Heart rate reactivity and type A behavior as modifiers of physiological response to active and passive coping.
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Adaptation, Psychological↗
Biomedical subjects
M F Wilson
Publications and source records attributed to M F Wilson.
Predicting response to a reaction time task: heart rate reactivity compared with type A behavior.
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Adult↗
Effects of caffeine on vascular resistance, cardiac output and myocardial contractility in young men.
The mechanisms by which caffeine typically elevates blood pressure (BP) in humans have not been previously examined using a placebo-controlled design. Accordingly, oral caffeine (3.3 mg/kg body weight, equivalent to 2 to 3 cups of coffee) was given on 2 days and a placebo was given on 1 day to 15 healthy young men using a double-blind, crossover procedure. All 3 test sessions were held during a week of caffeine abstinence. Multiple measurements were made on subjects at rest (baseline values) and over a 45-minute interval after ingestion of caffeine for BP, heart rate, systolic time intervals and thoracic impedance measures of ventricular function. Baseline measurements were highly reliable for each subject across all sessions and yielded means for placebo vs caffeine days that were not different. Caffeine increased systolic and diastolic BP (p less than 0.01) and decreased heart rate (p less than 0.05). The pressor effect was due to progressively increased systemic vascular resistance and resulted in greater stroke work (p less than 0.01). There was no indication that caffeine increased cardiac output or contractility. These actions of caffeine were replicable when each caffeine day was tested separately against the placebo day. These results suggest that caffeine use by persons with cardiovascular diseases should be examined to determine whether caffeine's enhancement of vascular resistance may contribute to systematic hypertension and/or create excessive demands for cardiac work.
Adult↗
A specific method for the determination of soluble sugars in plant extracts using enzymatic analysis and its application to the sugar content of developing pear fruit buds.
A simple manual method for the routine analysis of glucose, fructose, mannose, galactose, and sucrose in plant material is described. The technique is demonstrated using various seeds known to form part of the diet of the bullfinch (Pyrrhula pyrrhula L.), a pest of commercial orchards in southeast England. The method involves the overnight extraction of the sugars with 62.5% aqueous methanol, followed by the conversion of the individual sugars to gluconate 6-phosphate (or, in the case of galactose, to galactono-gamma-lactone) by specific enzymes, and their determination spectrophotometrically.
Carbohydrates↗
Activation patterns to aversive stimulation in man: passive exposure versus effort to control.
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Adult↗
The effects of H1 and H2 histamine receptor antagonists on the development of endotoxemia in the conscious, unrestrained rat.
This study was designed to use the H2 antagonist cimetidine and the H1 antagonist diphenhydramine alone and in combination to clarify the role of histamine in the development of endotoxin shock. The jugular vein and the carotid artery of male Sprague-Dawley rats were cannulated during enflurane anesthesia. After recovery, blood pressure, heart rate, and respiration rate were continuously monitored. Animals were pretreated with saline, a combination of the H1 and H2 receptor antagonists diphenhydramine (20 mg/kg) and cimetidine (80 mg/kg), or individual doses of diphenhydramine or cimetidine. After pretreatment an endotoxin bolus (40 mg/kg) was given. Arterial blood samples (0.35 ml) were taken before endotoxin and after endotoxin at 60 and 240 min for measurement of pH, PO2, PCO2, hematocrit, glucose, and lactate. Pathological examinations were made at 240 min. Four additional groups of animals (N = 10) were studied for the effect of each of the treatment modes on 24-hr survival rate. Treatment with cimetidine plus diphenhydramine prevented the endotoxin-induced blood pressure fall, increase in heart rate, and hypoglycemia; increased the 24-hr survival rate from 10 to 60%; and inhibited the small intestinal pathology found in control rats. Treatment with diphenhydramine alone produced similar results except that there was a gradual blood pressure decrease later in shock. The results obtained from the cimetidine-treated groups were much the same but there was a slight, transient decrease in blood pressure early after endotoxin and the survival rate was increased to 90%. These results demonstrate that in the conscious rat antagonism of the H1 and/or H2 receptors modifies hemodynamic and metabolic responses and the subsequent pathology, altering the course of endotoxin shock and survival. This study provides substantial evidence to implicate histamine as one of the key vasoactive mediators in the development of endotoxin shock.
Analysis of Variance↗
Evaluation of cardiac output, total peripheral vascular resistance, and plasma concentrations of vasopressin in the conscious, unrestrained rat during endotoxemia.
To eliminate the influence of anesthesia while investigating the role of vasoactive hormones during shock, we have developed an unanesthetized rat model that provides information on key cardiovascular parameters pertinent to shock. Enfluane anesthesia was used while the animals were being catheterized. After recovery from anesthesia, endotoxin (40 mg/kg) was given, and after 4 hr of measurements, animals (11) were killed. Cardiac index (CI) fell significantly 5 min after endotoxin and remained depressed for 4 hr. Mean blood pressure (MBP) decreased from 121 +/- 5.7 mmHg to 79 +/- 5.6 at 5 and 15 min, and increased to 113 +/- 3.0 at 180 min. Central venous pressure (CVP) was decreased from 30 min to the end of the study. Heart rate (HR) increased from 357 +/- 13 to a high of 448 +/- 14 at 5 min and remained at well over 400 for the 4-hr monitoring period. Total peripheral vascular resistance (TPVR) was twice that of the control at 30 min and remained elevated. Stroke volume decreased to 37% of that of the control at 15 and 30 min and remained at 50% of that of the control until sacrifice. Plasma concentrations of vasopressin measured by radioimmunoassay increased from 14 pg/ml (+/- 2.2, SEM) to 144 (+/- 56) and 144 (+/- 66) at 15 and 240 min after endotoxin. Pathological examination at the end of the study revealed extensive hemorrhage in all areas of the small intestine. We conclude that in the conscious endotoxic rat decreases in CI, MBP, and CVP are accompanied by compensatory increases in HR and TPVR; plasma vasopressin concentrations are greatly elevated; and severe small intestinal hemorrhage occurs. The control animals (12) were stable throughout the entire study period, establishing the conscious, instrumented, unrestrained rat presented here as an attractive model for the study of shock without the bias of anesthesia.
Animals↗
Laryngoscopic endotracheal intubation of rats for inhalation anesthesia.
Endotracheal intubation of the rat under direct vision is described together with the details of procedures and apparatus for conducting inhalation anesthesia in this species. Our intubation method requires no special manufacture of equipment, because it employs the human laryngoscope equipped with an infant blade (size 0). Using inhalation anesthetics such as enflurane or halothane for induction, clear laryngoscopic visualization of the glottis is reliably obtained, allowing rapid and routine intubation of the rat in a highly predictable amount of time. In contrast, the injected anesthetics such as ketamine or pentobarbital sodium seem unsuited to laryngoscopic intubation as a result of problems of variable induction times, copious oral secretions, and strong pharyngeal-laryngeal reflexes.
Anesthesia, Inhalation↗
Anesthetic-induced changes in cardiovascular and small intestinal responses to endotoxin in the rat.
The influence of anesthesia on endotoxin shock patterns in the rat was examined. Blood pressure, heart rate, arterial blood gases, glucose, lactate, and pathology of the small intestine were measured before and after endotoxin (40 mg/kg) challenge in male Sprague-Dawley rats. The three groups studied were: (1) enflurane anesthetized (N = 10), (2) ketamine anesthetized (N = 10), and (3) awake and unrestrained (N = 13). Measurements were made during 30 min prior to endotoxin injection (IV) and for 240 min afterward. Reflex tachycardia, which occurred in the awake group simultaneously with the initial endotoxin-induced hypotension, was not present during either enflurane or ketamine anesthesia. Significantly less gross intestinal pathology was found at 4 hr after endotoxin in the anesthetized groups compared to the awake group. These results suggest that the response of the sympathoadrenal system to the hypotension following endotoxin may be blunted in the anesthetized animal.
Anesthesia↗
Physiologic responses to epinephrine infusion: the basis for a new stress test for coronary artery disease.
Since many patients with chest pain cannot exercise adequately, an alternative stress would be useful to evaluate coronary reserve. We studied the physiologic responses to epinephrine to assess its potential. We report on 39 patients with chest pain. Doses from 0.03 to 0.30 micrograms/kg/min were administered intravenously. Heart rate increased from 72 +/- 10 to 86 +/- 12 bpm (mean +/- SD), systolic blood pressure (BP) from 122 +/- 20 to 158 +/- 18 mm Hg (increased afterload), and rate-pressure product/100 from 88 +/- 21 to 133 +/- 18. Rate-corrected pre-ejection period decreased from 141 +/- 23 to 92 +/- 14 msec and LVET/PEP ratio from 0.41 +/- 0.1 to 0.24 +/- 0.05 (increased contractility). Increased afterload and contractility increased myocardial oxygen demand. Simultaneously diastolic time and BP decreased, reducing myocardial blood supply. The endocardial viability ratio fell from 1.27 +/- 0.3 to 0.80 +/- 0.2. These data suggest that epinephrine infusion would be a useful stress test for coronary disease and are supported by a sensitivity of 87% and specificity of 100% in 23 patients with known coronary anatomy.
Adult↗
Detection of the 'hyperdynamic state' of sepsis in the baboon during lethal E. coli infusion.
This study was designed to document the early responses of the baboon to LD100 E. coli infusion with an emphasis on cardiovascular, respiratory, and metabolic alterations. Adult baboons were anesthetized, catheterized aseptically to monitor cardiopulmonary and systemic parameters, and infused with LD100 E. coli intravenously for 2 hours. Cardiac output was determined with an Edwards Laboratory Thermodilution Cardiac Output Computer. Oxygen contents of systemic and pulmonary artery blood were determined with a Van Slyke Manometric Apparatus. Results demonstrate early significant increases in cardiac output, oxygen uptake, heart rate, rectal temperature, respiratory rate and minute volume, and decreases in mean systemic arterial pressure and total peripheral resistance. Pulmonary vascular resistance remained relatively constant. In conclusion, an early 'hyperdynamic state' has been detected in the baboon during lethal E. coli infusion (similar to that documented in humans with sepsis) characterized by compensatory alterations in cardiovascular hemodynamics, respiration, and metabolism.
Animals↗
The benefits of corticosteroid given after the onset of hypotension during endotoxin shock in the conscious rat.
We have shown that prophylactic treatment with a high dose of corticosteroid stabilizes the cardiovascular system, prevents hemorrhage of the small intestine, and improves survival. In this study we evaluated the effect of corticosteroid administered early after the manifestation of shock induced by endotoxin on blood pressure, heart rate, respiration rate, hematocrit, blood glucose, acid-base parameters, small-intestinal hemorrhage, and survival in the conscious rat. Male Sprague-Dawley rats were anesthetized with 2% enflurane and cannulae were placed in the carotid artery and jugular vein. Following recovery the animals were challenged with endotoxin (20 mg/kg). After the mean blood pressure had fallen to below 70 mm Hg the animals received corticosteroid (300 mg/kg) or an equivalent volume of saline. Supplemental doses of 30 mg/kg were given 90 min and 180 min after the initial dose. In groups other than those dealing with survival, rats were sacrificed after 4 h for pathological examination. When endotoxin was administered to untreated animals, 0/10 were alive at 15 h. In the treated group, 6/10 were alive at 24 h. Treatment shortened the early hypotensive period, but resulted in lower blood pressure from + 60 min to sacrifice. Heart rates in the treated animals were lower, pulse pressures were higher, and respiration rates were the same. Corticosteroid treatment prevented hypoglycemia, hemoconcentration, and acidemia, and markedly inhibited hemorrhage of the small intestine. Large-dose corticosteroid treatment is highly effective even when administered after the first evidence of shock induced by endotoxin in the conscious rat.
Animals↗
Release of vasoactive hormones and circulatory changes in shock.
Circulatory shock mechanisms that may result in the acute renal failure (ARF) syndrome are summarized. Both circulatory and neurohumoral mechanisms leading to the shock state and ARF are emphasized. Release of vasoactive hormones, with a review of vasodilators and vasoconstrictors, is discussed in terms of release mechanisms, onset of release, magnitude and duration of plasma elevation, and the basal plasma level of each. Hemodynamic diagnoses in shock in both the classical low cardiac output and the early sepsis high cardiac output syndromes are commented upon with emphasis on the importance of early diagnosis and adequate measurements of the circulatory state for optimum therapy. The septic hyperdynamic syndrome is reviewed with particular regard to changes in the renal circulation and function. Mechanisms of lactic acidemia in the hyperdynamic syndrome in the presence of adequate nutrient tissue flow are discussed. Elevations of vasoactive hormones and their relationship to the early shock state are mentioned. Their elevations in late shock are reviewed with critical comments given as to the possible interactions and importance of the vasodilator and vasoconstrictor actions on organ function and survival. Blood pressure alone is not a good indicator of progress in the management of septic shock.
Acute Kidney Injury↗
Mechanisms of splenectomy protection in epinephrine-induced renal and cardiac necrosis.
This study was intended to elucidate the mechanism(s) of protection afforded by splenectomy against EPI-induced ATN and myocardial necrosis. Renal function parameters, hematocrit, circulating catecholamines (EPI and NE), serum enzymes (CPK and SGOT), and urinary PGE2 were measured before and during intravenous infusion of EPI (4 micrograms/kg/min for 6 hr) in intact and chronically splenectomized animals. All but serum enzymes were measured in another group of splenectomized animals that were implanted with small fragments of the autologous spleen (autoimplanted animals) 2 weeks prior to EPI infusion. Renal function tests and urinary PGE2 levels were monitored for several hours during the recovery period. The development of ARF in intact animals was accompanied by marked increases in circulating catecholamine levels, hematocrit, and serum enzymes and by a marked decrease in urinary PGE2 levels. These animals had diffuse ATN and hemorrhagic lesions of the heart (myocardial necrosis), and none survived. Chronically splenectomized animals were protected against the adverse effects of EPI infusion. The protected animals showed minimal elevation of circulating catecholamine levels and no changes in urinary PGE2 levels or hematocrit. Serum enzymes and renal and cardiac histopathology remained essentially normal in these animals. Implantation of autologous splenic tissue in splenectomized animals caused reversal of the protective effect of splenectomy. The response of autoimplanted animals to EPI infusion was in all respects similar to that in intact animals with the exception of hematocrit, which did not rise. All autoimplanted animals survived. They showed prompt recovery of renal function associated with significant increase of urinary PGE2 levels during the recovery period. Focal ATN was observed but no hemorrhagic lesion of the heart was found. From these observations we conclude the following: (1) high circulating NE and/or low renal (urinary) PGE2 activity are important in the pathogenesis of EPI-induced ARF, (2) the spleen may release some factor(s) that modulate plasma NE level and/or renal PGE2 activity during EPI infusion, (3) EPI-induced ARF may occur independently of myocardial necrosis, and (4) hematocrit has no major role in EPI-induced ARF.
Acute Kidney Injury↗
The role of vasopressin in the maintenance of cardiovascular function during early endotoxin shock.
This study was conducted as an initial step to elucidate the role of vasopressin in the events leading to irreversible shock. The influence of vasopressin on the maintenance of cardiovascular and respiratory function during early endotoxin shock was evaluated. Conscious, unrestrained male Sprague-Dawley rats (SD) and male homozygous Brattleboro rats (B) lacking vasopressin were anesthetized with 2% enflurane and cannulas were placed in the carotid artery and jugular vein. After recovery from anesthesia, endotoxin (20 mg/kg) was administered. Endotoxin in the B caused an immediate drop in blood pressure to below 40 mm Hg with no recovery. This resulted in death for all ten animals within 3 1/2 hours; eight of ten had expired within 90 min. In contrast, the blood pressure response of the SD dropped to 70 mm Hg but recovered to values near control until sacrificed 240 min after endotoxin. Corticosteroid treatment (300 mg/kg) administered 30 min before endotoxin in the B prevented the severe decrease in blood pressure with values falling to and remaining near 70 mm Hg for the 240-min observation period. All treated animals survived this period. Heart rates in the SD increased sharply after endotoxin and continued to rise, whereas both treated and untreated B increased slowly. Respiration rates for the untreated B were severely depressed until death after endotoxin, whereas the SD and treated B remained at or above control. The results implicate vasopressin in the maintenance of cardiovascular function during the early phase of shock induced by endotoxin, and demonstrate the ability of corticosteroid to substantially improve cardiovascular integrity in the absence of vasopressin.
Adrenal Cortex Hormones↗
Survival characteristics during septic shock in 39 baboons.
In septic shock nonsurvival is characterized by failure of multiple organ systems. The design of therapeutic measures to increase survival would be enhanced if critical responses could be identified early. Escherichia coli LD100 was given to 39 baboons by IV infusion over two hours followed by different therapy regimens in 31 [2--4]. There were 18 permanent survivors (seven days or more), all receiving antibiotic/steroid combination therapy. Responses of survivors and nonsurvivors were measured and compared during the first 12 hours from onset of infusion. Changes in blood pressure and acid-base parameters were not significantly different between groups. Five responses indicative of permanent survival were lower heart rates, less elevation of blood urea nitrogen, normal blood glucose at eight hours, hyperglycemia with normal insulin at 12 hours, and lower plasma lactate concentrations beginning at four hours.
Animals↗
Does LD100 E coli shock cause myocardial failure?
We have documented that myocardial dysfunction occurs in canine endotoxin shock and have designed this study to determine the effect of lethal live E coli-induced shock on the myocardium. Small adult heart "donor" dogs (wt range 6-9 kg) were infused with LD100 E coli (N = 12) or saline (N = 16) for 30 minutes. Two hours later, heart transfer surgery was initiated and once completed the isolated working left ventricle was allowed to equilibrate in the extracorporeal circuit of a "support" dog (wt range 22-32 kg). Myocardial performance was then evaluated by changing mean aortic pressure while controlling cardiac output. Three to five hours after E coli infusion, marked myocardial dysfunction occurred in 75% of the hearts as evidenced by increased left ventricular and diastolic pressures and depressed peak positive and negative dP/dt at every mean aortic pressure tested compared with control hearts. Myocardial efficiency and power were depressed, oxygen uptake was elevated, and coronary blood flow was unchanged in E coli-treated compared with control hearts. Data support the presence of heart dysfunction in gram-negative septic shock.
Animals↗
Influence of attenuation on radionuclide stroke volume determinations.
Using a method for determination of absolute volumes, including correcting for attenuation, we have explored the ability of the method to determine stroke volume in humans by radionuclide techniques. Thermodilution cardiac output determinations and multigated equilibrium blood-pool scintigraphy in the LAO view were performed simultaneously in twenty patients in which no evidence of intracardiac shunts or valvular disease was present. The correlation was good between the attenuated radionuclide and thermodilution stroke volume (r = 0.80, s.e.e. of estimate = 12 ml; SVtd = 2.31 x SVr + 18 ml). When correction for attenuation was made, the correlation improved (r = 0.96, s.e.e. = 6 ml) and approached the line of identity (SVtd = 0.99 x SVr + 1.2 ml). The correlation was also good between radionuclide cardiac output, corrected for attenuation, and the thermodilution cardiac output (r = 0.89, s.e.e. = 0.36 l/min; COtd = 0.86 x COr + 0.67 l/min). Thus our method of correction for attenuation in the determination of absolute left-ventricular volumes has been shown to provide a reliable, noninvasive means of calculating stroke volume and cardiac output in humans, without the use of geometric assumptions or regression equations.
Cardiac Output↗