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Biomedical subjects

T J Ebert

Publications and source records attributed to T J Ebert.

At least 73 records · Page 4Linked to original sources
PubMed1989

Impedance-derived cardiac indices in supine and upright exercise.

Impedance cardiography was used to determine the classical systolic time intervals (STI's) (i.e., pre-ejection period (PEP), left ventricular ejection time (LVET) and the quotient PEP/LVET), in young, healthy, male subjects during supine and seated exercise. With increasing exercise, there was a tendency toward decreases in PEP, LVET, and PEP/LVET. In the seated position, there was an increase in transthoracic Zo incident to the caudal migration of thoracic blood--a result of the postural change. With seated exercise, there were--in contrast to supine exercise-greater decreases in PEP/LVET and greater increases in the Heather index. Similarly, there was a tendency toward increases in dZ/dtmin and the Rapid Ejection Index. We suggest that these differences are related to increased myocardial contractility resulting from the postural augmentation of cardio-sympathetic activity, added to that of exercise per se. This study, as well as previous ones, indicates that impedance cardiography is reliable, effective, and more practicable than the arteriographic method for monitoring STI's. We also believe that certain impedance-derived indices (i.e., transthoracic Zo, dZ/dtmin and the Heather Index) have considerable potential value for physiologic and clinical investigation.

Adult↗
PubMed1989

Partial attenuation of hemodynamic responses to rapid sequence induction and intubation with labetalol.

The effectiveness of labetalol (a combination nonselective beta and alpha-1-adrenergic receptor antagonist) in modifying hemodynamic responses associated with rapid sequence induction and tracheal intubation was evaluated. In a double-blind study, 24 ASA physical status I or II male patients scheduled for elective surgery were given either IV labetalol, 0.25 mg/kg (n = 8) or 0.75 mg/kg (n = 8), or a saline placebo (n = 8). Five minutes later, patients were given oxygen by mask and IV vecuronium, 0.01 mg/kg. Ten minutes after giving labetalol or placebo, cricoid pressure was applied and anesthesia was induced with IV sodium thiopental (4 mg/kg) and succinylcholine (1.5 mg/kg) 1 minute prior to intubation. The mean duration of laryngoscopy was 17 +/- 3 seconds. Prior to induction, the 0.25 mg/kg and 0.75 mg/kg doses of labetalol significantly (p less than 0.05) reduced mean arterial pressure by 4.4 +/- 1.9 and by 8.6 +/- 2.0 mmHg, respectively, but did not significantly alter heart rate or cardiac output. The 0.75 mg/kg dose of labetalol also significantly (p less than 0.05) decreased total peripheral resistance by 10.1 +/- 3.0%. Within 30 seconds after intubation, patients in all three groups exhibited increases in heart rate, mean arterial pressure, total peripheral resistance, and rate pressure product and a decrease in stroke volume. However, patients in the 0.25 and 0.75 mg/kg labetalol groups, compared to those in the placebo group, had significantly lower increases in peak heart rate (33 +/- 2 and 27 +/- 3 vs. 44 +/- 7 beats/minute), peak mean arterial pressure (38 +/- 6 and 38 +/- 7 vs. 58 +/- 7 mmHg), and peak rate pressure product (7,726 +/- 260 and 7,215 +/- 300 vs. 14,023 +/- 250 units). The results show that these doses of labetalol significantly blunt, but do not completely block, autonomic responses to rapid sequence induction and intubation.

Adult↗
PubMed1989

Increased intraoperative cardiovascular morbidity in diabetics with autonomic neuropathy.

Thirty-eight consenting subjects scheduled for elective ophthalmologic surgery were classified as nondiabetics (n = 21) or diabetics (n = 17) and were tested preoperatively for autonomic dysfunction. The autonomic tests consisted of respiratory sinus arrhythmia and heart rate responses to the Valsalva maneuver to test cardiac vagal function and diastolic blood pressure responses to head-up tilt and cold pressor test to assess sympathetic efferent integrity. At a separate time, anesthesia was established with fentanyl (2 micrograms/kg), sodium thiopental (3-5 mg/kg), and vecuronium (0.1 mg/kg), and maintained with isoflurane, oxygen, and nitrous oxide. An anesthesiologist, blinded to the autonomic test results, recorded perioperative blood pressure and heart rate. The autonomic test results revealed significant autonomic dysfunction among the diabetics. Heart rate and blood pressure declined to a greater degree (P less than 0.05) during induction of anesthesia in diabetics compared with controls and there was less of an increase in these same parameters following tracheal intubation in diabetic patients. Thirty-five percent of diabetics required intraoperative vasopressors compared with only 5% of control patients (P less than 0.05). A major finding was that the diabetics who required intraoperative blood pressure support had significantly greater impairment of autonomic test results compared with those diabetics who did not need vasopressors. Diabetics are at increased risk for cardiovascular lability during anesthesia and preoperative screening of diabetics with simple noninvasive autonomic tests may be useful in identifying those at high risk for perioperative cardiovascular instability.

Anesthesia, Inhalation↗
PubMed1989

Hemodynamic, renal, and hormonal responses to incremental ANF infusions in humans.

The effects of incremental exogenous alpha-human atrial natriuretic factor (ANF) infusion (10 and 25 ng.kg-1. min-1) on the cardiovascular, renal, and hormonal systems were examined in 22 healthy males. Successive 45-min infusions of ANF increased plasma levels five- and ninefold from a basal 42 +/- 5 pg/ml (P less than 0.01 and P less than 0.001). Hemodynamic responses provoked by ANF consisted solely of progressive reductions in central venous pressure (CVP) (P less than 0.05). Heart rate and mean arterial pressure were unaltered. Plasma renin activity, aldosterone, and vasopressin were not modified by either dose of ANF. However, plasma norepinephrine increased 32% during the 10-ng.kg-1.min-1 infusion (P less than 0.05) and remained elevated during the higher dose of ANF. Renal function was unaltered by the 10-ng.kg-1.min-1 infusion of ANF when compared with base line and placebo responses. The 25-ng.kg-1. min-1 infusion of ANF increased sodium excretion 100% from base line (P less than 0.05), whereas potassium excretion decreased 47% (P less than 0.05). Urine output increased significantly from 7.7 +/- 0.6 to 12.5 +/- 0.7 ml/min (P less than 0.05). These responses were not observed in the placebo group or in an additional group of four volunteers who received a continuous low-dose infusion of ANF (10 ng.kg-1.min-1) for two consecutive 45-min periods. Neither dose of ANF altered creatinine clearance or free water clearance. The data indicate that fivefold elevations (physiological levels) of plasma ANF do not influence renal or hormonal function.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1989

Effect of plasma sodium on aldosterone secretion during angiotensin II stimulation in normal humans.

Studies were carried out in normal male subjects (n = 6, age 20-35 years) to determine the interaction of angiotensin II and plasma sodium on aldosterone secretion. These relations were quantified by elevation of plasma sodium with an infusion of 5% sodium chloride (4 ml/kg/30 min i.v.) with measurements of plasma aldosterone, atrial natriuretic factor (ANF), and arginine vasopressin (AVP) over 3 hours. Two hours before sodium chloride infusion, an intravenous infusion of angiotensin II was begun at 0.5 or 5.0 ng/kg/min and continued throughout the study. Plasma potassium was maintained constant by the addition of potassium to the infusate. NaCl/KCl infusion raised plasma sodium 4 meq/l with no decreases of plasma potassium. Plasma aldosterone averaged 7 +/- 1.8 ng/dl before NaCl infusion in subjects infused with 0.5 ng angiotensin II and was not significantly reduced with sodium chloride infusion. Angiotensin II infused at 5 ng/kg/min resulted in average plasma aldosterone levels of 31 +/- 3.6 ng/dl, which sodium chloride infusion decreased to 16.6 +/- 1.3 ng/dl (p less than 0.05) in 60 minutes. Plasma aldosterone remained depressed for the remaining period of study. Plasma ANF increased from 40 to 60 pg/ml with sodium chloride infusion. We conclude that small physiological elevations of plasma sodium concentrations can signal substantial decreases of plasma aldosterone in normal human subjects in situations where plasma angiotensin II is moderately elevated. The precise mechanisms of these responses remain to be determined.

Adult↗
PubMed1989

Nitrous oxide augments sympathetic outflow: direct evidence from human peroneal nerve recordings.

Direct evidence for postganglionic sympathetic nerve activation to blood vessels supplying skeletal muscle was sought by recording from the peroneal nerve of 13 volunteers with a 5-mu tipped tungsten needle. Eight subjects breathed through an anesthesia face mask connected to a semiclosed anesthesia circuit for two consecutive 10-min periods while 25% and 40% nitrous oxide (N2O) was administered sequentially. Five subjects served as controls and breathed equivalent concentrations of nitrogen. Blood pressure and central venous pressure were recorded from radial artery and jugular vein catheters. Forearm blood flow was measured by venous occlusion plethysmography. Peroneal nerve recordings were amplified 100,000-fold and integrated for analysis of burst frequency. N2O did not significantly alter respiratory rate, end-tidal CO2 (mass spectrometry), and diastolic or central venous pressures but did produce small but significant increases in heart rate and systolic pressure compared to time-control (P less than 0.05). In contrast, N2O was associated with progressive, large increases in muscle sympathetic nerve activity (peak % delta = 69 +/- 22 burst/min [X +/- SEM]) and forearm vascular resistance (30 +/- 4%) and a nonsignificant increase in plasma norepinephrine levels. Thus, brief exposure to 25% and 40% N2O produces striking increases in sympathetic outflow to skeletal muscle in humans.

Adult↗
PubMed1988

Reflex activation of sympathetic nervous system by ANF in humans.

Recent studies in experimental animal preparations suggest that ANF might alter sympathetic nervous system function. In the present investigation, direct recordings of postganglionic muscle sympathetic nerve activity were obtained from the peroneal nerve of conscious human volunteers. These data and hemodynamic parameters were recorded before and during infusions of atrial natriuretic factor (ANF, 99-126) or placebo (isotonic saline) in 10 subjects. Base-line ANF (36.5 +/- 3.8) increased to 329 +/- 22 pg/ml during 20-min infusions of ANF (15 ng.kg-1.min-1). This did not alter heart rate or blood pressure but reduced central venous pressure (CVP) by 47 +/- 10% (P less than 0.01). Base-line-integrated sympathetic activity (14.4 +/- 2.4 bursts/min) increased 30 +/- 12% during ANF infusion (P less than 0.05). However, when CVP was fixed at control levels with head-down tilt or lower body positive pressure, sympathetic activity was unchanged from pre-ANF base-line levels. These data indicate that exogenous infusions of ANF reduced CVP and unloaded cardiopulmonary baroreceptors. This elicits reflex increases of muscle sympathetic efferent activity. When CVP is maintained at control levels, ANF does not alter sympathetic neural outflow to muscles.

Atrial Natriuretic Factor↗
PubMed1988

Atrial natriuretic factor attenuates carotid baroreflex-mediated cardioacceleration in humans.

We tested the hypothesis that infusions of atrial natriuretic factor (ANF) attenuate carotid baroreflex-mediated tachycardia in humans. The afferent profile from carotid baroreceptors was altered by repeated, intermittent random applications of neck suction (40 mmHg) and neck pressure (20 mmHg) to healthy volunteers during supine control and during infusions of 15 (n = 6) or 25 ng.kg-1.min-1 (n = 9) of alpha-human ANF or during placebo (n = 9). ANF infusions resulted in five- and eightfold increases of plasma ANF, which did not alter base-line cardiac interval, blood pressure, respiratory sinus arrhythmia, plasma renin activity, vasopressin, or norepinephrine but did reduce central venous pressure. Reflex bradycardic responses were unaltered during these infusions. Reflex tachycardic responses to carotid compression were significantly blunted (up to 40%) during infusions of ANF and were unchanged during placebo. These responses may be due to a sensitization of cardiac receptors and augmentation of cardiac-vagal afferent traffic by ANF, which diminishes reflex cardiac-sympathetic outflow during carotid baroreceptor unloading.

Adult↗
PubMed1988

Carotid baroreflex responsiveness in high-fit and sedentary young men.

The influence of fitness on cardiac vagal activity and baroreflex-mediated control of heart rate has not been clearly established in humans. Therefore, we studied resting cardiac vagal activity by evaluating respiratory sinus arrhythmia (RSA) and examined carotid-cardiac baroreflex responsiveness with a neck collar in 11 high-fit and 9 sedentary [based on maximal O2 consumption (VO2max) and history of physical activity] healthy young men (19-31 yr of age). Resting cardiac vagal activity was determined from the standard deviation of 100 consecutive resting R-R intervals. Baroreflex responsiveness was determined from the R-R interval responses to neck suction and pressure (repeated trials of 5-s stimuli of -20, -40, and 35 mmHg). Both RSA and the bradycardic (R-R interval) responses to neck suction of -40 mmHg were significantly greater (P less than 0.05) in the high-fit individuals (RSA, 116.5 +/- 11.5 ms; neck-suction response, 145.3 +/- 17.0 ms; mean +/- SE) compared with sedentary subjects (RSA, 65.2 +/- 6.6 ms; neck-suction response, 86.9 +/- 12.5 ms). Responses of the high-fit volunteers to the other intensities of neck stimuli (-20 and 35 mmHg) showed a similar trend but were not significantly different from those of the sedentary volunteers. The baroreflex slope derived from these data was significantly greater in the high-fit subjects (4.00 +/- 0.39 ms/mmHg) compared with the sedentary controls (2.53 +/- 0.28 ms/mmHg). These data suggest that resting cardiac vagal activity is greater, carotid-to-cardiac activity is well maintained, and baroreflex sensitivity, i.e., slope, is augmented in high-fit subjects.

Adult↗
PubMed1988

Dynamic cardiovascular responses to infusions of atrial natriuretic factor in humans.

We sought to demonstrate a hypotensive effect from infusions of atrial natriuretic factor (ANF) into humans and to describe the mechanism(s) of this effect. Cardiovascular and hormonal responses to human ANF-(99-126) (125 ng/kg bolus followed by a 30-minute infusion at 25 ng/kg/min) were determined in eight conscious volunteers and compared with responses of eight time-control subjects who received isotonic saline. Baseline levels of ANF (52.8 +/- 5.5 pg/ml) increased 8.8-fold after 30 minutes of ANF infusion but were unchanged in the time controls. Plasma levels of renin, aldosterone, vasopressin, sodium, potassium, and osmolality did not change during infusions. A transient 5% reduction in mean arterial pressure related to a 12% reduction in peripheral resistance was observed 10 minutes after the priming bolus of ANF. This response was not sustained during the remainder of the ANF infusion period, nor did it occur in two additional subjects who received ANF infusions without the priming bolus. Steady state responses consisted of significant reductions in central venous pressure (15%), stroke volume (13%), and cardiac output (10%), but no reduction in blood pressure. Plasma norepinephrine levels and peripheral resistance increased (34% and 9%, respectively) during ANF administration. These data indicate that steady state responses to ANF in humans consist of decreases in cardiac filling pressures, which reduce cardiac output, unload cardiopulmonary baroreceptors, and activate the sympathetic nervous system. Blood pressure is well maintained despite striking increases in plasma ANF.

Adult↗
PubMed1988

Fentanyl-diazepam anesthesia with or without N2O does not attenuate cardiopulmonary baroreflex-mediated vasoconstrictor responses to controlled hypovolemia in humans.

Cardiopulmonary baroreceptors located primarily on the low-pressure side of the circulation sense slight reductions in cardiac filling pressures and elicit sustained peripheral vasoconstriction. Because most inhalation and many intravenous anesthetics attenuate arterial baroreflex function, the low-pressure baroreflex may serve a major role in maintaining blood pressure during intraoperative hypovolemia. To activate the low-pressure baroreflex, progressive nonhypotensive reductions in central venous pressure were produced with graded applications of lower body negative pressure (LBNP, -5, -10, -15 mm Hg) in 18 ASA class I patients before elective surgery. This produced linear reductions in stroke volume as determined by impedance cardiography and cardiac output. Cardiopulmonary baroreflex-mediated increases in total and forearm vascular resistance assisted in maintaining stable blood pressure. After ten patients were anesthetized with fentanyl (12.5 micrograms/kg) and diazepam (0.25 mg/kg) and an additional eight received these agents plus supplemental N2O (70%), reflex vasoconstrictor responses to LBNP were not attenuated and, therefore, blood pressure continued to be well maintained despite substantial reductions in cardiac filling pressures. Thus, these anesthetic regimens preserved vasoconstrictor responses mediated by cardiopulmonary baroreflexes. This promoted cardiovascular stability that may be particularly beneficial in patients with cerebral, cardiovascular, or renal disease undergoing surgical procedures with potential for rapid blood loss.

Adult↗
PubMed1987

The effect of age on hemodynamic response to graded postural stress in normal men.

We studied the hemodynamic effect of graded gravity (g) increments from 10 degrees headdown (-0.17 g) to 70 degrees headup (+0.94 g) tilt on young (20 to 29 years), middle-aged (40 to 49 years) and older (60 to 69 years), healthy men. Thoracic blood volume and ventricular stroke volume decreased linearly with increasing g levels. Heart rates and diastolic pressures increased, but only at the higher g levels; however, the increases were significantly less in the 60- to 69-year-old men. The results indicate that thoracic blood volume and ventricular stroke volume are remarkably gravity dependent over the entire tilt range in all groups, the lesser heart rate and diastolic pressure responses in older participants are significant circulatory handicaps and may contribute to the increased incidence of postural hypotension in elderly persons, the sharp rise in vascular resistance at lower +g levels (when arterial pressure is unchanged) suggests that cardiopulmonary reflexes play an important role in human circulatory adjustment to the headup posture.

Adult↗
PubMed1986

Effects of fentanyl-diazepam-nitrous oxide anaesthesia on arterial baroreflex control of heart rate in man.

The effects of fentanyl 7.5 micrograms kg-1 (group I), 10.0 micrograms kg-1 (group II) and 12.5 micrograms kg-1 (group III) with diazepam 0.25 mg kg-1 and 70% nitrous oxide on baroreflex control of heart rate in humans were investigated. Phenylephrine (the pressor test), sodium nitroprusside (the depressor test) and graded neck suction provoked baroreflex responses. In group I the pressor, depressor and neck suction baroreflex slopes decreased during anaesthesia. In groups II and III the depressor test slopes were also decreased during anaesthesia. However, the slopes derived from the pressor and neck suction tests did not decrease. These data suggest that baroreflex control of heart rate is attenuated during low doses of fentanyl (7.5 micrograms kg-1). Baroreflex mediated tachycardia is decreased by higher doses of fentanyl (10.0 and 12.5 micrograms kg-1). However, baroreflex-mediated bradycardia is maintained during the higher doses of fentanyl. We suggest this effect is the result of enhanced vagal efferent activity mediated by fentanyl.

Adult↗
PubMed1986

Baroreflex responsiveness is maintained during isometric exercise in humans.

The simultaneous rise in heart rate and arterial pressure during isometric handgrip exercise suggests that arterial baroreflex control may be altered. We applied incremental intensities of neck suction and pressure to nine healthy young men to alter carotid sinus transmural pressure. Carotid stimuli were delivered during 1) supine control, 2) "anticipation" of beginning exercise, and 3) handgrip (20% of maximum voluntary contraction). Anticipation was a quiet period, immediately preceding the beginning of handgrip, when no muscular work was being performed. Compared with control, the R-R interval prolongation and mean arterial pressure decline provoked by carotid stimuli were decreased during the anticipation period. These data suggest that influences from higher central neural locations may alter baroreflex function. Furthermore, we derived stimulus-response curves relating carotid sinus transmural pressure to changes in R-R interval and mean arterial pressure. These curves were shifted during handgrip; however, calculated regression slopes were not changed from control. The data indicate that isometric handgrip exercise has a specific influence on human carotid baroreflex control of arterial pressure and heart period: baroreflex function curves are shifted rightward during handgrip, whereas baroreflex sensitivity is unchanged. Furthermore, central neural influences may be partially involved in these alterations.

Adult↗
PubMed1986

Vasopressin reduces cardiac function and augments cardiopulmonary baroreflex resistance increases in man.

We examined the effects of physiologic infusions of arginine vasopressin (AVP) on cardiovascular hemodynamics and on reflex responses initiated by decreasing cardiopulmonary baroreceptor stimulation (with lower body negative pressure) in 10 healthy, captopril-pretreated young men (19-27 yr). Their responses were compared with those of four volunteers given isosmotic infusion. Heart rate, stroke volume, blood pressure, and forearm blood flow were measured by electrocardiography, impedance cardiography, radial artery cannulation, and strain gauge plethysmography. Two 55-min infusions of AVP at rates of 0.15 and 0.40 ng/kg per min increased average plasma concentrations from control levels of 5 pg/ml to 18 and 36 pg/ml, respectively. These infusions resulted in progressive reductions of heart rate and cardiac output and increases of forearm and total peripheral resistance. Blood pressure increases were significant only during the larger AVP infusion rate. Lower body negative pressure provoked reflex increases of total peripheral resistance. These increases were enhanced 60% during AVP infusion compared with increases during control (pre-AVP). Baseline measurements and reflex responses were unchanged by isosmotic infusions. These results demonstrate that AVP has profound effects on cardiovascular function and augments cardiopulmonary baroreflex-mediated increases of peripheral resistance in man.

Adolescent↗
PubMed1986

The use of thoracic impedance for determining thoracic blood volume changes in man.

In these studies, strong inferential evidence is provided which suggests that thoracic impedance provides reliable estimates of thoracic blood volume changes in man. There were 24 volunteers studied in 4 different experiments. The results of these studies are as follows: Impedance derived blood volume changes in the calf of man correlate closely with standard estimates of calf blood volume changes made with strain gauge plethysmography. There is a close linear relationship between the increase of thoracic impedance and the increase of calf blood volume during head-up tilt. Volunteers who develop syncope during head-up tilt (presumably due to excessive decreases of central blood volume) demonstrate exaggerated increases of thoracic impedance. Decreases in central venous pressure produced by lower body negative pressure are significantly correlated to thoracic impedance increases.

Adult↗
PubMed1985

Halothane anesthesia attenuates cardiopulmonary baroreflex control of peripheral resistance in humans.

The effects of halothane anesthesia on cardiopulmonary (low pressure) baroreflex control of peripheral resistance were studied in 10 ASA class I young men. Graded (-5, -7.5, -10, -12.5 mmHg) lower body negative pressure (LBNP) was used to produce progressive decreases in thoracic blood volume and central venous pressure. These stimuli activate reflexes from cardiopulmonary baroreceptors. Volunteers were studied while awake and during 1 MAC (0.75%) and 1.25 MAC (0.93%) halothane anesthesia. Hetastarch (6%) in 0.9% normal saline was infused into patients before baseline recordings were initiated. Blood pressure, stroke volume, cardiac output, and systemic and forearm vascular resistance decreased and forearm blood flow increased during halothane anesthesia. In awake subjects, LBNP did not alter heart rate or blood pressure, but stroke volume and cardiac output decreased. Blood pressure was maintained by cardiopulmonary baroreflex-mediated increases in peripheral resistance. In anesthetized subjects, decreases in stroke volume and cardiac output during LBNP were similar to awake responses, however, hypotension occurred because reflex resistance increases were markedly attenuated. The authors conclude that halothane anesthesia blunts cardiopulmonary baroreflex resistance responses provoked by mild decreases in thoracic blood volume in humans.

Adult↗