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Biomedical subjects

H H Erickson

Publications and source records attributed to H H Erickson.

54 records · Page 3Linked to original sources
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↗
PubMed1975

Heart biochemical responses in miniature swine subjected to +Gz acceleration.

Myocardial biochemical systems which are sensitive to hypoxic and ischemic insult were studied to determine the possible etiology of ventricular endocardial hemorrhage in miniature swine following +GZ stress. Unanesthetized animals were subjected to a single, 120-s +9 GZ acceleration. Approximately 1-2 h following +GZ exposure, the animals were anesthetized and the hearts removed for analyses. Acceleration exposure resulted in the loss of acid phosphatase enzyme activity from the membrane-bound lysosomal fraction with concomitant increased activity in the soluble fraction. This suggests that lysosomal membrane integrity had been disrupted. Mitochondrial preparations from +GZ-stressed hearts exhibited marked increases in active respiratory rate and rate of calcium transport while oxidative phosphorylation efficiency was unchanged. The results clearly indicate that +GZ acceleration is capable of altering myocardial biochemical systems. However, the results tend to suggest that these alterations in cellular processes may be mediated by influences other than hypoxia or ischemia.

Acid Phosphatase↗
PubMedDate not supplied

Cardiovascular effects of enflurane and halothane on the rhesus monkey.

Ten rhesus monkeys were chronically instrumented to compare the cardiovascular effects of enflurane and halothane. In 17 experiments, each monkey was evaluated in the awake state and after equilibration at each of many anesthetic levels. End-expired gas concentrations were expressed in multiples of human minimum alveolar concentrations (MAC) for comparison. There was a predictable dose-related decrease in heart rate, mean arterial pressure, peak left ventricular dp/dt, and the latter divided by left ventricular developed pressure (see article) with both agents. Central venous pressure was increased by both. At equal MAC levels, no significant differences were detected between halothane and enflurane. Cardiac output and aortic flow acceleration were obtained on one of the animals for both agents. Results were consistent with those for the other measured parameters.

Animals↗