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Biomedical subjects

H H Erickson

Publications and source records attributed to H H Erickson.

At least 19 recordsLinked to original sources
PubMed1992

Pulmonary artery and aortic pressure changes during high intensity treadmill exercise in the horse: effect of frusemide and phentolamine.

Intravenous frusemide (1.0 mg/kg bwt) or phentolamine (0.33 mg/kg bwt) was given to 7 horses 1 h before exercise and their effects on pulmonary artery and aortic pressure changes during strenuous exercise were examined. Short-term near-maximal treadmill exercise (10 m/sec, 3 degrees incline) produced increases in heart rate, mean pulmonary artery pressure (PAP), mean aortic pressure (AP), and packed cell volume (PCV). Frusemide did not affect heart rate, PAP or PCV during exercise. Frusemide significantly decreased mean AP by 10 to 15 mmHg during exercise. Phentolamine produced an increase in heart rate relative to control only early in exercise but not during later, more strenuous, exercise. Phentolamine had no statistically significant effect on AP, PAP, or PCV, but a significant reduction was observed between 180 and 230 sec of exercise when PAP and AP were standardised against heart rate. Frusemide did not prevent horses from haemorrhaging during exercise in this study. Treatment with phentolamine did not sufficiently reduce the PAP and AP to test our hypothesis that a reduction in PAP and AP would eliminate EIPH.

Animals↗
PubMed1992

Inhibition of equine mononuclear cell proliferation and leukotriene B4 synthesis by a specific 5-lipoxygenase inhibitor, A-63162.

The lipoxygenase metabolites of arachidonic acid have an important role in lymphocyte activation. We used a specific 5-lipoxygenase inhibitor, A-63162, to examine the role of 5-lipoxygenase (5-LO) in equine blood mononuclear cell (BMC) proliferation and leukotriene B4 (LTB4) synthesis after stimulation with mitogen (phytohemagglutinin, PHA) or calcium ionophore (A23187). The A-63162 inhibited PHA-induced equine BMC proliferation and, at the same concentration, also inhibited A23187-induced LTB4 synthesis. The presence of exogenous interleukin 2 (IL-2) or the cyclooxygenase inhibitor indomethacin, failed to reverse the immunosuppression caused by A-63162. Further, we found that A-63162, at the concentration that inhibited BMC proliferation and LTB4 synthesis, had no effect on BMC viability. The addition of the specific protein kinase C inhibitor, H-7, did not inhibit A23187-induced LTB4 synthesis. Results indicate that 5-lipoxygenase metabolites may have an important role in equine lymphocyte activation and that protein kinase C has no role in regulating LTB4 production after A23187 stimulation.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed1992

Influence of cyclooxygenase inhibitors on furosemide-induced hemodynamic effects during exercise in horses.

Furosemide, which commonly is used as a prophylactic treatment for exercise-induced pulmonary hemorrhage in horses, may mediate hemodynamic changes during exercise by altering prostaglandin metabolism. To determine if furosemide's hemodynamic effects during exercise in horses could be reversed, cyclooxygenase inhibitors were administered with furosemide. Four treatments were administered 4 hours prior to treadmill exercise at 9 and 13 m/s. They included a control treatment (10 ml of 0.9% NaCl solution, IV), furosemide (1 mg/kg of body weight, IV) administered alone, and furosemide in combination with phenylbutazone (4 mg/kg, IV, q 12 h for 2 days) or with flunixin meglumine (1.1 mg/kg, IV, on the day of experiment). Five horses were randomly assigned to complete all treatments. Physiologic variables at rest prior to exercise were not influenced by treatments. Furosemide, administered alone, reduced mean right atrial pressure and mean pulmonary artery pressure during exercise. The combinations of furosemide and flunixin meglumine or furosemide and phenylbutazone, at both levels of exercise intensity, returned mean right atrial pressure and mean pulmonary artery pressure to the value of the control treatment. During rest and exercise, plasma lactate concentration, PCV, heart rate, mean carotid artery pressure, oxygen consumption, carbon dioxide elimination, and cardiac output were not altered by any of the treatments. At 5 minutes after exercise, the administration of furosemide, alone or with phenylbutazone, reduced mean right atrial pressure. Other measured variables were not significantly influenced by treatments during recovery from exercise. These results suggested that cyclooxygenase inhibition partially reverses the decrease in mean right atrial pressure or pulmonary artery pressure induced by furosemide during exercise.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

Influence of furosemide on hemodynamic responses during exercise in horses.

Four hours prior to exercise on a high-speed treadmill, 4 dosages of furosemide (0.25, 0.50, 1.0, and 2.0 mg/kg of body weight) and a control treatment (10 ml of 0.9% NaCl) were administered IV to 6 horses. Carotid arterial pressure (CAP), pulmonary arterial pressure (PAP), and heart rate were not different in resting horses before and 4 hours after furosemide administration. Furosemide at dosage of 2 mg/kg reduced resting right atrial pressure (RAP) 4 hours after furosemide injection. During exercise, increases in treadmill speed were associated with increases in RAP, CAP, PAP, and heart rate. Furosemide (0.25 to 2 mg/kg), administered 4 hours before exercise, reduced RAP and PAP during exercise in dose-dependent manner, but did not influence heart rate. Mean CAP was reduced by the 2-mg/kg furosemide dosage during exercise at 9 and 11 m/s, but not at 13 m/s. During recovery, only RAP was decreased by furosemide administration. Plasma lactate concentration was not significantly influenced by furosemide administration. Furosemide did not influence PCV or hemoglobin concentration at rest prior to exercise, but did increase both variables in dose-dependent manner during exercise and recovery. However, the magnitude of the changes in PCV and hemoglobin concentration were small in comparison with changes in RAP and PAP, and indicate that furosemide has other properties in addition to its diuretic activities. Furosemide may mediate some of its cardiopulmonary effects by vasodilatory activities that directly lower pulmonary arterial pressure, but also increase venous capacitance, thereby reducing venous return to the atria and cardiac filling.

Animals↗
PubMed1989

Changes in circulating equine erythrocytes induced by brief, high-speed exercise.

Five horses were exercised at 10m/sec at a 3 degree incline for 2 mins. Packed cell volume, erythrocyte count, haemoglobin concentration, mean corpuscular volume, plasma protein, total white cell count and lymphocytes increased significantly in blood samples taken after exercise, compared with those taken before exercise; but mean corpuscular haemoglobin and mean corpuscular haemoglobin concentration decreased. Erythrocytes were more resistant to osmotic stress after exercise, but their shape and degree of deformity were unaffected by exercise.

Animals↗
PubMed1989

Mechanism of exercise-induced hypoxemia in horses.

Arterial hypoxemia has been reported in horses during heavy exercise, but its mechanism has not been determined. With the use of the multiple inert gas elimination technique, we studied five horses, each on two separate occasions, to determine the physiological basis of the hypoxemia that developed during horizontal treadmill exercise at speeds of 4, 10, 12, and 13-14 m/s. Mean, blood temperature-corrected, arterial PO2 fell from 89.4 Torr at rest to 80.7 and 72.1 Torr at 12 and 13-14 m/s, respectively, whereas corresponding PaCO2 values were 40.3, 40.3, and 39.2 Torr. Alveolar-arterial PO2 differences (AaDO2) thus increased from 11.4 Torr at rest to 24.9 and 30.7 Torr at 12 and 13-14 m/s. In 8 of the 10 studies there was no change in ventilation-perfusion (VA/Q) relationships with exercise (despite bronchoscopic evidence of airway bleeding in 3) and total shunt was always less than 1% of the cardiac output. Below 10 m/s, the AaDO2 was due only to VA/Q mismatch, but at higher speeds, diffusion limitation of O2 uptake was increasingly evident, accounting for 76% of the AaDO2 at 13-14 m/s. Most of the exercise-induced hypoxemia is thus the result of diffusion limitation with a smaller contribution from VA/Q inequality and essentially none from shunting.

Animals↗
PubMed1986

Effects of propranolol on cardiopulmonary function in the pony during submaximal exercise.

Cardiopulmonary responses of four ponies were monitored during standard exercise tests (SET), before and after beta-adrenergic receptor blockade with propranolol. The SET consisted of four 5 min increments of increasing speed from 1.0 to 2.8 m/sec on a treadmill at a 7 degrees incline. Data were collected at rest, throughout the SET and recovery. Administration of propranolol to ponies at rest had no effect on cardiopulmonary function. During the SET, increases in heart rate, mean pulmonary artery flow velocity (an index of cardiac output) and right ventricular dP/dt (an index of myocardial contractility) were progressively attenuated as running speed increased. Body temperature and mean pulmonary artery and right ventricular pressures were significantly elevated over normal. Propranolol treatment had no effect on the responses of mean arterial pressure, haematocrit, haemoglobin, blood lactate and arterial blood gases and pH to the SET. These results suggest that in the pony there is no sympathetic activity to the heart at rest and that during exercise there is pulmonary vasodilation mediated by beta-adrenergic receptors.

Animals↗
PubMed1984

Pain perception and alleviation in animals.

In the last 2 decades there have been substantial advances in our knowledge of the scientific basis of the mechanisms of pain. Nociceptors or pain receptors are widespread in the skin and tissues of animals; chemical mediation of nociceptor excitation may provide a key for understanding the peripheral phenomena related to pain. The expression of pain in animals involves multiple ascending and descending branches, as well as specialized pain-signaling mechanisms in the spinal cord. The importance of these different pathways varies with species and circumstances. Endogenous neural systems in the brain stem and forebrain including both opioid and nonopioid mechanisms may modulate the central transmission of nociceptive signals in animals. Noxious stimuli mediate a variety of different functions; each animal has a consistent response to noxious stimuli or a consistent pattern of escape from pain. As we better understand the mechanisms of pain, the humane treatment and alleviation of pain in experimental animals can be placed on a much firmer scientific basis.

Afferent Pathways↗
PubMed1984

Effect of exercise on oxygen consumption, heart rate, and the electrocardiogram of pigs.

Pigs were exercised for 5 min at five different treadmill speeds (1.0-1.8 m X s-1) (3 degrees incline), while oxygen consumption (MO2), carbon dioxide production (MCO2), and the electrocardiogram (ECG) were recorded continuously. Data were taken at rest, during exercise, and at 2, 5, 15, and 30 min after exercise. Values for MO2, MCO2, and heart rate (HR) showed progressive increases with increasing treadmill speed. The respiratory exchange ratio (R) increased during exercise and approached 1.0, but peak values were seen shortly after exercise. Heart rate, MO2, MCO2, and R reached steady-state values after 2 min of exercise, which were maintained for the duration of exercise. In most cases, these variables had returned to control levels 15 min after exercise. A high correlation between HR and MO2 was found in these animals. Prominent increases in T-wave amplitude of the ECG were associated with exercise and early recovery. The metabolic and cardiac changes associated with exercise in these animals were all qualitatively similar to responses seen in exercising humans. Thus, this study further supports the belief that the pig is a good model for studying the cardiopulmonary responses to exercise in humans.

Animals↗
PubMed1982

Cardiodynamics in the rhesus macaque during dissociative anesthesia.

Effects of dissociative anesthesia on cardiovascular dynamics and respiration were investigated in rhesus macaques to determine its use in nonhuman primates for restraint and minor surgical procedures. Respiration was spontaneous, and premedicants or anesthetic adjuvants were not used. Two doses of the anesthetic were administered (IM): 1.5 and 3.0 mg/kg. Depressant effects were observed in all variables initially; some cardiovascular variables eventually exceeded preinjection values after the higher (3.0 mg/kg) dose level. At a dose of 1.5 mg/kg, significant depression in myocardial contractility persisted for 20 minutes, and at 3.0 mg/kg for 50 minutes. Stroke volume was minimally affected initially, although significant increases occurred at 40 and 50 minutes after the 3.0 mg/kg injections. Heart rate was depressed by 5% and 7% in the animals given the small and large doses. Values were within control levels by 90 minutes after the anesthetic was injected, except respiratory rate and body temperature. We conclude that the dissociative anesthetic used produces neither marked nor prolonged cardiovascular effects. Since cardiovascular effects are absent by 90 minutes after the anesthetic was injected, dissociative anesthesia is a desirable technique for minor surgical procedures and restraint, especially before physiologic studies.

Anesthesia↗
PubMed1977

Anti-G suit effect of cardiovascular dynamic changes due to +GZ stress.

Lightly anesthetized dogs underwent 1-min exposure to +Gz acceleration without and with a bladder-type anti-G suit. Prior chronic instrumentation permitted through evaluation of cardiac dynamics. During +3 Gz acceleration all recorded dynamic variables were lowered and transient tachycardia occurred. After acceleration ceases, all pressures and dP/dt exceeded control levels. Inflation of the anti-G suit during +3 Gz eliminated the dramatic effects observed during and after acceleration stress. During +6 Gz with the anti-G suit inflated, arterial pressure and dP/dt were maintained whereas left ventricular end-diastolic pressure and total peripheral resistance were much elevated and heart rate was lower. At the onset of G stress, internal diameter of the heart always fell transiently. Otherwise, diameter was not significantly affected by any of the experimental conditions. The results suggest that the anti-G suit maintains perfusion pressure at high sustained G; however, with the anti-G suit inflated at +6 Gz, central venous pressure is dramatically elevated and heart rate depressed. Thus, beneficial effects which provide tolerance to high G are accompanied by potentially detrimental effects.

Animals↗
PubMed1977

Cardiovascular response to fentanyl-droperidol and atropine in the dog.

A combination of fentanyl-droperidol was administered intravenously alone or with atropine sulfate (2 doses--0.04 or 0.02 mg/kg of body weight) to determine if stable neuroleptanalgesia could be produced in the dog. Cardiovascular responses were recorded at 5, 15, and 30 minutes. Fentanyl-droperidol given alone caused a significant increase of peripheral resistance and mean arterial pressure at 5 minutes and then a decrease of these values over a postinjection period of 30 minutes. Left ventricular dP/dt increased significantly at postinjection minutes 15 and 30. In dogs given atropine concurrently with fentanyl-droperidol, there was significant increase in heart rate and decrease in stroke volume. Also, there were significant initial increases in diastolic and mean arterial blood pressures, ventricular contractility, and coronary blood flow. The dose of 0.02 mg of atropine/kg seemed optimal for intravenous administration with fentanyl-droperidol in the dog; when the atropine dose was 0.04 mg/kg, large inotropic and chronotropic effects were produced.

Animals↗
PubMed1976

Ultrastructural effects of +Gz stress on swine cardiac muscle.

Miniature swine were subjected to 9 +Gz acceleration for 60-120s. Within 2 h following the +Gz force, the anterior papillary muscle was removed and prepared for scanning and electron microscopy. Ultrastructural changes observed in the cardiac myocytes included cellular redistribution of mitochondria and nuclei. Tears in the contractile fibers, bizarre profiles or nuclei, and peculiar membrane-bounded bodies in the cytoplasm also were observed. Hemorrhagic areas were localized around the Purkinje fibers. The T system and plasma membrane appeared unperturbed. The conclusion was drawn that, following high +Gz levels of acceleration, damage to myocardial ultrastructure ensues.

Acceleration↗
PubMed1976

Cardiovascular function during sustained +Gz stress.

The development of aerospace systems capable of very high levels of positive (+Gz) stress, has created a need for a better understanding of the cardiovascular responses to acceleration. Using a canine model, the heart and cardiovascular system were instrumented to continuously measure coronary blood flow, cardiac output, left ventricular and aortic root pressure, and oxygen saturation in the aorta, coronary sinus, and right ventricle. The animals were exposed to acceleration profiles up to +6 Gz, 120 s at peak G; a seatback angle of 45 degrees was simulated in some experiments. Radiopaque contrast medium was injected to visualize the left ventricular chamber, coronary vasculature, aorta, and branches of the aorta. The results suggest mechanisms responsible for arrhythmias which may occur, and subendocardial hemorrhage which has been reported in other animals.

Blood Pressure↗
PubMed1975

Ventricular function following acute carbon monoxide exposure.

Cardiac output function curves were used to investigate the effects of carbon monoxide on the heart in the conscious dog. Each dog was briefly exposed to 1,500 ppm carbon monoxide through a permanent tracheostomy. Immediately upon attaining either 10%, 20%, or 30% HbCO a rapid infusion of Ringer's lactate was given to test cardiac capabilities. The combined effects of carbon monoxide and infusion produced significant increases in cardiac output, heart rate, mean left ventricular pressure, dP/dt and (dP/dt)/IP. Cardiac output was sufficient to prevent peripheral hypoxia at all HbCO levels; however, there was evidence of impending cardiac depression beginning at 20% HbCO.

Animals↗
PubMed1975

Coronary hemodynamics during positive (+G-z) acceleration.

Left circumflex (LC) and left anterior descending (LAD) coronary flows, coronary perfusion pressure (P-ca), and arterial O-2 content (Cao-2) were determined in five dogs, lightly anesthetized with chloralose, during exposures to +2.0 and +3.0 G-Z stress; and for three of these dogs at +3.5-G-Z. At +2.0 G-Z, except for one dog with the most marked decrease in P-ca, KC and LAD flows increased above control by 15 s and thereafter gradually returned toward control; coronary resistances were significantly below control at 15 and 30 s (p smaller then 0.05). At +3.0 G-Z, LC and LAD flows were significantly greater than control (p smaller 0.05) from 30 to 60 s, while resistances were below control (p smaller than 0.05). At +3.5 G-Z, LC flow was maintained above control by a much reduced resistance, with P-ca below control; LAD flow increased in one dog, remained unchanged in one, and decreased slightly in one, although resistance always decreased. Cao-2 did not change significantly at any +G-Z level, and myocardial O-2 transport paralleled the changes in coronary flow.

Acceleration↗
PubMed1975

Cardiovascular changes during and following 1-min exposure to +Gz stress.

Magnitude and duration of cardiovascular responses following anesthetized dogs. During lower G forces (+1 to +3GZ), responses were variable. In most dogs during higher G forces (+4 or +5GZ), aortic pressure, cardiac output, left ventricular pressure, and dp/dt were dramatically compromised. These changes were observed whether the onset of the gravitational inertial force was slow (0.1 G/s) or rapid (1.0 G/s). Cardiovascular changes after acceleration were consistent. Left atrial pressure and arterial pressure rose and a transient rise in dp/dt was often observed. Cardiac output rose briefly, then fell; hence, peripheral resistance increased. Magitude and duration of these changes were directly related to G forces during acceleration. Our results confirm that +GZ stress produces major cardiovascular changes. Our experiments also demonstrate that responses following +GZ stress may be dramatic and prolonged. Increased peripheral resistance elevates perfusion pressure and, concurrently, the increased preload may cause acute cardiopulmonary congestion.

Acceleration↗