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Biomedical subjects

G A Zeballos

Publications and source records attributed to G A Zeballos.

29 records · Page 2Linked to original sources
PubMed1991

The role of vasopressin and atrial natriuretic factor in postoperative fluid retention after the Fontan procedure.

The Fontan procedure results in right atrial distention and is complicated by fluid retention. Since systemic fluid balance may be hormonally mediated in part and related to right atrium size, we measured plasma atrial natriuretic factor and plasma arginine vasopressin levels in 19 patients undergoing the Fontan procedure and in 12 control patients undergoing other types of heart operations. Preoperative plasma atrial natriuretic factor levels were higher in patients undergoing the Fontan procedure than in control patients (95 +/- 16 pg/ml preoperatively versus 50 +/- 8 pg/ml; p less than 0.05) and increased in patients undergoing the Fontan procedure to 330 +/- 48 pg/ml by postoperative day 2 (p less than 0.05) but not in control patients. Increased plasma atrial natriuretic factor levels could enhance capillary transudation, but elevated plasma atrial natriuretic factor levels should also enhance diuresis and prevent fluid retention. Vasopressin levels, however, were also increased in patients undergoing the Fontan procedure (from 9 +/- 2 pg/ml preoperatively to 144 +/- 37 pg/ml at end of operation) and were higher and remained elevated longer than in control patients undergoing heart operations (37 +/- 7, 20 +/- 4, 16 +/- 6 pg/ml on postoperative days 1, 2, and 3 to 10 for the Fontan group compared with 15 +/- 4, 4 +/- 1, 4 +/- 2 pg/ml for control patients). Vasopressin levels were highest in the Fontan group with the most severe fluid retention and effusions (for example, 51 +/- 10 pg/ml versus 23 +/- 4 pg/ml, on postoperative day 1). Increased vasopressin and atrial natriuretic factor could act synergistically to result in the development of effusions after the Fontan procedure when atrial natriuretic factor-induced capillary transudation is combined with vasopressin-induced antidiuresis.

Atrial Natriuretic Factor↗
PubMed1990

Regulation of plasma ANF after increases in afterload in conscious dogs.

Although atrial stretch is the primary stimulus for atrial natriuretic factor (ANF) secretion, hormones may directly affect ANF secretion or may indirectly influence ANF by changing left ventricular afterload, thereby altering atrial stretch. To determine whether direct effects are important for the release of ANF in vivo, we measured changes in plasma ANF and in atrial wall function in the conscious dog after the administration of vasopressin, angiotensin II, and phenylephrine and by mechanically increasing left ventricular afterload by partial aortic occlusion. Injections of phenylephrine, angiotensin II, and arginine vasopressin (AVP) that were chosen to cause similar changes in systemic arterial pressure resulted in similar changes in atrial pressure and diameter. Maximum V wave atrial wall stress increased to 283 +/- 12, 311 +/- 41, 327 +/- 24, and 277 +/- 22 g/cm2 for AVP, angiotensin, phenylephrine, and occlusion, respectively, and plasma ANF increased to 242 +/- 81, 248 +/- 62, 299 +/- 95, and 190 +/- 53 pg/ml. There were significant linear correlations between left ventricular afterload and left atrial pressure, and each method for increasing left ventricular afterload shifted the position to the left on an atrial pressure-diameter, compliance curve, by a similar degree. Thus changes in left ventricular afterload result in changes in atrial wall function and similar changes in plasma ANF. No hormonal-specific increase in plasma ANF was found in conscious dogs after increases in afterload.

Angiotensin II↗
PubMed1989

Atrial wall function and plasma atriopeptin during volume expansion in conscious dogs.

Mean left atrial pressure is believed to be an accurate estimate of atrial stretch in vivo and is used to assess the stimulus for atriopeptin release in both animals and humans. However, for a number of years it has been known that atrial stretch receptor discharge occurs during specific phases of the atrial cycle and that B-receptor discharge correlates with the passive filling of the atrium, which occurs during the V wave. The purpose of this study was to develop the concept that phase-specific changes in atrial wall stress are responsible for atriopeptin secretion. In chronically instrumented conscious dogs, volume expansion (1,000 ml of saline in 5 min) increased left atrial pressure and dimensions and caused a 663 +/- 189% increase in plasma immunoreactive atriopeptin from 44 pg/ml. At this time, mean left atrial pressure increased only 202 +/- 36% (mean +/- SE), whereas A wave pressure increased 146 +/- 19% and V wave pressure increased 290 +/- 67%. A and V wave dimensions increased only a few percent. After developing atrial wall thickness constants for diastole (KCl fixation) and systole (BaCl2 fixation), calculated atrial A wave wall stress increased 163 +/- 25%, and V wave wall stress increased 346 +/- 85%. Minute wall stress (wall stress times heart rate) gave an even better correlation with changes in plasma atriopeptin. V wave minute wall stress increased 690 +/- 168%, whereas A wave wall stress increased 366 +/- 56%.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Variable arginine vasopressin levels in neonatal congestive heart failure.

Arginine vasopressin levels in 17 neonates with cardiac disease were compared with control levels in 10 healthy newborn infants. Infants with congestive heart failure who were free of left ventricular outflow tract obstruction had a mean level of 80 +/- 18 pg/ml, which was significantly greater than the mean control level (p less than 0.001). Infants with congestive heart failure and left ventricular outflow tract obstruction had a mean vasopressin level of 3 +/- 0.7 pg/ml, which was lower than the mean control level of 6 +/- 0.7 pg/ml (p less than 0.05). The data suggest that impaired forward flow to high pressure sinoaortic and ventricular baroreceptors is necessary for vasopressin release in congestive heart failure. In left ventricular outflow tract obstruction with heart failure these receptors may be impaired or absent, leading to decreased vasopressin release. Low plasma arginine vasopressin may adversely affect circulatory homeostasis.

Acute Disease↗
PubMed1985

Ultrastructure and electrical activity of the rat neurohypophysis.

Ultrastructural and electrophysiological studies of the rat neurohypophysis was carried out following stimulation to cause vasopressin release. Unit activity was investigated with microelectrodes, filtered, integrated, and recorded simultaneously with blood pressure in a polygraph. The basal unit activity was challenged by perfusing the hypothalamus and pituitary gland with hypertonic, hypotonic, and isotonic solutions through the internal carotid and by bleeding. Posterior lobes were fixed in osmium tetroxide and stained with uranyl acetate for electron microscopy. Single unit activity from the neural lobe showed mostly a continuous pattern of activity with a rate of discharge (RD) of 7 to 30 pulses per 10 s during control periods. Following hypertonic stimulation, out of 20 units studied, 35% increased, 10% decreased, and 55% did not change their RD. The effect of bleeding was studied in 34 units. Following the withdrawal of 1 ml of blood from the jugular vein, 29% increased, 32% decreased, and 38% did not change their RD. It is concluded that the existence in the neurohypophysis of fibers which are excited or inhibited by stimuli known to cause vasopressin release supports the hypothesis of the existence of a modulatory mechanism for neuropeptide release in the neural lobe.

Animals↗
PubMed1975

Neurohypophysial electrical activity in the anesthetized cat.

The spontaneous electrical activity of the neural lobe of the cat hypophysis has been recorded. We have observed two types of activity: (1) 0.5-1.0 mV in amplitude and 4-6 msec in duration, and (2) 0.03-0.07 mV in amplitude and 1-2 msec in duration. The discharge rates of both types of activity are affected by osmotic stimuli known to influence vasopressin release. Nevertheless, only the smaller potentials were studied because they were easier to obtain. The typical response to injections of hypertonic saline was an increase in the discharge rate characterized by two peaks in the frequency-time curve. This activity seems to correspond to the unit activity described by several authors for neurosecretory hypothalamic units. Hypotonic injections cause, in about 45% of the injections, a 50% decrease in the firing rate. Injections of isotonic saline did not alter the discharge rate by the neurohypophysis. We conclude that elements in the neural lobe of the pituitary are electrically excitable and respond to stimuli known to cause vasopressin release.

Animals↗
PubMedDate not supplied

Contribution of the ventricles and the atrial appendages to the elevation of plasma atrial natriuretic factor (ANF) during pacing-induced heart failure in conscious dogs.

The goal of our study was to determine whether the elevation in plasma ANF was produced by the atrial appendages or ventricular tissue during pacing-induced heart failure in chronically instrumented conscious dogs (sham) or dogs with bilateral atrial appendectomy. Acute volume expansion caused a significant elevation of plasma ANF from 80 +/- 8 to 149 +/- 26 pg/ml (p < 0.01) in sham dogs, but caused no significant change from 67 +/- 7 to 84 +/- 8 pg/ml in atrial appendectomized dogs. There were increases in left ventricular end-diastolic pressure (LVEDP) and left atrial pressure (LAP) in both groups of dogs. After rapid left ventricular pacing (210-240 beats/min) for 4 weeks to induce heart failure, dogs in both groups had tachycardia, elevated LVEDP and higher LAP. Plasma ANF was increased by 250% to 283 +/- 64 pg/ml (p < 0.01) in sham dogs, and only 40% to 94 +/- 15 pg/ml (p > 0.05) in atrial appendectomized dogs. In response to volume expansion, there were further increases in LVEDP and LAP in both groups of dogs, but plasma ANF was not elevated (288 +/- 39 pg/ml) in sham dogs and only slightly increased (132 +/- 7 pg/ml) in atrial appendectomized dogs. Our results suggest that, during pacing-induced heart failure, the atrial appendages are the major source of elevated plasma ANF, and the remaining atrial and ventricular tissue, even when maximally stretched, can only modestly increase plasma ANF.

Animals↗