Biomedical subjects

T Lauri

Publications and source records attributed to T Lauri.

6 recordsLinked to original sources

PubMed2000

Effects on dogs of surface-induced hypothermia and rewarming on the right heart function and pulmonary circulation.

Hypothermia is commonly found in accidents on land and at sea, yet its pulmonary circulatory effects have not been studied before. To study the effects of hypothermia on the right heart function and pulmonary circulation, cardiac catheterization was carried out on nine anaesthetized beagle dogs. The dogs were cooled between ice bags until the temperature in the pulmonary artery was 25 degrees C and then rewarmed using a heating box especially constructed for this purpose. Heart rate decreased significantly (P < 0.01) during cooling. Cardiac output also diminished mainly because of decreased heart rate. Total pulmonary resistance increased in the cold (P < 0.05) and returned to the initial level during rewarming. The peak rate of increase in pressure (dP/dtmax) of the right ventricular pressure curve did not show any significant change. Retardation in relaxation in hypothermia was indicated by an increase (P < 0.01) in the peak negative dP/dt of the right ventricular pressure curve. According to our results, the contraction rate did not change, but the relaxation rate decreased significantly during cooling. No signs of heart failure were observed and all parameters returned to normal during rewarming. In conclusion, right ventricular function was not compromised even during deep hypothermia.

Animals↗

PubMed1997

Effects of surface-induced hypothermia and rewarming on canine cardiac contraction-relaxation cycle.

The aims of this study were to elucidate the effects of cooling and rewarming on cardiac contraction-relaxation cycle. Cardiac catheterization was carried out on eleven anaesthetized beagle dogs. The dogs were cooled between icebags until the temperature of the blood in the ascending aorta was 25 degrees C and then rewarmed. Heart rate increased transiently at the beginning of cooling down to 33 degrees C (P < 0.05). Cardiac output first tended to increase until a body temperature of 33 degrees C was achieved but then decreased (P < 0.05). The systolic period lengthened significantly (P < 0.001) when the body temperature decreased from 37 degrees C to 25 degrees C. Cardiac relaxation slowed down linearly with temperature during cooling. The peak value of the first order derivative of the ventricular pressure curve (dP/dtmax) increased at the beginning of cooling down to 33 degrees C, indicating enhanced systolic pressure rise in left ventricle but returned to baseline values at lower temperatures. However the ejection fraction, systolic period and the systemic vascular resistance increased at the temperatures below 33 degrees C despite the unaltered peak dP/dt and thus we conclude that the contraction force is augmented in the hypothermia. All the parameters measured recovered to normal during rewarming and no signs of heart failure were noted during the experiments.

Animals↗

PubMed1996

Cardiovascular responses to an acute volume load in deep hypothermia.

Intravenous administration of warm fluids is used clinically as first aid either alone or as a contributing method, to rewarm hypothermic patients back to normal body temperature. The aim of this study was to determine the effects of an acute volume load in hypothermic conditions on the canine circulatory system. Cardiac catheterization was performed on 18 anaesthetized beagle dogs. Eleven of them were cooled and at a body temperature of 25 degrees C they received 40 ml.kg-1 dextran administered intravenously. The control group received dextran at normal body temperature. During cooling the body from 37 degrees C down to 25 degrees C most of the volume load escaped from the circulation due to extravazation. During rewarming, the opposite effect could be seen and the volume load persisted up to 29 degrees C and signs of cardiac decompensation were observed. According to these results, the intravenous administration of warm fluids to rewarm hypothermic patients should not be used routinely when hypovolaemia is the only result of hypothermia.

Animals↗

PubMed1996

Cardiovascular responses to beta-stimulation with isoproterenol in deep hypothermia.

The aim of this study was to investigate the effects of beta-stimulation in deep (25 degrees C) hypothermia. Cardiac catheterization was performed on seven anesthetized beagle dogs. They were cooled between ice bags down to 25 degrees C and received isoproterenol administered intravenously three times: at the normal body temperature (37 degrees C) before cooling, after cooling at 25 degrees C, and after rewarming at 37 degrees C. Circulatory function was measured for every 1 degree C of temperature change. Isoproterenol infusion at 37 degrees C induced cardiac acceleration, including the increases of heart rate, cardiac output, and peak first derivative of the left ventricular pressure curve. Systemic vascular and mean outflow resistances and mean aortic pressure decreased. During cooling, shivering thermogenesis continued, even down to 25 degrees C. At 25 degrees C, cardiac acceleration after isoproterenol infusion did not exist but relaxation rate increased slightly. Systemic vascular and mean outflow resistances decreased, but left ventricular end-diastolic and filling pressures increased. beta-Stimulation at normal body temperature increases shivering thermogenesis during cooling. The venous return to the left ventricle at 25 degrees C increased after isoproterenol infusion while systemic vascular resistance decreased, indicating systemic vasodilatation. This increase in preload is probably due to vasoconstriction in pulmonary vessels, which may be mediated by prejunctional beta-adrenoceptors. For cardiac inotrophy, the isoproterenol had no physiologically significant effects at 25 degrees C. After rewarming at 37 degrees C, the effects of isoproterenol were physiologically similar to the effects at the same temperature before cooling.

Adrenergic beta-Agonists↗

PubMed1991

Cardiac function in hypothermia.

Hypothermia retards cardiac contraction and prolongs the subphases of the cardiac cycle in varying degrees. Six anaesthetized beagle dogs were catheterized and cooled between ice bags until the aortic blood temperature was 25 degrees C and then rewarmed to normothermia. The speed of relaxation decreased to a half from its value in normothermia as indicated by the time constant of exponential isovolumic ventricular pressure fall and by the change in the negative dp/dt. It is suggested that retardation of relaxation is connected with temperature dependent changes in calcium kinetics. Decrease of cardiac output was mediated mainly by decreased stroke volume indicating sympathetic tone in spite of cold narcosis.

Animals↗

PubMedDate not supplied

Influence of ethanol on circulation in surface-induced hypothermia and subsequent rewarming.

Hypothermia and ethanol are often closely linked and in hypothermic accidents ethanol is often a contributing factor. To study the effects of ethanol on the circulation in hypothermic conditions, cardiac catheterization was carried out on 18 anaesthetized beagle dogs. They were divided into two groups. One gram of ethanol/kg of b.wt. diluted in saline was infused into the vena cava superior within 30 min to seven dogs. The dogs were then cooled between ice bags until the blood temperature in the ascending aorta was 25 degrees C and they were then rewarmed. The control group of 11 dogs was cooled and rewarmed without ethanol infusion. The heart rate first increased when cooling down to 33 degrees C and decreased thereafter in the control group. In the ethanol group heart rate increased during the ethanol infusion and remained high when cooling down to 33 degrees C and decreased thereafter. Heart rate was higher in the ethanol group throughout the experiments, and during rewarming the difference was significant. In the control group cardiac output first increased until a body temperature of 33 degrees C was achieved but then decreased. In the ethanol group cardiac output started to decrease after ethanol infusion. During rewarming there was a significantly higher cardiac output in the ethanol group, probably due to the higher heart rate. In the cardiac cycle the systolic period prolonged significantly (p < 0.001) in both groups when the body temperature decreased from 37 degrees C to 25 degrees C whereas the diastolic period remained quite stable. The contraction phase was also affected by the cooling. The changes in contraction force cannot be seen in dP/dt alone because dP/dt values first increased significantly when cooling from 37 degrees C to 33 degrees C but then decreased. Ejection fraction, systolic period, and the systemic vascular resistance increased despite the reduction of the dP/dt and thus we conclude that the contraction force is augmented in hypothermia. In the ethanol group the myocardium seems to be depressed due to ethanol. In the early phase of cooling heart rate increased but cardiac output decreased in the ethanol group, indicating the decreased ability of the heart to respond to cooling in the presence of ethanol. The time constant of exponential pressure fall (tau) increased linearly with cooling from 37 degrees C to 25 degrees C and recovered with rewarming in both groups. Changes in negative dP/dt coincided with the changes in the time constant of exponential isovolumic pressure fall. Ethanol did not influence relaxation. All the parameters we checked recovered to normal during rewarming.

Animals↗