Prevention of sudden death after repair of tetralogy of Fallot: treatment of ventricular arrhythmias.

The majority of sudden deaths after repair of tetralogy of Fallot have been presumed to be due to ventricular arrhythmia; however, it remains to be demonstrated that antiarrhythmic medication reduces the incidence of sudden death. Since 1978, ventricular arrhythmias have been treated aggressively; these include any ventricular arrhythmia on routine electrocardiogram and more than 10 uniform premature ventricular complexes per hour on 24 hour electrocardiogram. A review was undertaken of 488 patients followed up for more than 1 month after repair of tetralogy of Fallot (mean follow-up time 6.1 years); 13.5% had ventricular arrhythmia on routine electrocardiogram. Ventricular arrhythmia appeared from 2 months to 21 years postoperatively (mean 7.3 years). Ventricular arrhythmias were significantly (p less than 0.01) related to: longer follow-up duration, older age at follow-up, older age at operation and higher postoperative right ventricular systolic and end-diastolic pressures. Ventricular arrhythmia on routine electrocardiogram occurred in 100% of those who later died suddenly compared with 12% of those who did not die (p less than 0.01). Treatment for ventricular arrhythmia was given to 46 patients and considered "successful" if there were fewer than 10 uniform premature ventricular complexes per hour on 24 hour electrocardiogram. A successful drug was found in 44 of the 46: 30 of 34 given phenytoin, 6 of 9 given propranolol, 1 of 7 given quinidine, 1 of 2 given disopyramide, 8 of 9 given mexiletine and 4 of 5 given amiodarone.(ABSTRACT TRUNCATED AT 250 WORDS)

Eliminating unnecessary lactate dehydrogenase testing. A utilization review study and national survey.

BACKGROUND: Consensus recommendations call for the elimination of lactate dehydrogenase (LDH) tests from routine rule out myocardial infarction (ROMI) protocols. METHODS: We conducted a utilization review project in which we evaluated the institutional impact of removing LDH and LDH isoenzyme tests from our hospital diagnostic panel. We then conducted a scripted telephone survey of 100 US hospitals to assess the generalizability of this project. RESULTS: All our cardiology staff members supported this intervention. Lactate dehydrogenase isoenzyme test results did not add clinically useful data for any of 200 consecutive patients discharged with a diagnosis of acute myocardial infarction, and selective use of LDH isoenzyme testing in cases where it was clinically believed to be indicated cut costs 99% during the year after our intervention. Furthermore, our telephone survey demonstrated that 66% of US hospitals polled continue to test for LDH isoenzymes in every patient with possible myocardial infarction. CONCLUSIONS: Our results corroborate prior recommendations for the removal of LDH testing from the routine ROMI protocol. Such an intervention may be accomplished easily, with excellent staff acceptance and considerable savings. Most US hospitals continue to include LDH testing in their ROMI panels despite national guidelines recommending otherwise.

Protein accumulation in cerebrospinal fluid during -90 degrees head-down tilt in rabbit.

Plasma proteins are only somewhat larger than the intercellular spaces of the cerebral microvessels that constitute the blood-brain barrier or of the choroid plexus villi that elaborate cerebrospinal fluid (CSF). We hypothesized that the integrity of these barriers in anesthetized rabbits might be compromised during head-down tilt (HDT). Plasma protein and osmolality, hematocrit, and CSF protein concentration were compared in rabbits exposed to 1 h of HDT (n = 20) and prone rabbits (n = 10). In addition, the concentration of trypan blue dye, injected intravenously at the end of HDT or the prone position, was measured in brain homogenate. Finally, arterial blood pressure was measured via a catheterized carotid artery. HDT disrupted the barrier between blood and CSF, as indicated by a significantly (P < 0.01) greater brain trypan blue concentration in the HDT rabbits [172.2 +/- 14.4 (SD) micrograms/g dry wt] than in the prone rabbits (29.8 +/- 4.4 micrograms/g dry wt). Moreover CSF protein 5 min after HDT onset was significantly increased compared with control in HDT rabbits (54.6 +/- 1.9 vs. 81.4 +/- 5.2 mg/dl; n = 8) but not in prone rabbits (55.6 +/- 2.7 vs. 57.2 +/- 5.0 mg/dl; n = 6). Changes in the plasma protein-to-hematocrit ratio in the HDT animals, but not in the prone animals, were also compatible with a loss of fluid from the vascular compartment.(ABSTRACT TRUNCATED AT 250 WORDS)

Endurance training in dogs increases vascular responsiveness to an alpha 1-agonist.

The effects of endurance training on vascular responsiveness to an alpha 1-agonist and the associated changes in baroreflex modulation of heart rate and vascular resistance were studied. Graded dosages of phenylephrine were given to eight treadmill-trained dogs and to eight untrained dogs; both groups were chronically instrumented and were sedated and resting when tested. These dosages were repeated after ganglionic blockade. Aortic pressure, cardiac output, central venous pressure, peripheral resistance, and heart rate were each averaged over 30 s before injection and 90 s after injection. The slope of the peripheral resistance-dose relationship was significantly increased in trained compared with untrained dogs in both the unblocked and blocked cases [unblocked: trained 0.89, untrained 0.47; blocked: trained 4.30, untrained 2.05 (mmHg.l-1.min)/(microgram.kg-1)]. The unblocked resistance slopes were reduced with respect to the blocked slopes by 77 (untrained) and 79% (trained). The slope of the heart rate-aortic pressure response was reduced, but not significantly, by endurance training. We conclude that 6 wk of endurance training in dogs resulted in a doubling of the vascular responsiveness to an alpha 1-agonist, with no significant change in the baroreflex regulation of resistance or heart rate.

A temporally detailed reanalysis of the conditional heart rate response in dog.

We used rapid (500 Hz) digital sampling to derive a detailed analysis of the HR conditional response in dog (n = 11) to a 30-sec tone (CS+) followed by a 1/2-sec shock. We found an initial bradycardia at 1.5 +/- 1.0 sec in 6 of 11 dogs from a pre-CS+ control of 85 +/- 26 bpm (mean +/- SD) to 74 +/- 25 bpm (p less than 0.05). In 9 of the 11 dogs there was a subsequent rapid (19.9 +/- 6.7 bpm/sec) increase (+26 +/- 10 bpm) in HR lasting from 1.3 +/- 0.9 to 2.7 +/- 1.0 sec. This was followed by a second, larger (+41 +/- 16, p less than 0.05), but slower (4.0 +/- 2.4 bpm/sec, p less than 0.05) tachycardia which lasted from 4.9 +/- 1.0 to 13.5 +/- 2.6 sec. The peak HR (131 +/- 27 bpm) was attained at 15.0 +/- 3.8 sec, after which HR fell slowly (-2.4 +/- 1.4 bpm/sec) to an average of 92 +/- 29 bpm at 28.6 +/- 1.4 sec (i.e., approximately 1.4 sec prior to shock delivery). This analysis revealed trends in the conditional HR response which were not discernible in individual trials and were obscured in the more traditional analyses of the conditional HR response.

Coronary alpha-adrenergic tone and contraction of ischemic myocardium in awake dog.

The effect of neurogenic coronary vasomotor tone upon contraction in ischemic myocardium was investigated in awake, mongrel dogs. The animals were chronically instrumented with a hydraulic occluder around the left circumflex coronary artery; a small catheter was also implanted within the vessel. Ultra-sound crystal pairs were placed distal to the occluder in myocardium perfused by the left circumflex artery. Pacing electrodes were sutured onto the right ventricular conus. During the experiment (n = 6) the occluder was inflated to stenose the vessel; the imposition of cardiac pacing (210/min) in conjunction with this stenosis resulted in depressed contraction of the myocardium distal to the occluder as assessed by the ultra-sound crystals: Segmental shortening decreased to 45.4 +/- 5.4% of unpaced control. Phentolamine, an alpha-antagonist, was then infused into the left circumflex catheter for ten minutes (0.1 mg/min) and the experiment repeated. After the alpha-blockade the combination of coronary stenosis and heart rate pacing decreased segmental shortening to only 84.6 +/- 10.1% of control, which was significantly (P less than 0.01) improved relative to the unblocked condition. In another experiment (n = 4), a less severe stenosis was imposed upon the left circumflex vessel. During pacing, muscle shortening decreased to 94 +/- 8.5% of control. Infusion of phenylephrine, an alpha-agonist, for ten minutes (0.1 mg/min) resulted in a 56.7 +/- 5.9% decrease in shortening during pacing; this was significantly greater (P less than 0.01) than the previous decrease. These data indicate that coronary alpha-adrenergic tone can significantly compromise regional myocardial function even in ischemic muscle whose coronary blood flow reserve has been exhausted.

Hibernation "trigger": opioid-like inhibitory action on brain function of the monkey.

A hibernation "trigger" factor derived from the blood of the hibernating woodchuck acts to suppress vital physiological processes in the primate. When infused into the cerebral ventricle of the conscious monkey, the factor induced hypothermia, behavioral depression, bradycardia and aphagia. The opiate antagonists, naloxone and naltrexone, either reverse or retard these behavioral and physiological signs. We hypothesize that the "trigger" molecule is an endogenous opioid-like peptide which may be unique to the hibernator. Moreover, the non-hibernating primate apparently possesses receptor sites in the brain that are capable of responding to this potent molecule.

Human Pavlovian HR decelerative conditioning with negative tilt as US: a review of some S-R, stimulus-substitution evidence.

Interest in human Pavlovian heart rate (HR) conditioning with conventional shock and loud noise unconditional stimuli has declined, as measured by reports in the literature. Accompanying this decline have been the following views: (a) that HR should be abandoned as a psychophysiological index of the psychological (learning) process of Pavlovian conditioning; (b) that, following psychology's shift to a more cognitive emphasis, the self-regulation (S-R), stimulus-substitution view of pavlovian conditioning is wrong, because there is no equivalence in direction between shock- and loud noise-induced HR-accelerative unconditional response and the conditional response. This paper reviews recent reports of human Pavlovian conditioning of HR deceleration with negative tilt as the unconditional stimulus. The results support an S-R, stimulus-substitution interpretation of conditioning. In addition, these studies have potential therapeutic application in the teaching of (medically desirable) HR deceleration, especially when Pavlovian procedures are combined with instrumental (biofeedback) ones. However, such physiological aspects of the decelerative unconditioned response as the degree of vagal involvement are difficult to investigate in the human preparation.

Human Pavlovian HR-decelerative conditioning with negative tilt as US: evidence of vagal and sympathetic influences on the UR in dogs.

Following a review of studies employing negative tilt in human Pavlovian conditioning of heart rate (HR) deceleration (Furedy et al, in press), this paper reports data based on animal subjects on such physiological aspects of the decelerative unconditioned response (UR) as the degree of vagal involvement. Five anesthetized dogs underwent 90 degrees negative body tilts pre- and postbilateral vagotomy, while interbeat interval (IBI), left ventricular pressure (LVP) and its first derivative, d(LVP)/dt, which is a measure of sympathetic cardiac drive, were recorded. Consistent with the vagal interpretation of the tilt-induced decelerative UR, the results indicated that vagotomy markedly changed the tilt-induced bradycardic reflex from a fast-recruiting, large-magnitude (over 45%), and sustained (throughout the 20-27-s tilt) IBI increase, to slower-recruiting, and markedly smaller (less than 5%) IBI increase. However, there was also evidence of an initial sympathetic excitation of about 5 s, as indicated by a 45% increase in d(LVP)/dt, which returned to baseline level by 9 s following tilt onset. Vagotomy increased this tilt-induced sympathetic excitation to about 100%, and it remained at above 70% throughout the tilt. Prevagotomy LVP showed a slight (about 10%) and delayed (about 6 s following tilt onset) depressor response, which was eliminated by vagotomy. Finally, unaveraged data from individual dogs suggested that prevagotomy, LVP changes preceded IBI changes. Regarding implications of these results for human HR deceleration-inducing preparations, we conclude that the different physiological mechanisms that accompany and/or produce a given change in HR need continuing investigation with multiple dependent physiological variables (which are assessed for topographical differences), and in both human and animal preparations.

Stability of visceral behavior in the awake rat during rest.

Brady and colleagues have championed the importance of careful delineation and control of a subject's behavioral state. In this paper we develop the concept of visceral behavior from a physiological perspective. Sprague-Dawley rats were instrumented to record arterial blood pressure, renal sympathetic nerve activity, and respiration. The rats were restrained in a conical cloth sock. Rats that were well adapted to the sock restraint showed a regular respiratory pattern and consistent pressure recordings; they rested quietly in the sock and moved only occasionally to adjust their position. Fourier analysis of blood pressure and nerve activity showed a concentration of power below 1 Hz. The coherence between the two signals was strong (0.83 +/- 0.03) at 0.42 Hz. Conversely, during their initial adjustment to the sock restraint, the rats tended to show large fluctuations in blood pressure associated with episodic apneic breathing; 1 animal displayed this pattern of visceral behavior throughout most of the experiment. Despite this instability in pressure, the rats' overt behavior was stable: They rested quietly in the sock with only occasional position shifts. Spectral analysis and coherence computations showed large shifts in the distribution of power and frequency range over which arterial pressure and sympathetic activity were tightly coupled. These data are consistent with the view that an animal's circulatory adjustments, as well as adjustments in other aspects of its physiological state, constitute an important aspect of behavior, and that this behavior can influence the interpretation of biobehavioral data.

Laboratories which produce veterinary vaccines.

Borders, continents and oceans no longer provide a significant barrier to the movement of goods and services. Under the regulations of the General Agreement on Tariffs and Trade and the World Trade Organisation, governments may no longer prevent the importation of veterinary vaccines without scientific proof that the product would pose a threat to the health and safety of the nation. The origins of production laboratories for veterinary vaccines and the management of those laboratories are as diverse as the government programmes by which they are regulated. Both processed-based and performance-based approaches can be equally effective in the quality assurance of products. Seven international and regulatory initiatives have been developed to review these regulatory systems and, where possible, to harmonise standards and/or recognise equivalents to ease the movement of products. Continued exchange of information on a regional and world-wide basis can ensure the quality and availability of veterinary vaccines for animal health programmes around the world.

Control of left ventricular function during acceleration-induced blood volume shifts.

Peripheral pooling of blood was produced in chronically instrumented, sedated dogs (n = 7) by subjecting them to a +2 Gz force (along their spinal axis) for 3 min. The acceleratory force was then quickly removed, thereby mobilizing blood toward the thoracic cavity. Left ventricular volume, calculated from ultrasound measurements of major and minor axes and wall thickness, increased (p less than 0.05) from 21.7 +/- 3.6 ml (diastolic, mean +/- S.E.M.) and 14.1 +/- 3.3 ml (systolic) during the peripheral pooling of blood to 28.2 +/- 4.1 ml (diastolic) and 16.0 +/- 2.9 ml (systolic) as measured at 2 min after release of the acceleratory force. The d(LVP)/dt was essentially unchanged (i.e., from 3415 +/- 482 mm Hg.s-1 to 3536 +/- 249 mm Hg.s-1). The experiment was repeated after total pharmacologic autonomic blockade (propranolol, atropine, phenoxybenzamine). Left ventricular volumes during +2 Gz after blockade were 27.7 +/- 2.5 ml (diastolic) and 21.2 +/- 2.9 (systolic). The acceleration-induced changes in cardiovascular function, including the changes in ventricular volume, were not significantly different from those of the reflexive state. These results, therefore, do not reveal a substantial role for the autonomic nervous system in the regulation of left ventricular volume responses to the sudden cessation of G-induced peripheral blood pooling. Since the cessation of the G force induced essentially identical increases in left ventricular volumes and stroke volumes both before and after the autonomic blockade, it is concluded that the heart relied mainly upon the Frank-Starling mechanism to adapt to the changes in load.

A longitudinal subspecialty experience for internal medicine residents.

OBJECTIVE: Market and technology innovations have greatly changed the teaching and practice of medicine in the past 10 years. This report describes an innovation in the ambulatory education of internal medicine residents: a subspecialty continuity clinic. METHODS: A subspecialty continuity clinic was developed to improve the training of internal medicine residents in caring for complex ambulatory patients. The clinic structure is discussed from the perspective of patients, residents, and subspecialists. Logistical challenges and solutions are described. RESULTS: Two and one-half years into the program, feedback from residents and subspecialists has been positive. In-training examination scores are relatively higher in the involved specialties, and residents are managing illnesses they rarely saw in an outpatient setting before this program. CONCLUSION: This experience suggests that a subspecialty continuity clinic is worthwhile and practical in educating primary care residents.

Potentiation of the pressor response to stress by tolbutamide in dogs.

Tolbutamide has previously been shown to amplify the pressor effects of "exogenous" catecholamines in conscious dogs, possibly due to sensitization of the alpha 1-adrenoreceptor-mediated vasoconstriction. The objective of this study was to examine if tolbutamide also amplifies the pressor effects of "endogenous" catecholamines released during psychological stress (classical Pavlovian aversive conditioning). Experiments were conducted in beta-adrenoreceptor-blocked (propranolol, 1 mg/kg, i.v.) conscious dogs (n = 4) trained in classical aversive conditioning. Conditioning was accomplished by following a tone (CS+) with a 1/2 second shock; another tone (CS-) was not followed by any shock and served as control. With saline pretreatment, aversive conditioning (i.e., CS+) increased mean arterial pressure (MAP) only by approximately 4.7% when compared to CS-, whereas with tolbutamide (45 mg/kg, i.v.) pretreatment, the increase in MAP induced by CS+ beyond what was induced by the CS- (approximately 6.2%) was significantly (p < 0.05) larger than that with saline pretreatment. In isolated canine femoral arterial segments (n = 4), the vasoconstrictor effect of phenylephrine (an alpha 1-agonist) at 5 x 10(-6) M (which was the EC50 value) was amplified by 2 x 10(-2) M of tolbutamide from 54.0 +/- 2.0% to 66.9 +/- 2.1%. In conclusion, tolbutamide amplifies the pressor effects of "endogenous" catecholamines in conscious dogs, possibly by sensitization of the alpha 1-adrenoreceptor-mediated vasoconstriction. This mechanism of action is novel and has not been reported with other agents.

Two-component arterial blood pressure conditional response in rat.

The objective of these experiments was to quantify the pattern of change in arterial blood pressure (BP) during a discriminative aversive classical conditioning paradigm in rat using a new "high resolution" computer analysis. Sprague-Dawley rats (n = 5) were restrained in a soft, conical cloth pouch and conditioned using a 6 sec. pulsed tone (CS+) followed by a 0.5 sec. tail shock; a steady tone, never followed by shock, served as a CS-. BP peaked at 16.4 +/- 6.5 mm Hg (mean +/- SD) above control at 1.5 +/- 0.1 sec. after onset of CS+. This "first component" ("C1") also occurred during CS- (12.1 +/- 3.8 mm Hg), although the magnitudes of the two were significantly (p < 0.05) different. Another group of rats (n = 8) was treated identically except the tones were 15 seconds long. The conditional BP response consisted of two components. C1 was reminiscent of that seen using the short tone: for CS+ a peak of 13.6 +/- 5.6 mm Hg at 1.5 sec. or, for CS-, of 10.0 +/- 4.3 at 1.3 sec. (p < 0.05). In CS+ trials BP peaked again ("C2," 7.4 +/- 2.5 mm Hg) at 8.3 +/- 1.2 sec. There was no statistically significant C2 for CS- trials, clearly demonstrating discrimination between tones. The unconditional BP response in both groups consisted of two large, closely spaced peaks in BP. Respiration was recorded in 3 additional rats. After shock delivery these subjects often showed a sudden shift between (1) a regular respiratory pattern with moderate chest excursion and (2) apneic episodes interspersed with single, deep breaths. This latter pattern was associated with large, low frequency fluctuations in BP. Continued development of the rat conditioning paradigm is especially warranted because of the ability to record sympathetic nerve activity in intact, awake subjects and the large number of readily available genetic strains, which model human pathological states.

Autonomic nervous control of heart rate orienting and alpha responses in dog.

The object of this experiment is to study the autonomic nervous control of alpha responses elicited in classical conditioning. Twenty-two mongrel dogs were trained in classical discriminative conditioning. Typical two-phase tachycardic responses were observed in positive (CS+) trials while only the earliest, phase 1, response was observed in negative (CS-) trials. The phase 1 response, which was identical in CS+ and CS-trials, was compared in dogs before and after selective SA-nodal parasympathectomy (N = 7) and beta-adrenergic blockade (N = 11). The phase 1 tachycardic response was eliminated by selective SA-nodal parasympathectomy but not by beta-adrenergic blockade. We conclude that the phase 1 response observed in both CS+ and CS-trials with similar time sequence and magnitude is an alpha response. The heart rate orienting response results from a withdrawal of parasympathetic activity with little or no change in sympathetic tone.

Immunohistochemical characterization of reparative tissue present in human osteoarthritic tissue.

Studies involving disease progression in osteoarthritis (OA) have typically focused on the deterioration of native articular cartilage (AC) rather than the de novo cartilage which is frequently present. In general, there are two categories of de novo tissue observed in OA: (1) a pannus-like fibrocartilage that overlays native AC and (2) osteophytes. In this study, 30 AC samples representing a range of disease stages consistent with early to intermediate OA were examined for the occurrence of pannus-like tissue. All AC samples were examined immunohistochemically and compared with cartilage from three mature-looking osteophytes. To accomplish this, serial cartilage sections, derived from total knee arthroplasty specimens, were stained with hematoxylin and eosin and probed with antibodies raised against collagen type I, collagen type II, and aggrecan. Pannus-like tissue ranging from fibrous tissue to fibrocartilage was observed in 3 out of 30 AC samples. The appearance of this tissue was restricted to cartilage displaying signs of intermediate deterioration consistent with Outerbridge grade 2. Collagen type I, collagen type II, and aggrecan were abundant in both pannus-like tissue and osteophyte cartilage. In OA, the intrinsic repair process can yield a range of tissue types between fibrous tissue and fibrocartilage that is well integrated with the underlying, eroded AC. The absence of repair tissue from osteoarthritic samples representing the early stages of AC deterioration indicated that a relationship exists between macroscopic damage and a localized cellular repair response. Several histological and immunohistochemical similarities were also observed between the pannus-like tissue and osteophyte-derived cartilage, suggesting a common developmental process.

Inspection of veterinary biologics in the United States.

Inspection of veterinary biologics in the United States (U.S.) has changed significantly over the years since the Virus-Serum-Toxin Act (V-S-T) was passed by the U.S. Congress in 1913. At first, government inspectors were appointed to every production location, observing the preparation, testing and initial shipment of veterinary biologics. In the 1950s, a new plan was developed to provide a more scientific basis of inspection. Over a 10-year period, a programme to test finished products at the National Veterinary Services Laboratories and a new procedure for inspecting facilities and products was implemented. Our current programme retains our extensive pre-licensing review of products, labeling, facilities and personnel and adds the new inspection system of random checking of finished batches, unannounced in-depth inspections, control of product batches and post-licensing monitoring. This combination of activities ensures that pure, safe, effective and economical veterinary biologics are available for use in the U.S.

Behaviorally conditioned changes in atrio-ventricular transmission in awake dog.

The purpose of this study was to examine the effects of behaviorally conditioned changes in autonomic activity on atrio-ventricular (AV) transmission in dog. To produce consistent activation of the cardiac nerves in the awake animal (n = 7), a classical appetitive conditioning paradigm was used. A conditioning trial consisted of a 30 s control period followed by one of two differing situations: (1) a 60-s conditional stimulus (CS+) tone wherein food (i.e. 'UCS' or unconditioned stimulus) was given during the last 30 s; or (2) at 30-s discriminative stimulus (CS-) tone which was never followed by food reward. Eight of each type trial were given daily until a stereotypic cardiovascular response was developed for the CS+ but not the CS-. The hemodynamic conditional response (i.e. 'CR', the response to the CS+) consisted of a moderate tachycardia (+14.5%, P less than or equal to 0.05), a small pressor response (+6.7%, P less than or equal to 0.01), and a moderate increase in the first time derivative of left ventricular pressure (+14.9%, P less than or equal to 0.01) reflecting an increase in inotropic state. The unconditional response (i.e., 'UCR', the response to the food reward) consisted of a substantial increase in HR (25.7%, P less than or equal to 0.01) above CR values while left ventricular pressure (LVP) and d(LVP)/dt increased 5.0% and 10.0% (P less than or equal to 0.01 for both) above their CR values. The effect of the conditioned changes in neural activity on the AV node was observed by pacing the atrium from 110 to 180 bpm during the first 15 s of each trial period (i.e. control, CS+, UCS). The discrepancy between the atrial pace rate and the transmitted ventricular rate is expressed as a 'mean difference score' and serves as an index of the fidelity of the AV transmission process: the smaller the difference, the closer a 1:1 ratio of atrial vs ventricular beats is approached. The relatively large mean difference score for the control periods (46.0 +/- 9 bpm) indicates that the paced atrial impulse did not faithfully precede ventricular contraction during these periods. The mean difference significantly decreased (34.6%, P less than or equal to 0.05) during the CS+, and approached an almost 1:1 ratio (75.6% decrease from CS+ values, P less than or equal to 0.01) during food delivery. beta-Adrenergic blockade (propranolol, 1 mg/kg, i.v.) eliminated the changes in mean difference during the CS+ but not during food delivery. There were no statistically significant physiological changes during CS-.(ABSTRACT TRUNCATED AT 400 WORDS)