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Biomedical subjects

D W Ferguson

Publications and source records attributed to D W Ferguson.

At least 19 recordsLinked to original sources
PubMed2001

Hypogonadism following prostate-bed radiation therapy for prostate carcinoma.

BACKGROUND: The degree of testicular damage resulting from primary treatment of prostate carcinoma by external beam radiation therapy (EBRT) to the prostate bed has not been determined. If significant testicular damage has occurred, the resulting endocrine changes may result in modified tumor behavior, contribute to postradiation impotence, and may aggravate other signs and symptoms of hypogonadism, potentially influencing a patient's choice of primary treatment for his tumor. METHOD: Three to eight years after primary treatment for localized prostate carcinoma, serologic evaluation for hypogonadism was undertaken in 33 men who had received EBRT and in 55 similar men who had received radical prostatectomy (RP). No subjects had developed recognized tumor recurrence, and none had undergone hormonal treatment since primary therapy. RESULTS: Among men of similar age, prior treatment with EBRT was associated with significantly more frequent hypogonadism than prior treatment with RP. In men with EBRT, total testosterone levels averaged 27.3% less, free testosterone levels 31.6% less, dihydrotestosterone levels 33.4% less, luteinizing hormone (LH) levels 52.7% greater, and follicle-stimulating hormone (FSH) levels 100% greater than those values in men who had prior treatment with RP. Differences between postradiation and postsurgical men in LH and FSH levels were most prominent in men older than 70 years. CONCLUSIONS: Three to eight years after primary treatment for prostate carcinoma, striking hormone differences were present between men who had received EBRT to the prostate bed and those with prior RP. These differences strongly suggested that prominent and permanent testicular damage was sustained during EBRT, frequently severe enough to cause hypogonadism.

Aged↗
PubMed2000

Progressive osteoporosis during androgen deprivation therapy for prostate cancer.

PURPOSE: Hypogonadism is a prominent risk factor for osteoporosis in older men. However, bone loss during androgen ablation therapy for prostate cancer has rarely been quantitated. MATERIALS AND METHODS: Femoral neck bone mineral density was determined in 26 men before orchiectomy or chemical castration as initial hormone therapy for prostate cancer and at 6-month intervals thereafter for 6 to 42 months. Measurements were made in 16 other men at 12 to 24 months beginning 3 to 8 years after the onset of castration. Baseline and post-castration bone loss was related to several host and tumor characteristics, and compared to similar measurements in 12 control subjects. RESULTS: Average age corrected baseline femoral neck bone mineral density was higher in controls than in treated men and remained essentially unchanged for 2 years. Following orchiectomy average bone mineral density decreased 2.4% and 7.6%, respectively, during years 1 and 2 (2-year loss 2.5% to 17.0%), with similar losses documented in men undergoing chemical castration. Average bone mineral density decreased 1.4% to 2.6% per year 3 to 8 years after uninterrupted androgen deprivation. Age corrected baseline bone mineral density was greater in men who were obese, younger than 75 years or participated in regular exercise but the influence of each characteristic could not be isolated. Post-castration bone loss was greater in men who were obese, younger than 75 years without regular exercise. CONCLUSIONS: Chemical or surgical castration in men with prostate cancer is usually followed by greatly accelerated bone loss which may be superimposed on a bone mass already depleted before hormonal therapy. Baseline bone mass and subsequent bone loss may be influenced by host obesity, age and exercise habits.

Aged↗
PubMed1999

Trimming and shoeing the chronically affected horse.

Several of the technical approaches applied to the foot overlap with regard to intent. Frog or solar support, for example, may be provided either to stabilize the distal phalanx within the hoof capsule or in an effort to unload regional pain arising from the solar surface of the foot. It is likewise obvious that some techniques such as lowering the heels to achieve phalangeal realignment and raising the heels to relieve deep digital flexor tendon tension are contradictory. In these instances, it is not that one technique is always correct but that differences exist among horses. Currently, it is something of an art to define what specific technique is needed or, alternatively, how to best apply a specific technique. As more facts regarding how the normal and foundered foot function, the farrier's role in the rehabilitation of affected horses is likely to increase.

Animals↗
PubMed1998

Digital perfusion, evaluated scintigraphically, and hoof wall growth in horses with chronic laminitis treated with egg bar-heart bar shoeing and coronary grooving.

Nuclear scintigraphy was used to assess digital perfusion before and after treatment in 10 horses with clinical and radiographic evidence of chronic laminitis. Horses were evaluated for lameness, degree of distal phalanx rotation, and heel-toe hoof wall growth ratio, and randomly divided into two treatment groups. Group 1 horses received only egg bar-heart bar shoeing; Group 2 underwent egg bar-heart bar shoeing and coronary grooving. Horses were re-evaluated for digital perfusion, lameness, degree of distal phalanx rotation, and hoof wall growth at 6 week intervals over the 18 week follow-up period. Prior to treatment, relative scintigraphic activity at the dorsal laminar area was decreased and relative scintigraphic activity at the toe and adjacent solar area was increased. Egg bar-heart bar shoeing was associated with significantly increased dorsal laminar scintigraphic activity and significantly decreased solar scintigraphic activity over the 18 week period. Coronary grooving, in combination with egg bar-heart bar shoeing, resulted in a significantly lower heel-toe hoof wall growth ratio but did not enhance digital perfusion. Seven of 10 (70%) horses were responsive to treatment, defined as an improvement in lameness by at least one grade. Horses that were refractory to treatment had significantly lower dorsal laminar scintigraphic activity and higher palmar coronary scintigraphic activity prior to treatment than horses that responded to treatment. Our results are the first to demonstrate that egg bar-heart bar shoeing is associated with improved dorsal laminar perfusion, and support the use of this technique. In addition, we found that pre-treatment nuclear scintigraphy was predictive of clinical outcome in horses with chronic laminitis treated with corrective shoeing.

Animals↗
PubMed1995

Influence of resting sympathetic activity on reflex sympathetic responses in normal man.

Reflex sympathetic responses to physiologic stress are known to be modulated by afferent sensory mechanisms. However, the potential influence of baseline sympathetic tone on these reflex-mediated responses is unclear. To test the hypothesis that the resting level of muscle sympathetic nerve activity (MSNA) influences reflex-mediated changes in MSNA in normal man, MSNA, blood pressure (BP), central venous pressure (CVP), and heart rate (HR) was measured in 38 normal subjects at rest and during deactivation of cardiopulmonary baroreceptors (CPBR) with lower body negative pressure (LBNP; 0 to -15 mmHg). A cold pressor test (CPT) also was performed in 25 subjects. Incremental LBNP decreased CVP (from 5.8 +/- 0.4 to 2.1 +/- 0.4 mmHg) without altering BP or HR, and increased in MSNA burst frequency (from 22.5 +/- 1.4 to 30.2 +/- 1.4 bursts/min). There was no significant correlation between levels of MSNA and any haemodynamic parameter at rest. There was a significant inverse correlation between CPBR sympathetic gain (CPBRSG, slope of the regression line correlating percentage change in MSNA (bursts/min) per mmHg decrease in CVP during non-hypotensive LBNP) and resting MSNA (r = -0.72, p < 0.0001). A significant inverse correlation was also observed between MSNA responses to the CPT (expressed as percentage change in burst frequency from control) and the resting MSNA (r = -0.63, p = 0.008). Sixteen subjects were restudied 3 weeks to 14 months later to determine reproducibility of measurements; resting BP and CVP, HR, and MSNA levels were not different between the two sessions, as was CPBRSG. In ten of these 16 subjects, in whom the CPT was repeated the MSNA response also was not significantly different. These studies demonstrate an inverse relationship between resting MSNA and both cardiopulmonary baroreflex sensitivity and sympathetic neural responses to the non-baroreflex mediated cold pressor stimulus. These findings suggest that resting levels of sympathetic neural activity influence reflex-mediated changes in muscle sympathetic nerve activity.

Adult↗
PubMed1994

Differential effects of digitalis on chemoreflex responses in humans.

To investigate the effects of digitalis on chemoreflexes in humans, we measured muscle sympathetic nerve activity (microneurography), minute ventilation, oxygen saturation, end-tidal carbon dioxide, mean arterial pressure, heart rate, and central venous pressure during stimulation of peripheral chemoreceptors with hypoxia, during stimulation of central chemoreceptors with hypercapnia, and during a cold pressor test before and after digitalis and placebo in 10 healthy volunteers on two different days (randomized, double-blind, cross-over design). Digitalis did not affect baseline measurements significantly. Despite similar changes in oxygen saturation and end-tidal carbon dioxide during hypoxia and hypercapnia with both placebo and digitalis, digitalis significantly potentiated overall ventilatory responses to hypoxia (+67 +/- 12% before versus +98 +/- 3% after digitalis; mean +/- SEM; P < .01) but did not affect the response to hypercapnia. Sympathetic nerve activity increased by 25 +/- 9% during hypoxia before digitalis and 30 +/- 10% during hypoxia after digitalis (P = NS) and increased by 38 +/- 18% during hypercapnia before digitalis and 26 +/- 11% during hypercapnia after digitalis (P = NS). Digitalis did not significantly change responses to the cold pressor test. Placebo had no effect on ventilatory and sympathetic nerve activity responses. We conclude that digitalis selectively augments ventilatory responses to peripheral chemoreceptor stimulation by hypoxia.

Adult↗
PubMed1993

Importance of left atrial baroreceptors in the cardiopulmonary baroreflex of normal humans.

In animals, sympathetic responses to orthostasis are regulated in part by cardiopulmonary afferents arising from atrial and ventricular baroreceptors. To determine the relative importance of these baroreceptor regions in the cardiopulmonary baroreflex of normal humans, simultaneous measurements of left atrial and right and left ventricular volumes (cine computed tomography), invasive hemodynamics, forearm vascular resistance (plethysmography), and efferent sympathetic nerve activity to muscle (microneurography) were obtained under control conditions and with nonhypotensive lower body negative pressure (-10 mmHg, LBNP-10) in nine normal human subjects. LBNP-10 did not alter heart rate or mean systemic arterial pressure, but it did produce significant decreases in pulmonary artery diastolic and right atrial pressures. This reduction in cardiac filling pressures resulted in efferent sympathoexcitation evidenced by increases in forearm vascular resistance and efferent sympathetic nerve activity to the muscle. LBNP-10 did not alter end-diastolic volume of the left or the right ventricle. Similarly, ventricular stroke volume was unchanged during LBNP-10, as assessed by cine computed tomography or thermodilution techniques. In contrast, LBNP-10 resulted in a significant decrease in left atrial volume. Thus, LBNP produced a significant decrease in cardiac filling pressures and left atrial volumes with resultant reflex sympathoexcitation, whereas ventricular volumes were unchanged. These observations suggest an important role for left atrial (nonventricular) baroreceptor afferents in the cardiopulmonary baroreflex of normal humans.

Adult↗
PubMed1992

Digitalis and neurohormonal abnormalities in heart failure and implications for therapy.

A pathophysiologic hallmark of heart failure is neurohormonal excitation, a prominent feature of which is activation of the sympathetic nervous system. Studies from our laboratories demonstrate that clinical heart failure is characterized by marked increases in efferent sympathetic neural outflow to muscle; the magnitude of this sympatho-excitation parallels the degree of cardiac dysfunction. Impairments of cardiopulmonary and arterial baroreflex sensory mechanisms appear to be responsible to a significant degree for this sympatho-excitation, consistent with findings in animal models of heart failure. Digitalis glycosides exert modest inotropic actions when administered to patients with heart failure. Digitalis also has potent autonomic effects that can potentiate impaired arterial and cardiopulmonary baroreflex mechanisms in experimental models of cardiac dysfunction. Acute digitalis administration to patients with moderate-to-severe heart failure produces profound and sustained sympatho-inhibition, which precedes any observed hemodynamic action of the agent. Further, acute digitalization of such patients rapidly normalizes impaired baroreflex-mediated mechanisms. Data now suggest that the mechanism of action of digitalis in humans is an acute potentiation of baroreceptor-mediated afferent regulation of sympathetic neural mechanisms. Prospective, randomized and controlled studies now are required to test the hypothesis that the acute effects of digitalis on autonomic mechanisms also are observed during chronic administration. In theory, the chronic sympatho-inhibitory action of digitalis, combined with its chronic potentiation of impaired baroreflex mechanisms, may offer beneficial effects independent of its inotropic actions in patients with heart failure.

Digitalis Glycosides↗
PubMed1992

Clinical, hemodynamic and sympathetic neural correlates of heart rate variability in congestive heart failure.

Heart rate (HR) variability has long been recognized as a sign of cardiac health. In the presence of heart disease, HR variability decreases, an observation that has been associated with poor prognosis in a number of recent studies. HR variability is particularly altered in congestive heart failure (CHF), a condition associated with a number of typical functional hemodynamic and neurohumoral alterations. The relation of measurements of HR variability to these abnormalities in patients with heart failure has not been carefully examined. Twenty-three patients (19 men, 4 women, mean age 49 years) with New York Heart Association class II to IV CHF were studied prospectively without cardiac medications; radionuclide ventriculography, right-sided heart catheterization, peroneal microneurography, plasma norepinephrine and 24- to 48-hour ambulatory electrocardiography were performed. Average RR interval and its standard deviation, and HR power spectrum (0 to 0.5, 0.05 to 0.15 and 0.2 to 0.5 Hz) were derived from the ambulatory electrocardiographic recordings and compared with left ventricular ejection fraction, thermodilution cardiac output, pulmonary arterial wedge pressure, New York Heart Association class, age, muscle sympathetic nerve activity (peroneal nerve) and norepinephrine level by linear regression. None of the measures of HR variability were significantly related to age, left ventricular ejection fraction, cardiac output or functional classification, whereas the 0.05 to 0.15 and 0.20 to 0.50 Hz components were weakly but significantly related to cardiac output (r = 0.49 and 0.42, p = 0.02 and 0.045, respectively). In contrast, a generally stronger and negative relation was demonstrated between spectral and nonspectral measurements of HR variability, and indicators of sympathoexcitation, muscle sympathetic nerve activity and plasma norepinephrine.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1992

Effects of heart failure on baroreflex control of sympathetic neural activity.

Baroreflex control of heart rate, vascular resistance and norepinephrine is impaired in patients with heart failure, but recent animal studies demonstrate preserved baroreflex control of sympathetic nerve activity in this disorder. Studies were therefore performed to compare baroreflex control of efferent sympathetic nerve activity to muscle in 10 normal subjects (age mean +/- SEM 21 +/- 1 years) and in 11 patients with moderate to severe heart failure (age 48 +/- 5 years, New York Heart Association class II to IV, left ventricular ejection fraction 19 +/- 2%, pulmonary capillary wedge pressure 27 +/- 2 mm Hg, cardiac index 2.04 +/- 0.22 liters/min/m2). Baroreflex activation was produced by intravenous infusion of phenylephrine (0.5 to 2.0 micrograms/kg/min) and deactivation by infusion of nitroprusside (0.4 to 2.5 micrograms/kg/min). During phenylephrine infusion, comparable increases in mean arterial pressure were produced in normal subjects (89 +/- 2 to 99 +/- 3 mm Hg, p less than 0.01) and in patients with heart failure (90 +/- 2 to 99 +/- 3 mm Hg, p less than 0.01). The patients with heart failure exhibited significantly attenuated (p less than 0.01 for normal vs heart failure) decreases in heart rate (93 +/- 5 to 90 +/- 6 beats/min, p = not significant [NS]) compared with normal subjects (67 +/- 3 to 58 +/- 4 beats/min, p less than 0.01) and tended to demonstrate attenuated sympathoinhibitory responses to this pressor stimulus. More strikingly, patients with heart failure demonstrated significant impairment of baroreflex responses during nitroprusside-induced baroreceptor deactivation. In normal subjects, nitroprusside produced a decrease in mean arterial (90 +/- 2 to 80 +/- 3 mm Hg, p less than 0.001) and right atrial (4 +/- 1 to 2 +/- 1 mm Hg, p less than 0.01) pressures with a resultant reflex increase in heart rate (68 +/- 3 to 81 +/- 4 beats/min, p less than 0.001) and muscle sympathetic nerve activity (326 +/- 74 to 746 +/- 147 U/min, p less than 0.01). In patients with heart failure (n = 10), nitroprusside produced comparable (p = NS for normal vs heart failure) decreases in mean arterial (89 +/- 2 to 77 +/- 2 mm Hg, p less than 0.001) and right atrial (6 +/- 1 to 1 +/- 1 mm Hg, p less than 0.001) pressures, but did not significantly alter heart rate (91 +/- 6 to 97 +/- 4 beats/min, p = NS) or sympathetic nerve activity (936 +/- 155 to 1179 +/- 275 U/min, p = NS).(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed1992

Naloxone potentiates cardiopulmonary baroreflex sympathetic control in normal humans.

Naloxone, an opioid antagonist, augments baroreflex mechanisms in animals; this occurrence suggests that endogenous opioids blunt baroreflex responses. Limited human studies suggest an inhibitory action of endogenous opioids on baroreflex-mediated vagal responses during arterial baroreceptor deactivation. To evaluate the potential effect of endogenous opioids on cardiopulmonary baroreflex mechanisms in humans, we measured arterial and central venous pressures, heart rate, and efferent muscle sympathetic nerve activity (MSNA, by peroneal microneurography) during unloading of cardiopulmonary baroreceptors with incremental lower body negative pressure (LBNP, from 0 to -15 mm Hg) and during the cold pressor test in 21 normal subjects (aged 24 +/- 1 [mean +/- SEM] years). In 14 subjects, we performed LBNP before and after naloxone (0.15 mg/kg i.v.) and placebo (n = 11) on separate days. In six of these 14 subjects and an additional seven subjects (n = 13), studies were also performed before and after administration of a lower dose of naloxone (0.075 mg/kg i.v.) on separate days. Neither dose of naloxone significantly altered control arterial or central venous pressures or heart rate. Control MSNA was reduced after the higher but not after the lower dose of naloxone. Comparable reductions in central venous pressure were produced by LBNP in all groups before and after naloxone or placebo, whereas LBNP did not alter arterial pressure. Cardiopulmonary baroreflex sympathetic sensitivity, which was derived as the slope of the linear regression relation between percent change in total MSNA (units) per absolute change in central venous pressure (mm Hg) during incremental LBNP, was significantly augmented after both the high dose (from 18.6 +/- 4.7%/mm Hg to 39.3 +/- 8.1%/mm Hg, p = 0.001) and low dose of naloxone, whereas placebo had no effect. MSNA responses to the cold pressor test were not altered by either dose of naloxone. Thus, naloxone selectively potentiates cardiopulmonary baroreflex regulation of sympathetic neural activity in normal humans. These findings suggest that endogenous opioids exert a tonic inhibitory effect on sympathetic responses to orthostatic stress in normal humans.

Adult↗
PubMed1991

Sympathetic responses of patients with congestive heart failure to cold pressor stimulus.

Studies in patients with congestive heart failure (CHF) demonstrate blunting of sympathoexcitatory responses to baroreflex perturbation. Whereas experimental and limited clinical evidence suggests impairment of baroreflex mechanisms as the etiology of these attenuated responses, an alternative mechanism would be an inability of patients with CHF to increase sympathetic neural outflow above markedly elevated baseline levels. Hemodynamic and sympathetic neural responses (peroneal microneurography) were therefore compared of normal subjects (n = 10) and patients with CHF (n = 10) during the non-baroreflex sympathoexcitatory stimulus of the cold pressor test. The cold pressor stimulus produced increases in arterial pressure and heart rate in both groups. During hand immersion in ice water, normal subjects demonstrated significant increases in muscle sympathetic nerve activity expressed as burst frequency (20 +/- 2 to 28 +/- 3 bursts/min, p less than 0.01), total integrated nerve activity (224 +/- 41 to 342 +/- 62 U/min, p less than 0.05), and total activity corrected for accompanying changes in heart rate (375 +/- 81 to 538 +/- 118 U/100 heart beats, p less than 0.05). Similarly, despite elevated control levels of sympathetic activity, patients with CHF also demonstrated significant sympathoexcitatory responses to the cold pressor stimulus, with increases in muscle sympathetic nerve burst frequency (60 +/- 7 to 67 +/- 7 bursts/min, p less than 0.01) total integrated nerve activity (818 +/- 159 to 1,015 +/- 191 U, p less than 0.001), and total activity corrected for accompanying changes in heart rate (1,008 +/- 178 to 1,173 +/- 201 U/100 heart beats, p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1991

Percutaneous balloon pericardiostomy for non-surgical management of recurrent pericardial tamponade: a case report.

We report the case of a 26-year-old male with recurrent hemorrhagic cardiac tamponade occurring after initial management by needle pericardiocentesis and pigtail catheter drainage. As an alternative to open surgical pericardial fenestration, a percutaneous balloon pericardiostomy was performed with an 18 mm balloon catheter and over-the-wire insertion of a 16 F chest tube for 72 h of pericardial drainage. This non-surgical approach resulted in successful resolution of recurrent cardiac tamponade.

Adult↗
PubMed1991

Contrasting effects of digitalis and dobutamine on baroreflex sympathetic control in normal humans.

BACKGROUND: Digitalis glycosides augment cardiopulmonary baroreceptor mechanisms in animals. This could result from inotropic actions or from direct sensitization of cardiac mechanoreceptors. METHODS AND RESULTS: To determine if digitalis has similar actions in humans and to evaluate the mechanisms involved, we measured muscle sympathetic nerve activity (MSNA; microneurography) during unloading of cardiopulmonary baroreceptors with incremental lower body negative pressure (LBNP; 0 to -15 mm Hg) and during the cold pressor test in 22 normal subjects (age 22 +/- 1 year, mean +/- SEM). Arterial and central venous pressures, heart rate, and MSNA were measured during LBNP before and after intravenous digitalis (Cedilanid 0.02 ng/kg, n = 8), dobutamine (2.8 +/- 0.5 micrograms/kg/min, n = 8), or placebo (n = 6). Digitalis and dobutamine produced similar increases in baseline mean arterial pressure and decreases in central venous pressure and MSNA. LBNP produced similar decreases in central venous pressure in all groups before and after drug administration. The MSNA responses to LBNP were markedly potentiated by digitalis but not by dobutamine or placebo. CONCLUSIONS: Digitalis did not alter responses to the cold pressor test. Thus, digitalis selectively potentiated cardiopulmonary baroreflex regulation of sympathetic neural responses in normal humans, whereas dobutamine (another positive inotropic agent) did not produce this effect. We conclude that digitalis augments cardiopulmonary baroreflex control of sympathetic activity, probably by direct baroreceptor sensitization.

Adult↗