Effects of cromolyn in horses with chronic obstructive pulmonary disease.

The effect of disodium cromoglycate (cromolyn) in preventing the pulmonary dysfunction caused by the inhalation of barn and hay dust was studied in 5 horses with confirmed chronic obstructive pulmonary disease (COPD). The horses were studied before (Con) and after exposure to hay and dust allergens (Expos) and after pretreatment with cromolyn followed by exposure (Cr-Expos). There was a significant reduction in PaO2 from 86.8 +/- 8.3 to 73.1 +/- 8.8 when the horses were exposed to hay and dust allergens. The PaO2 after pretreatment with cromolyn and exposures was 78.1 +/- 5.5. There were no significant changes in PaCO2, FRC, pH and A-aDO2 when the Con, Expos, and Cr-Expos periods were compared. There were significant increases in VE from a control value of 77.9 +/- 18.2 to 128.7 +/- 55.1 and 133.7 +/- 17.1 L/min during the exposures, which was due primarily to increases in respiratory frequency. Respiratory dead space (VD/VT) increased from 0.55 +/- 0.10 to 0.71 +/- 0.07 and 0.65 +/- 0.05, and alveolar ventilation (VA) remained constant. Pulmonary resistance (RL) and transpulmonary pressure (Ptr) increased from a control of 0.77 +/- 0.28 cm H2O/L/sec and 7.73 +/- 3.38 cm H2O to 2.93 +/- 1.01 and 20.17 +/- 4.81 during the Expos period and tidal volume (VT) fell from 7.5 +/- 1.0 to 5.7 +/- 1.3 L. The pre-treatment with cromolyn before exposures significantly reduced the increase in RL and Ptr and returned VT to Con levels.

Effects of training on cardiorespiratory function in the horse.

The effects of 5- and 10-wk treadmill exercise training on cardiorespiratory function were evaluated in the horse. Cardiac output (Q), heart rate (HR), and stroke volume (SV), as well as left ventricular (LVP), aortic (AoP), and mean right atrial (RAP) pressures and the peak first time derivative of LVP (LV dP/dtmax), were measured at rest and at five different levels of exercise up to 90% of initial predicted maximal HR (HRmax). Oxygen uptake (VO2) and respiratory exchange ratio (R) were also obtained under the same conditions. At rest, although HR was no different after training, LV dP/dtmax was lower at 10 wk (2,369 +/- 502 vs. 1,615 +/- 302 mmHg/s). At the different measured work loads during exercise, Q and VO2 remained unchanged with training, whereas there were consistent trends toward lower LVP, AoP, and LV dP/dtmax and significant reductions in HR and R (both P less than 0.05). In contrast, SV and mean RAP were elevated (P less than 0.05) during exercise after the 10-wk training program. Although the observed changes in cardiorespiratory function in response to a training program in the horse are generally similar to those reported for other species, our data also suggest a training-induced increase in venous pressures during exercise as measured by elevated mean RAP values.

Deanol affects choline metabolism in peripheral tissues of mice.

Administration of 2-dimethylaminoethanol (deanol) to mice induced an increase in both the concentration and the rate of turnover of free choline in blood. Treatment with deanol also caused an increase in the concentration of choline in kidneys, and markedly inhibited the rates of oxidation and phosphorylation of intravenously administered [3H-methyl]choline. In the liver, deanol inhibited the rate of phosphorylation of [3H-methyl]choline, but did not inhibit its rate of oxidation or cause an increase in the level of free choline. These findings suggest that deanol increases the choline concentration in blood by inhibition of its metabolism in tissues. Deanol may ultimately produce its central cholinergic effects by inhibition of choline metabolism in peripheral tissues, causing free choline choline to accumulate in blood, enter the brain, and stimulate cholinergic receptors.

Cardiorespiratory adjustments to tethered-swimming in the horse.

The cardiorespiratory and metabolic responses to various levels of tethered-swimming were evaluated in 5 sedentary horses. Cardiac output (Q) and heart rate (HR) correlated highly (r = 0.89 and 0.94 respectively) with work effort (WE) expressed as kg pulled . kg body wt-1 . 10-2. While swimming, stroke volume (SV) was reduced at the lowest workloads, but increased with increasing WE so that at the highest workloads it had returned to the on-land standing SV. Pressures in the pulmonic as well as on both sides of the systemic circulation were considerably elevated by this form of exercise, although only mean carotid artery pressure (CAP) correlated highly (r = 0.83) with WE. During tethered-swimming plasma lactic acid (LA) rose exponentially from 1 to 10 mmol . 1-1 with increasing HR over the range 150-200 beats . min-1. Oxygen uptake (VO2) increased linearly (r = 0.95) from 25-112 ml . kg-1. min-1 over the We range of 3.0-7.8 kg pulled . kg body wt-1. 10-2. The aerobic capacity of the equine species would appear to be twice that of man. The greater increase in VO2 in the exercising horse cannot be explained solely on the basis of increases in Q. Therefore alterations in hematocrit, hemoglobin and oxygen extraction appear to play a more important role in the horse during exercise than they do in man.

Swimming--a method to study the physiologic response of the horse to exercise.

The literature on exercise physiology in the horse with special reference to swimming is briefly reviewed. The use of a pool for swimming horses is described and a technique discussed for the collection of haematologic and haemodynamic data using this form of exercise.

Effect of lidocaine on the atrial fibrillation threshold.

The effect of lidocaine on the atrial fibrillation threshold (AFT) and the ventricular fibrillation threshold (VFT) was studied in anesthetized dogs. In ten animals, injection of lidocaine 2 mg./Kg. intravenously resulted in a markded increase of the ventricular fibrillation threshold (from 11.0 +/- 1.5 to 33.3 +/- 6.2 mA., P less than 0.001). In another group of ten animals, lidocaine did not have consistent effect on the atrial fibrillation threshold. However, a dose of lidocaine of 3 mg./Kg intravenously produced a significant increase in AFT (from 14.0 +/- 0.56 to 41.1 +/- 0.32 mA., P less than 0.001). No changes in AFT or VFT were noted in control experiments. The data suggest that lidocaine possesses an antiarrhythmic effect on the atria but higher than usual doses are required.

Effect of alcohol on the atrial fibrillation threshold in dogs.

The atrial fibrillation threshold was measured in 10 anesthetized dogs by delivering a series of impulses directly to the right atrium after infusion of 4.5 ml of 5% glucose per kilogram of body weight, and after 1.5 ml of absolute alcohol per kilogram in 3 ml/kg of 5% glucose. There were no changes in the atrial fibrillation threshold after glucose. The mean AFT before alcohol was 6.8 volts. Immediately after alcohol infusion, the arterial blood alcohol concentration (BAC) was 300.7 mg/100 ml, and the AFT increased to 9.75 volts (P less than 0.01); 20 minutes later the BAC was 181.2 mg/100 and the AFT 8.5 (P less than 0.02). There was no rebound decrease in AFT up to 65 minutes. The findings suggest that in anesthetized normal dogs, alcohol may have a direct mild antiarrhythmic effect on the atria. Atrial fibrillation in alcoholics may be due to alcohol indirectly through electrolyte, autonomic, or histologic changes.

Altered intracardiac conduction after acute administration of ethanol in the dog.

Varying concentrations of ethyl alcohol were injected either into the left main coronary artery or intravenously in anesthetized intact dogs. Effects of alcohol on intracardiac conduction (by His bundle electrogram) were examined at spontaneous and paced (atrial) heart rates. Alcohol by the intracoronary route prolonged atrioventricular node and intraventricular conduction times by approximately 5 to 15%. These changes preceded a depression of left ventricular systolic pressure and of the rate of rise of left ventricular pressure and an elevation of left ventricular end-diastolic pressure. Intracoronary injections of contrast medium (sodium diatriozoate) or iso-osmolar solutions of sucrose and injections of similar amounts of alcohol in the ascending or descending aorta did not affect intracardiac conduction. Increasing atrial pacing rates resulted in prolongation of atrioventricular nodal conduction intervals, but did not influence intraventricular conduction time. At each pacing rate, alcohol depressed both atrioventricular nodal and intraventricular conduction. The data suggest that alcohol has a direct depressant effect on intracardiac conduction.