Use of nutritional supplements by high school football and volleyball players.

The known use of performance enhancing agents by athletes has occurred throughout history. In the 1960s and 1970s steroids and amphetamines were the supplements most often used. Now athletes are turning to supplements that are either natural or stimulate the release of natural hormones. The purpose of this study is to evaluate the prevalence of use of nutritional supplements among high school football and volleyball players. This study surveyed 495 male football players and 407 female volleyball players from 20 high schools in Northwest Iowa. These athletes completed anonymous surveys and returned them to their coaches. Results showed that 8% of the male athletes and 2% of the female athletes were using supplementation. Supplements used included creatine, androstiendione, HMB, amino acids, DHEA, phosphogen, weight gainer 1850, Tribulus, muscle plus, multivitamins, calcium, GABA, and Shaklee Vita Lea and Physique.

Differences in men's and women's mean ankle ligamentous laxity.

The incidence of ligamentous ankle injuries is known to be one of the most common athletic injuries that exists. Recently, there has been a great deal of interest regarding the increased risk of female ligamentous injury, such as the anterior cruciate ligament, lateral ankle sprains and others. The purpose of this study is to evaluate whether or not normal lateral ankle ligamentous laxity is similar in male and female athletes. This study selects 22 male and 27 female college athletes who have had no significant ligamentous ankle injuries requiring medical treatment. They were placed on a Telos ligamentous stress device and stressed to a level of 15 daN. Radiographs were then obtained to determine talar tilt at this level of ankle stress. Results were compared between men and women showing that there was a statistically significant difference. Women had a much greater ligamentous laxity of the lateral ankle than men.

Role of the sympathoadrenal axis in the cardiovascular response to cocaine in conscious unrestrained rats.

We investigated the role of peripheral sympathetic neurons and the adrenal medulla in the cardiovascular responses to cocaine in conscious, unrestrained Sprague-Dawley rats. Surgical adrenal demedullation (ADM) and/or chemical peripheral sympathectomy was used to eliminate one or both components of the sympathoadrenal axis. Phentolamine (5 mg/kg i.v.) was used to evaluate whether cocaine elicited epinephrine (EPI) release from the adrenal medulla. Significant EPI release by cocaine would result in "epinephrine reversal" after phentolamine pretreatment. Cocaine (2.5 mg/kg i.v.) was used in all experiments except the dose-response relationship study. In normal rats, cocaine caused a transient increase in mean blood pressure (MBP). Pretreatment with phentolamine reversed this BP response and this depressor effect was blocked by propranolol (2 mg/kg i.v.) suggesting that the pressor effect of cocaine was mediated by EPI. Chemical sympathectomy alone partially inhibited the pressor effect of cocaine, but pretreatment with phentolamine still reversed the residual action of cocaine on MBP at this time. Two weeks after ADM, the effect of cocaine on MBP was not significantly different from that of the sham-operated rats. However, pretreatment with phentolamine inhibited but did not reverse the effect of cocaine on MBP at that time. In rats with both ADM and chemical sympathectomy, cocaine caused only a decrease in MBP that was not blocked by propranolol or atropine methylnitrate, presumably because of its direct depressive actions. Results of this study suggest that both peripheral sympathetic neurons and the adrenal medulla play important roles in the cardiovascular actions of cocaine.

Interaction of propranolol, verapamil, and nifedipine on the myocardial depressant effect of cocaine.

We wished to determine if drugs with negative inotropic properties would exacerbate the transient myocardial depression associated with intravenous (i.v.) cocaine administration. The influence of propranolol, nifedipine, or verapamil pretreatment on the myocardial depressant effect of cocaine was examined in 13 chronically instrumented, conscious dogs. Cocaine alone (4 mg/kg i.v.) caused significant increases in heart rate (HR), mean arterial pressure (MAP), and rate-pressure product (RPP), effects consistent with sympathetic stimulation. Regional ejection fraction (EF) (determined by two-dimensional echocardiography), however, decreased from 56 +/- 5% (mean +/- SE) at baseline to 34 +/- 6% at 1 min and to 41 +/- 5% at 2 min after cocaine administration but recovered to 49 +/- 4% at 10 min. Pretreatment with propranolol (0.5 mg/kg i.v.) blunted the rate-pressure response to cocaine by 28%. Regional EF decreased from 53 +/- 5% at baseline to 26 +/- 3% (p < 0.01 as compared with cocaine alone) at 2 min after cocaine and was still reduced at 33 +/- 3% (p < 0.001 as compared with cocaine alone) at 10 min. Pretreatment with verapamil (10 mg i.v. 10 min before cocaine) blunted the rate-pressure response very little, but regional left ventricular (LV) EF decreased less, from 58 +/- 3% to only 46 +/- 5% at 2 min, and was almost normal at 10 min (57 +/- 5%). Nifedipine [90 mg sustained-release orally (p.o.) administered 5 h earlier] also reduced the myocardial depressant effect of cocaine at 2 min [regional EF decreased from 50 +/- 2% at baseline to 38 +/- 4% (cocaine alone), 56 +/- 3 to 49 +/- 4% (nifedipine and cocaine), p < 0.05].(ABSTRACT TRUNCATED AT 250 WORDS)

The effects of cocaine on cardiac electrophysiology in conscious, unsedated dogs.

This study was performed to determine the cardiac electrophysiological effects of cocaine and specifically to determine the time course of these actions. Eighteen chronically instrumented conscious dogs were tested with i.v. cocaine at doses of 1 or 4 mg/kg. The following statistically significant changes were observed 1 min following the 4 mg/kg dose of cocaine: heart rate increased from 135 +/- 8 to 186 +/- 9 beats/min, QRS duration increased from 60 +/- 5 to 74 +/- 5 ms, corrected QT interval increased from 298 +/- 7 to 339 +/- 8 ms, intraatrial conduction time increased from 27 +/- 2 to 31 +/- 3 ms, atrioventricular conduction time increased from 125 +/- 5 to 140 +/- 8 ms, and the atrial effective refractory period (ERP) increased from 101 +/- 6 to 130 +/- 9 ms. All of these parameters had returned to baseline by 10 min after cocaine administration. Corrected sinus node recovery time and the ventricular ERPs were not significantly affected by either cocaine dose. The only significant change produced by the 1 mg/kg cocaine dose was prolongation of the atrial ERP. These results suggest that cocaine causes very transient electrophysiological changes that undoubtedly represent the integrated effects of the adrenergic and local anesthetic actions of this drug.

Characterization of 5-hydroxytryptamine receptors in bovine coronary arteries.

This study was designed to determine the subtypes of 5-HT receptors present in bovine large coronary arteries and to characterize the response mediated by each subtype of receptor. Concentration-response relationships for 8-hydroxy-2-(di-n-propylamino)-tetralin (5-HT1A agonist) (0.3-100 microM), CGS-12066B maleate (5-HT1B agonist) (0.01-30 microM), alpha-methylserotonin maleate (5-HT2 agonist) (0.01-30 microM), 1-(m-chlorophenyl)-biguanide (5-HT3 agonist) (0.1-100 microM) and serotonin (0.1-300 microM) were studied in vitro using 2-mm segments of bovine proximal left anterior descending coronary artery. Each segmental ring was mounted in a 70-ml tissue bath for the measurement of isometric tension. 8-Hydroxy-2-(di-n-propylamino)-tetralin (10-100 microM), alpha-methylserotonin maleate (0.01-30 microM) and serotonin (0.1-300 microM) induced endothelium-independent contraction, whereas CGS-12066B maleate and 1-(m-chlorophenyl)-biguanide had no effect in this species. Contractions induced by 8-hydroxy-2-(di-n-propylamino)-tetralin or alpha-methylserotonin maleate were attenuated by pretreatment with S(-)propranolol (2.6 microM), a relatively selective 5-HT1A and 5-HT1B receptor antagonist, and ketanserin (0.3 microM), a selective 5-HT2 receptor antagonist, respectively. Pretreatment with S(-)propranolol or ketanserin also attenuated serotonin-induced contraction, demonstrating that serotonin mediates contraction through both 5-HT1A and 5-HT2 receptors in bovine large coronary arteries.

Contraction of bovine coronary vascular smooth muscle induced by cocaine is not mediated by norepinephrine.

This study was designed to assess the effects of cocaine on coronary arterial smooth muscle and to determine whether previously reported cocaine-induced coronary vasospasm is mediated by substances released from the endothelium or by increased adrenergic receptor stimulation. Concentration-response relationships for cocaine (0.1-300 microM) and norepinephrine (0.1-300 microM) were studied in vitro using 2 mm segments of bovine proximal left anterior descending coronary artery. Each segmental ring was mounted in a 70 ml tissue bath for the measurement of isometric tension. Cocaine (3-300 microM) caused significant, concentration-dependent, increases in developed tension (p less than 0.05). Removal of the endothelium or pretreatment with prazosin (0.1 microM) or propranolol (1 microM) did not significantly alter this action of cocaine. In contrast to cocaine, norepinephrine (10-300 microM) caused significant decreases in developed tension (p less than 0.01). These findings suggest that cocaine-induced contraction of bovine coronary vascular smooth muscle is not mediated by endothelium derived contracting substances or norepinephrine.

Mechanism of cocaine-induced myocardial depression in dogs.

Cocaine causes pronounced depression of left ventricular function in conscious dogs immediately after intravenous administration. To examine this effect, 14 mongrel dogs were anesthetized with pentobarbital sodium (32 mg/kg) and instrumented with arterial and venous catheters and a Doppler blood flow transducer on the left circumflex coronary artery. Two weeks later, heart rate, blood pressure, coronary blood flow, and regional left ventricular ejection fraction (by two-dimensional echocardiography) were measured before and 1, 2, 5, and 10 minutes after cocaine (4 mg/kg i.v.), while the animals were fully conscious. Heart rate, blood pressure, and coronary blood flow were increased significantly at each time after cocaine. Regional ejection fraction, however, was depressed by 50 +/- 7%, 35 +/- 4%, and 21 +/- 4% at 1, 2, and 5 minutes after cocaine treatment, respectively. Ten minutes after cocaine treatment, regional ejection fraction had recovered to a level not significantly different from baseline. Because the observed myocardial depression after cocaine was accompanied by a large increase in the rate-pressure product, and presumably, myocardial oxygen consumption, this depression could have been secondary to increased myocardial oxygen demand not appropriately matched by an increase in coronary blood flow. To minimize the effects of cocaine on myocardial oxygen demand, a subset of six dogs received cocaine (4 mg/kg i.v.) while sedated with pentobarbital (25 mg/kg). In these dogs, cocaine did not significantly alter heart rate or blood pressure; however, regional ejection fraction was significantly depressed by 44 +/- 5% and 36 +/- 6% at 1 and 2 minutes after cocaine treatment, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiovascular effects of cocaine: enhancement by yohimbine and atropine.

The cardiovascular effects of cocaine, alone and in combination with yohimbine and/or atropine, were studied in dogs anesthetized with pentobarbital sodium. All dogs were instrumented for the measurement of arterial blood pressure, left ventricular contractile force, left circumflex coronary artery blood flow, lead II ECG and heart rate. Dogs were divided into two groups; one group received no pretreatment, the other group was pretreated with atropine sulfate, 2 mg/kg. Both groups received two i.v. doses of cocaine, 1 mg/kg, approximately 3.5 hr apart. Thirty minutes before administration of the second cocaine dose, yohimbine, 0.25 mg/kg, i.v. was administered. In control animals which did not receive atropine or yohimbine, there was no difference in the cardiovascular responses to the two cocaine doses administered on this schedule. Administration of cocaine alone increased mean arterial blood pressure 9.6 +/- 2.2 mm Hg and increased the rate-pressure product, an index of myocardial oxygen consumption, 12.6 +/- 4.7%. Coronary blood flow was increased 13.1 +/- 4%. Yohimbine pretreatment significantly enhanced the cardiovascular actions of cocaine and this enhancement was most pronounced in the presence of atropine. When cocaine was administered after treatment with both atropine and yohimbine, mean arterial blood pressure was increased 44.2 +/- 7.2 mm Hg, heart rate was increased 30 +/- 7.9 beats/min and the rate-pressure product was increased by 72 +/- 10.1%, whereas coronary blood flow was increased only 42.8 +/- 12%. These data suggest that presynaptic alpha adrenergic and cholinergic muscarinic blockade may significantly increase the risk of cocaine-induced cardiovascular toxicity.

Acute myocardial ischemia detected in dogs by temporal variation in two-dimensional ultrasound gray level.

This study tests the hypothesis that acute myocardial ischemia induces a characteristic temporal variation in regional ultrasound amplitudes. Myocardial ischemia was created by circumflex coronary artery occlusion in seven closed-chest mongrel dogs. Ultrasound images were acquired prior to occlusion and post-occlusion on a phased-array two-dimensional system. Unprocessed ultrasound data from end-diastolic images were taken digitally for quantitative gray level analysis. Temporal variation in ultrasonic gray level of a nonischemic control region was compared to the temporal variation in gray level of the ischemic area. In the ischemic area, the average gray level for all seven dogs increased from 39.2 +/- 4.2 prior to occlusion to 42.5 +/- 4.9 at 15 minutes after occlusion, and then to 44.4 +/- 5.9, 45.3 +/- 6.2, and 47.0 +/- 6.0 at 30, 60, and 120 minutes, respectively (p less than 0.05 for control vs 15 minutes and 15 minutes vs 120 minutes). No significant changes in the average gray level of all seven dogs occurred in the nonischemic area from pre-occlusion to 2 hours post-occlusion (38.8 +/- 8.8, 38.4 +/- 8.0, 37.7 +/- 8.4, 37.8 +/- 8.5, and 38.0 +/- 8.2 for control, 15, 30, 60, and 120 minutes, respectively. These data show that regions of acute myocardial ischemia can be characterized by temporal variation in intramyocardial ultrasonic gray level, not only from the time before coronary occlusion to 15 minutes after occlusion, but also between 15 and 120 minutes in the post-occlusion period. Gray level values in nonischemic regions of the left ventricle are remarkably constant over time.

Cardiovascular effects of cocaine in conscious dogs: importance of fully functional autonomic and central nervous systems.

The cardiovascular effects of i.v. cocaine were studied in conscious dogs with chronically implanted arterial and venous catheters. The effects of i.v. cocaine on arterial blood pressure, heart rate and rate-pressure product were studied at doses ranging from 0.063 to 8 mg/kg. To avoid any possibility that development of acute tolerance to the actions of cocaine might interfere with our results, each dose of cocaine was administered on a separate day. Cocaine-induced changes in mean arterial blood pressure ranged from an increase of 11.8 +/- 2.1 mmHg at a dose of 0.063 mg/kg to an increase of 95.8 +/- 11 mmHg at a dose of 8 mg/kg. Similarly, cocaine-induced changes in heart rate ranged from a decrease of 4.5 +/- 0.9 beats/min to an increase of 83 +/- 10 beats/min at the 0.063 and 8 mg/kg cocaine doses, respectively. Although the rate-pressure product was not significantly altered by doses of cocaine below 0.25 mg/kg, doses above that level produced dose-dependent increases in this parameter. The rate-pressure product, which was increased approximately 27% by the 0.25 mg/kg dose of cocaine, was more than doubled by the 2 mg/kg cocaine dose and was increased almost 4-fold by the 8 mg/kg dose of cocaine. The blood pressure response observed after cocaine administration was significantly decreased by pretreatment with 10 mg/kg hexamethonium.(ABSTRACT TRUNCATED AT 250 WORDS)

Increase in serum digoxin concentration produced by quinidine does not increase the potential for digoxin-induced ventricular arrhythmias in dogs.

Chronic treatment of dogs with digoxin alone, quinidine alone and digoxin in combination with quinidine was initiated in dogs to assess changes in arrhythmogenic potential associated with the quinidine-induced increase in serum digoxin concentration observed during combined digoxin and quinidine treatment. The arrhythmogenic potential of digoxin was evaluated through the use of the acetylstrophanthidin (AcS) tolerance test. AcS was infused at a rate of 5 micrograms/kg/min until ventricular arrhythmias occurred during a drug-free period and during chronic treatment with digoxin, quinidine and digoxin plus quinidine. The dose of AcS required to initiate ventricular arrhythmias is inversely related to the arrhythmogenic potential of digoxin present at the time of AcS infusion. Administration of quinidine alone in two different dosage regimens produced serum quinidine concentrations of 5.99 +/- 1.18 and 2.99 +/- 0.43 micrograms/ml and significantly increased AcS tolerance, whereas digoxin alone, over a wide range of serum digoxin concentrations, significantly decreased AcS tolerance. This decrease in AcS tolerance was linearly related to the serum digoxin concentration. The addition of quinidine treatment to animals receiving digoxin resulted in a significant elevation in the steady-state serum digoxin concentration. However, the AcS tolerance determined during the elevated serum digoxin concentration induced by quinidine was greater than that determined during treatment with the same dose of digoxin alone. Thus, quinidine administration to animals receiving digoxin resulted in a significant increase in the steady-state serum digoxin concentration but did not increase the arrhythmogenic potential of digoxin over that observed during treatment with the same dose of digoxin alone.(ABSTRACT TRUNCATED AT 250 WORDS)

Nocardia asteroides sepsis of the knee.

Nocardia asteroides as an infecting agent has been an increasingly identified pathogen in humans, especially in immunosuppressed hosts. The Nocardia organisms as a cause of septic arthritis have been very unusual and in all previously reported cases have occurred in immunosuppressed patients. This is a report of two additional patients, one of whom has had no history of immunosuppression either before infection or subsequent to treatment and resolution of the infection. The second is a case of a questionably immunosuppressed patient with Nocardia asteroides septic arthritis. These cases reemphasize the importance of performing not only the most common aerobic and anaerobic bacterial cultures but also fungal and acid-fast bacilli cultures for early identification of less common organisms and for the initiation of appropriate therapy.

Altered acoustic reflectance on two-dimensional echocardiography as an early predictor of myocardial infarct size.

P6 area of increased acoustic reflectance was readily observed by 2-dimensional echocardiography (2-D echo) in the acutely ischemic canine myocardium. Fifteen mongrel dogs subjected to closed-chest coronary artery occlusion were used to test the hypothesis that these areas of altered acoustic reflectance were predictors of subsequent myocardial infarction (MI). Each dog was studied by 2-D echo in short-axis views of the left ventricle at 4 levels before and after coronary artery occlusion. The dogs were killed after 48 hours and heart sections were stained with triphenyltetrazolium chloride to identify the areas of necrosis. Four sections were then selected, approximating the same location within the left ventricle as the short-axis views taken for 2-D echocardiographic analysis. The in vivo 2-D echocardiographic examination revealed alteration of acoustic reflectance immediately after coronary occlusion, which detected the presence of MI with a sensitivity of 92% and a specificity of 90%. The extent of altered acoustic reflectance seen by echo correlated closely (r = 0.81) with the extent of MI detected by triphenyltetrazolium staining of the excised heart. Altered acoustic reflectance seen by 2-D echo immediately after coronary artery occlusion reflects acute ischemic changes and may be an early predictor of MI size.