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J D Symons

Publications and source records attributed to J D Symons.

33 records · Page 2Linked to original sources
PubMed1993

Response of collateral-dependent myocardium to vasopressin release during prolonged intense exercise.

We hypothesized that vasopressin concentrations during exercise attenuate the increase in collateral-dependent blood flow leading to left ventricular dysfunction in Ameroid-occluded miniswine. An Ameroid occluder was placed around the proximal left circumflex coronary artery (LCX) of 19 miniswine. Ten weeks later V1 receptor blockade with the use of [d(CH2)5Tyr-(Me)]arginine vasopressin (10-12 micrograms/kg iv) increased resting transmural flow (radioactive microspheres) in the LCX region, indicating the presence of V1 receptors. Neither injection of lysine vasopressin (125 pmol/kg) after V1 receptor blockade nor injection of two specific V2 receptor agonists caused changes in mean arterial pressure, heart rate, or left anterior descending coronary arterial flow velocity, indicating that V2 receptors mediate no appreciable vasodilation in the swine coronary circulation. Next the ratio of collateral to noncollateral flow and regional systolic wall thickening (sonomicrometer dimension gauges) were measured at rest and after 20 min of prolonged, intense treadmill exercise (85-90% of heart rate reserve) in the presence and absence of V1 receptor antagonism. This degree of exertion increased plasma lysine vasopressin from 6.2 +/- 1.0 at rest to 21.0 +/- 7.0 pg/ml (P < 0.05) during the unblocked run. However, the decrease in transmural blood flow ratio (collateral to noncollateral flow) from rest was similar during exercise before and after V1 receptor blockade (0.78 +/- 0.07 and 0.80 +/- 0.05, respectively; P < 0.05 vs. rest). Likewise, percent systolic wall thickening in the collateral-dependent region decreased from rest to exercise in the absence and presence of V1 receptor antagonism (35.9 +/- 4.5 and 39.5 +/- 3.8%, respectively; P < 0.05 vs. rest).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

Vasopressin contributes to the cardiovascular response to dynamic exercise.

Vasopressin is a powerful vasoconstrictor that is released into the systemic circulation during exercise. We tested the hypothesis that this peptide contributes to the cardiovascular response during treadmill exercise in the pig. Seventeen miniswine were instrumented with epicardial electrocardiogram leads, left atrial and aortic catheters, and a left ventricular pressure transducer for measurement of heart rate (HR), regional blood flow, arterial blood pressure (MAP), and myocardial contractility [first derivative of left ventricular pressure (dP/dt) at 40 mmHg developed pressure] at rest and during exercise. At a work intensity of 80% of each animal's maximal HR reserve, exercise-induced increases in MAP, HR, dP/dt at 40 mmHg developed pressure, and cardiac output were measured. On a separate day, the workload performed by each animal was replicated in the presence of selective vasopressin V1-receptor inhibition using the specific V1 antagonist, [d(CH2)5Tyr(Me)]arginine vasopressin (10-14 micrograms/kg iv). During exercise, MAP was lower (96 +/- 3 vs. 104 +/- 2 mmHg) and cardiac output was higher (13.5 +/- 0.6 vs. 12.6 +/- 1.0 l/min) in the presence of V1-receptor blockade than during unblocked conditions, respectively. Furthermore, we observed an attenuation of exercise-induced decreases in blood flow to the colon. Increases in vascular resistance in the stomach, small intestine, colon, and pancreas also were diminished by V1-receptor inhibition. However, HR and myocardial contractile responses to exercise were not affected. These results suggest that vasopressin contributes to increases in MAP and to the redistribution of cardiac output during dynamic exercise in the miniswine.

Animals↗
PubMed1993

Repeated dipyridamole administration enhances collateral-dependent flow and regional function during exercise. A role for adenosine.

Two main hypotheses concerning the mechanisms responsible for coronary collateral growth suggest the involvement of chemical or mechanical factors. Since we recently demonstrated that the development of the coronary collateral circulation is not closely related to the extent or duration of myocardial ischemia, we hypothesized that chronic repeated vasodilation and increased myocardial blood flow using dipyridamole would enhance collateral development in miniswine with an ameroid-occluded left circumflex coronary artery (LCx). Two days after surgical instrumentation, the animals received dipyridamole (n = 9), diltiazem as an adenosine-independent vasodilator (n = 8), or control vehicle (n = 7) 90 minutes per day, 5 days per week for 8 weeks. At 5 and 8 weeks, transmural blood flow and systolic wall thickening were measured during infusion of dipyridamole, diltiazem, or vehicle. Transmural blood flow increased similarly in the LCx and nonoccluded regions at 30 and 60 minutes during infusion of either vasodilator. Thus, we believe that similar mechanical stimulation resulted from dipyridamole and diltiazem infusion. There was no change in blood flow during administration of the vehicle. Systolic wall thickening in the collateral-dependent region was not altered by infusion of dipyridamole, diltiazem, or vehicle. Therefore, both vasodilators increased blood flow without eliciting ischemia. After 8 weeks of repeated treatment with each pharmacological agent, at least 24 hours after the last drug infusion, near maximal physiological capacity of the coronary collateral vessels was assessed during treadmill running (approximately 240 beats per minute). Transmural myocardial blood flow ratios, expressed as flow in the LCx divided by flow in the nonoccluded region of the left ventricle, were similar at rest for animals treated with dipyridamole (0.90 +/- 0.03), diltiazem (0.97 +/- 0.05), and control vehicle (0.89 +/- 0.02). However, collateral-dependent myocardial blood flow during exercise was greater (P < .05) in the dipyridamole-treated animals (0.78 +/- 0.04) than in either diltiazem-treated (0.63 +/- 0.09) or vehicle-treated (0.62 +/- 0.02) animals. LCx systolic wall thickening at rest was similar in animals treated with dipyridamole (44.4 +/- 6.3%), diltiazem (42.2 +/- 3.0%), and control vehicle (38.1 +/- 2.8%). During exercise, however, myocardial function in the collateral-dependent region was greater (P < .05) in the dipyridamole-treated (39.2 +/- 5.2%) compared with diltiazem-treated (23.9 +/- 4.0%) and vehicle-treated (26.9 +/- 2.9%) animals.(ABSTRACT TRUNCATED AT 400 WORDS)

Adenosine↗
PubMed1993

Effects of prior exercise or ammonium chloride ingestion on muscular strength and endurance.

Previous studies linked muscular fatigue with a decrease in blood pH. This study investigated if the means of altering pH affected the extent of muscular fatigue. Drug-induced and exercise-induced acidosis were compared to test the hypothesis that exercise-induced acidosis impairs subsequent muscular performance more than chemically induced acidosis. In eight male subjects acidosis was induced by ingesting 0.3 g.kg-1 ammonium chloride (AC) for one trial, by upper body exercise (UBE) for another trial, and after placebo (PL) treatment. They then completed a performance test (PT) of 50 maximal, bilateral isokinetic knee extensions. Whole blood pH before (pHpre) and after (pHpost) the PT was 7.412, 7.264, and 7.261 for PL, UBE, and AC, respectively; both AC and UBE decreased pH similarly compared with PL. Peak torque and total work during the PT were similar for PL and AC, and were significantly greater than after UBE. Six subjects performed a fourth trial after combined AC and UBE treatments causing a pHpre of 7.081, but there was no greater performance impairment than that caused by UBE alone. The results dissociate the extent of the impairment from the magnitude of the disruption in blood pH.

Acid-Base Equilibrium↗
PubMed1993

Effects of sleep deprivation and exercise on glucose tolerance.

Previous studies suggest that sleep deprivation (SD) decreases glucose tolerance in humans. The present study examined the ability of 10 males to process a glucose load during two conditions separated by at least 10 d. Condition I consisted of sedentary daily activity and sleep deprivation (SDS). Condition II consisted of daily physical activity and sleep deprivation (SDX). In both the SDS and SDX conditions, subjects were sleep deprived for 60 h followed by 7 h of normal sleep. An oral glucose tolerance test (OGTT) was administered at 10 and 60 h of SD, and after a night of recovery sleep in each condition, and plasma glucose and insulin concentrations were measured. No differences in the total plasma glucose response to the OGTT were observed over the total experimental period during Conditions I and II. However, the insulin response to the OGTT was elevated in the two conditions after 60 h of SD. Furthermore, the sedentary Condition I (SDS) resulted in higher insulin responses at all times compared to exercise Condition II (SDX). It is suggested that SD contributes to the development of an insulin resistance that can be partially reversed by physical activity. The results support the suggestion that SD results in decreased insulin sensitivity at peripheral receptor sites which can eventually lead to insulin exhaustion at pancreatic sites after longer periods of SD.

Activities of Daily Living↗
PubMed1992

Analysis of beat-to-beat cardiovascular hemodynamic variables obtained from long-term biotelemetry.

Manual methods of large volume data storage, retrieval, and analysis are difficult, time consuming, and present numerous opportunities for calculation errors. We have designed and implemented a comprehensive computer-based system for performing these functions. Development of this system was necessary since left ventricular (LV) blood pressure and two regional LV wall thickness measurements were obtained during long-term extracorporeal biotelemetry of miniswine for 24-h periods. During a single recording period over 100,000 individual cardiac cycles were recorded on analog tape and later analysed for determination of global myocardial oxygen demand and regional myocardial function. In addition, custom designed software was developed to determine the extent and duration of myocardial dysfunction. Batch file commands enabled the customized software to operate without prompting by the user thus optimizing the time usage of the computer, and the computer based data acquisition and analysis system. Although this system was designed specifically for analysing cardiovascular hemodynamic variables, it is flexible and can be applied to other experimental applications.

Analog-Digital Conversion↗
PubMed1992

Biotelemetry of cardiovascular hemodynamic measurements in miniswine.

A three-channel biotelemetry system has been designed and implemented for use in a chronically instrumented animal model of cardiovascular disease. A dual-channel ultrasonic transit-time micrometer allows monitoring of left-ventricular wall motion for the regions perfused by the left circumflex and left anterior descending coronary arteries. A third channel provides left ventricular blood pressure obtained from a high-fidelity blood pressure transducer implanted in the left ventricle. The biotelemetry system features a high voltage dc-dc converter for improved ultrasonic signal strength, a time-to-voltage converter that is highly immune to synchronization frequency variations, low power consumption (approx. 100 mW), small size (4 x 6 x 12 cm), and low weight (approx. 200 g). This three-channel system has enabled our laboratory to continuously monitor untethered animals for 24-h periods. Data obtained from this miniature biotelemetry system can be utilized to quantify myocardial oxygen demand and regional left-ventricular wall thickening.

Animals↗
PubMed1992

Chronic reduction of myocardial ischemia does not attenuate coronary collateral development in miniswine.

BACKGROUND: Myocardial ischemia is considered to be a possible stimulus for development of the coronary collateral circulation. We therefore hypothesized that chronic reduction of myocardial oxygen demand to lessen ischemia would attenuate coronary collateral development over an 8-week period using left circumflex coronary artery (LCx) ameroid-induced constriction in pigs. METHODS AND RESULTS: Collateral development was assessed by myocardial blood flow (radioactive microspheres) and left ventricular regional function (sonomicrometer dimension gauges). beta-Adrenoceptor blockade with propranolol (160 or 320 mg b.i.d.p.o.) was initiated in 15 animals 1 day after surgery. Compared with 16 untreated animals, beta-adrenoceptor antagonism was documented in the treated group by 1) pharmacological stimulation with isoproterenol, 2) physiological stimulation during graded treadmill exercise, and 3) repeated long-term biotelemetry recordings of oxygen demand (heart rate and blood pressure) and regional myocardial function. In addition to pharmacological and physiological verification of beta-blockade, biotelemetry showed that, compared with the untreated animals, propranolol significantly reduced the daily number, individual duration, and severity of events representing myocardial dysfunction. This suggests that in the beta-blocked group, little if any ischemia was present throughout the first 5 weeks when collateral growth occurs. Transmural myocardial blood flow (expressed as a ratio of flow in the LCx region to the nonoccluded region of the left ventricle) and systolic wall thickening in the LCx region were determined at rest and during treadmill exercise (240 beats per minute) 31-38 days (5 weeks) and 60-67 days (8 weeks) after surgery. Propranolol was withdrawn 3 days before flow and function determinations and was resumed immediately after testing. Blood flow ratios at 5 weeks decreased similarly from rest to exercise in the untreated (0.83 +/- 0.04 to 0.60 +/- 0.05, p less than 0.05) and beta-blockade group (0.82 +/- 0.09 to 0.57 +/- 0.10, p less than 0.05). Systolic wall thickening from rest to exercise was attenuated to the same degree in the untreated (59 +/- 6% to 38 +/- 6%, p less than 0.05) and beta-blockade group (50 +/- 8% to 30 +/- 5%, p less than 0.05). Similar flow and function responses were observed in both groups at 8 weeks. CONCLUSIONS: We conclude that growth and development of the coronary collateral circulation measured functionally during exercise at 90% of maximal heart rate is unrelated to the extent and duration of myocardial ischemia in this model.

Animals↗
PubMed1991

Intramuscular accumulation of prostaglandins during static contraction of the cat triceps surae.

We previously demonstrated that muscle afferent endings are sensitized by exogenous prostaglandins during static contraction of skeletal muscle. The purpose of this study was to determine whether 30 s of static hindlimb contraction, induced by electrical stimulation of the cat sciatic nerve, increases the concentration of immunoreactive prostaglandin E2 (iPGE2) and 6-ketoprostaglandin F1 alpha (i6-keto-PGF1 alpha, the stable metabolite of prostaglandin I2) in muscle tissue. In addition, the role of ischemia in augmenting prostanoid production was examined. Gastrocnemius muscle was obtained by freeze-clamping tissue, and prostaglandins were extracted from muscle homogenates and measured by radioimmunoassay. Compared with precontraction values, high-intensity (68% of maximal tension) static contraction elevated gastrocnemius iPGE2 and i6-keto-PGF1 alpha by 45 and 53%, respectively (P less than 0.01). Likewise, when blood flow to the gastrocnemius was attenuated by arterial occlusion during and 2 min before low-intensity contraction (29% maximal tension), the intramuscular iPGE2 concentration was increased by 71% (P less than 0.01). Conversely, low-intensity contraction (30% of maximal tension) and arterial occlusion without contraction did not alter the concentration of either prostanoid. Our findings demonstrate that prostaglandins accumulate in muscle during static contraction. We believe that local muscle ischemia may provide a stimulus for this phenomenon. These prostaglandins therefore are available to sensitize afferent endings responsible for reflex adjustments during static muscle contraction.

6-Ketoprostaglandin F1 alpha↗
PubMed1990

Longitudinal and cross-sectional studies of the relationship between 6-keto PGF1 alpha and high density lipoproteins.

Two studies were performed to examine the relationship between Prostacyclin (PGI2) and high density lipoprotein cholesterol (HDL-C). A longitudinal study examined the stable metabolite of PGI2, 6-keto PGF1 alpha, along with HDL-C, and total cholesterol (TC) before (Week 0), during (Week 4), and after (Week 9) an eight week aerobic conditioning program. 6-keto PGF1 alpha was measured by radioimmunoassay using 125I, and HDL-C and TC were spectrophotometrically analysed. Maximal oxygen uptake and resting heart rate data obtained at Week 0 confirmed that the training group (E) was not different from the sedentary group (C). Results obtained at Week 9 indicated that maximal oxygen uptake was higher (p less than 0.05) and resting heart rate lower (p less than 0.05) in the E group, while these variables remained unchanged in group C. Levels of 6-keto PGF1 alpha, HDL-C, and TC did not differ between groups E and C when Week 0 was compared with Week 9. However, within the E group, significantly lower concentrations of 6-keto PGF1 alpha (p less than 0.05) and HDL-C (p less than 0.05) were found at Week 4 compared with Week 0. A cross-sectional study involving 52 subjects examined the relationship between 6-keto PGF1 alpha and several cardiovascular disease risk factors which included HDL-C. The only significant correlation (r = 0.50 p less than 0.05) observed was between 6-keto PGF1 alpha and HDL-C.

6-Ketoprostaglandin F1 alpha↗
PubMed1990

Role of thromboxane A2 in the cardiovascular response to intracoronary C5a.

Intracoronary administration of complement component C5a induces transient decreases in coronary blood flow and regional left ventricular segment shortening, associated with intramyocardial granulocyte trapping. We evaluated the influence of a cyclooxygenase inhibitor (acetylsalicylic acid, n = 8) or a thromboxane A2/prostaglandin H2 receptor antagonist (SQ29548, n = 6) on these C5a-induced cardiovascular responses. Open-chest anesthetized pigs were instrumented to monitor heart rate, arterial blood pressure, left anterior descending coronary blood flow, regional left ventricular segment shortening, and dP/dt. Oxygen content, lactate concentration, leukocyte count, and thromboxane B2, the stable metabolite of thromboxane A2, were measured in arterial and regional coronary venous blood. Repetitive injections of intracoronary C5a (500 ng) given 60 minutes apart showed no tachyphylaxis of the hemodynamic response. However, tachyphylaxis was seen in coronary blood flow changes when injections were spaced 30 minutes apart. An increase in myocardial oxygen extraction and lactate production was observed after intracoronary C5a. Administration of acetylsalicylic acid (50 mg/kg i.v.) attenuated C5a-induced decreases in coronary blood flow (-8 +/- vs. -3 +/- 1 ml/min) and regional left ventricular segmental shortening (-10 +/- 3% vs. -2 +/- 1%) and blocked the maximal increase in coronary venous thromboxane B2 (2.0 +/- 0.1 vs. 0.2 +/- 0.1 pmol/ml plasma). Furthermore, SQ29548 (30 micrograms/kg/min) reduced C5a-induced changes in coronary blood flow (-13 +/- 2 vs. -4 +/- 2 ml/min) and segmental shortening (-14 +/- 2% vs. -3 +/- 1%). Neither cyclooxygenase inhibition nor thromboxane A2/prostaglandin H2 antagonism blocked the decrease in coronary venous granulocyte count.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

High-intensity exercise performance is not impaired by low intramuscular glycogen.

The purpose of this study was to evaluate the effects of glycogen availability on short-term, high-intensity exercise performance. Eight males completed performance evaluation tasks (PET) consisting of maximum isokinetic strength and endurance, isometric strength, and electrically evoked force of the leg extensors, twice during each of two conditions. On day 1 (D1) of the control condition (C) subjects performed the PET, followed by strenuous exercise designed to deplete glycogen stores of the leg extensors. After consuming a mixed diet for 48h (days 2 and 3) they performed the PET again on day 4 (D4). The experimental condition (E) was identical to C, except that a strictly controlled low carbohydrate diet was consumed during Days 2 and 3. Biopsies from the vastus lateralis before the PET on D4 confirmed differences between conditions in intramuscular glycogen (426 +/- 43 vs 153 +/- 60 mmol glucose units.kg-1 d.w. for C and E respectively, P less than 0.001). Results obtained from the PET were not different between conditions on D4, nor within conditions when D1 and D4 were compared. Resting blood glucose, hematological variables indicative of hydration and acid-base status, and post PET blood lactate were similar for all trials. It is concluded that short-term, high-intensity exercise performance of glycogen depleted leg extensors is not impaired.

Acid-Base Equilibrium↗
PubMed1988

Physical performance and physiological responses following 60 hours of sleep deprivation.

The effect of 60 h of sleep deprivation (SD) upon physical performance and physiological responses to exercise was examined in 11 male subjects. The experiment consisted of two conditions separated by at least 10 d. In the experimental condition (E) subjects remained awake for 60 h and in the control condition (C) the same subjects had 7 h of sleep per night. In both conditions subjects reported to the laboratory on the evening prior to d 1 and slept for 7 h. Physical performance testing was carried out on d 1 and again on d 3 after either two nights of sleep or two nights of SD. Results obtained on d 3 are expressed relative to d 1, the control day. Maximal isometric and isokinetic muscular strength and endurance of selected upper and lower body muscle groups, performance of the Wingate Anaerobic Power Test, simple reaction time, the blood lactate response to cycle exercise at 70% VO2max, and most of the cardiovascular and respiratory responses to treadmill running at 70% and 80% VO2max, were not significantly altered as a result of SD. These results suggest that sleep loss of up to 60 h will not impair the capability for physical work, a finding of considerable importance in sustained military operations which frequently involve the combination of both physical and mental tasks.

Adult↗
PubMed1988

Electro-mechanical response times and muscle strength after sleep deprivation.

This study examined the effect of 60 h of sleep deprivation (SD) on electromechanical response times (EMRT), maximal voluntary isometric contraction (MVC), rate of force development (RFD), and times required to reach various percentages of MVC, during a maximal voluntary isometric contraction of both the forearm flexors and leg extensors. Eleven male subjects were either sleep deprived for 60 h (E) or performed similar daily activities and slept 7 h per night (C). Performance variables were evaluated at the same time intervals during both conditions. No significant differences were observed between the E and C conditions for EMRT (pre-motor time, electro-mechanical delay, total reaction time) or muscular performance (MVC, RFD). The results suggest that subjects who have undergone 60 h of SD can react as fast, and with as much force, as those who have had 7 h of sleep per night.

Adult↗