Cardiovascular effects of platelet-activating factor

Sudden release of platelet-activating factor (PAF) into the circulation can cause hypotension, tachycardia, and circulatory collapse. To further examine this response, we performed detailed studies of cardiovascular function after PAF administration to young domestic pigs and newborn piglets. Our results indicate that circulatory dysfunction after PAF reflects severe constriction of pulmonary resistance vessels and consequent acute right ventricular failure. Although PAF-induced coronary artery constriction and contractile depression may be complicating problems, left ventricular underperfusion and dysfunction after PAF are mainly the result of systemic arterial hypotension and diminished left ventricular filling. The adverse hemodynamic effects of PAF are accompanied by substantial release of thromboxane A₂ (TxA₂). These effects are mimicked by the TxA₂ agonist U-46619 and partially blocked by specific and nonspecific inhibitors of TxA₂ synthesis (OKY-046 and indomethacin). Even more potent blockade of PAF action is exerted by the TxA₂ receptor blocker, SQ 29,548. Taken together, these findings indicate that severe pulmonary vascular constriction and hemodynamic collapse soon after intravenous PAF are at least partially mediated by PAF-induced TxA₂ release. Tachyphylaxis to PAF influence has been observed in studies of leukocyte and platelet function. We hypothesized that tachyphylaxis to PAF might also occur in our studies of constrictor responses in pulmonary vessels. Recently, we have examined the capacity of PAF to produce sustained pulmonary vasoconstriction in openchested, anesthetized newborn piglets. Infusions sufficient to produce 100% increase in mean pulmonary artery pressure after 3 min showed no loss of efficacy when sustained for 30 min. The same was true for infusions of U-46619. Thus, the pulmonary vasoconstrictor influence of PAF or U-46619 is not readily diminished by tachyphylaxis. These findings favor the viewpoint that PAF or TxA₂ release during inflammatory processes could have prolonged adverse actions on pulmonary and systemic circulations. Based on a paper presented at the Third International Conference on Platelet-Activating Factor and Structurally Related Alkyl Ether Lipids, Tokyo, Japan, May 1989. The opinions or assertions contained here are those of the authors. They do not reflect the views of the Department of Defense or the Uniformed Services University of the Health Sciences. The experiments reported here were conducted according to the principles set forth in the “Guide for the Care and Use of Laboratory Animals,” Institute of Laboratory Animal Resources, U.S. Department of Health and Human Services (NIH Publ. 85-23, 1985).     

Taste aversion learning in young and adult rats.

Compared a total of 159 male Long-Evans rat pups and adults on their ability to learn taste aversions with 1- and 2-bottle tests, 2 different illness-inducing agents and flavors, and varying taste–illness delays. Rat pups learned taste aversions with either 1- or 2-bottle tests, but only with short taste–illness delays. Delays of 60 min were sufficient to block taste aversion learning in pups. Pups also failed to demonstrate neophobia to a novel taste. These findings suggest that pups forget taste information more rapidly than adults, perhaps because taste information is not so salient for pups as for adults. (29 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Erratum: "Studies in Early Infant Learning: Classical Conditioning of the Neonatal Heart Rate."

Reports an error in the original article by D. H. Crowell et al (Developmental Psychology, 1976[Jul], 12(4), 373-397). Corrections to equations 1, 2, and 3 on pages 381 and 382 are presented. (The following abstract of the original article appeared in record 1976-20687-001.) Three experiments demonstrated that human newborn heart rate level can be reliably modified through classical conditioning procedures. The theory of sensitization served as a frame of reference for Exps I and II, and drive reduction served for Exp III. In Exp I the delay, delay-trace, and control groups, with 10 2-day-old newborns in each, received 5 preconditioning trials of the CS alone, 16 conditioning trials with CS-UCS pairings differing for each group, and 5 extinction trials. Exp II was a replication of the 1st study and involved only the delay and delay-trace groups with 10 infants each. In both studies the delay group curves showed significant monophasic acceleratory responses during extinction. Results support the sensitization hypothesis (i.e., the CR occurring in the interstimulus interval was fashioned out of the response to the CS). In Exp III, the measure of conditioning was the response to the probe technique. 10 experimental Ss received preconditioning trials of nitrogen puff (UCS-sub-1) administered to the abdomen, followed by 10 CS-UCS-sub-2 (500-Hz tone acetic acid) pairings with an interstimulus interval of 3 sec. 10 controls received the same design with a CS-UCS-sub-2 interval of 40 sec. Analyses of the probe stimulus trials showed significant changes for the control group and none for the experimental group. The CS-UCS-sub-2 pairings in the experimental group are interpreted as producing increased drive and adaptive damping of the heart rate response. Findings show that early learning may occur under a variety of conditions and that the results can be incorporated by different theories. (PsycINFO Database Record (c) 2010 APA, all rights reserved)