discharge from the rostral hypothalamus resulting in increased discharge from the lower brainstem respiratory control centers.

In vitro labeling of the sialic acid moiety of glycoconjugates with carbon-14

Labeling of sialoglycoproteins with carbon-14 in vitro was performed by reacting the aldehyde groups, generated by mild periodate oxidation of the terminal sialyl groups, with 14C-labeled sodium cyanide to produce the labeled cyanohydrin derivatives (Kiliani reaction). Labeling with tritium was carried out by reduction of the aldehyde groups generated on the sialyl residues with 3H-labeled sodium borohydride following standard procedures. The behavior of both types of labeled specimens of fetuin and ovine submaxillary mucin, individually and in mixtures, was investigated by gel-filtration chromatography, gel electrophoresis, and cesium bromide gradient ultracentrifugation. The labeled sialyl residues were subjected to partial characterization: color yield with the resorcinol and thiobarbituric acid reagents, behavior on ion-exchange chromatography, and susceptibility to mild acid and enzymatic hydrolyses. In addition to these model glycoproteins, this procedure was also utilized to label the sialoglycoproteins present in human tracheobronchial secretions collected from normal subjects and patients with chronic bronchitis. The potential uses of this approach for comparative studies of normal and pathological sialoglycoconjugates available in minute amounts is described. The extension of this approach to the labeling of the galactosyl and N-acetylgalactosaminyl moieties of glycoconjugates following treatment with galactose oxidase is outlined.