Biomedical subjects

L E Stuhr

Publications and source records attributed to L E Stuhr.

10 recordsLinked to original sources

PubMed2001

Cardiovascular effects of verapamil and quinidine at normal and elevated ambient pressure.

Cardiovascular parameters were measured in rats before and after administration of verapamil and quinidine, a slow Ca2+ and fast Na+ channel blocker, respectively, at normal and elevated ambient pressure [5 bar (500 kPa)]. Left ventricular pressure (Pivt), maximal velocity of Plvt rise (+dP/dt) and fall (-dP/dt), and heart rate (HR), arterial systolic pressure (Pasys), and mean arterial pressure (MAP) were measured in all animals using catheters connected to pressure transducers. Cardiac output (Q), and myocardial blood flow (MBF) were detected by the microsphere technique. Total peripheral vascular resistance (TPVR), myocardial vascular resistance (MVR) and oxygen consumption of the heart (VO2) was calculated. In Groups 1a (control group; 1 bar) and 1b (test group; 1-5 bar), verapamil (1.5 mg x kg(-1)) caused a reduction in Plvt, +dP/dt, -dP/dt, Pasys, MAP, VO2, TPVR, and MVR in both groups at 1 bar (100 kPa), and these parameters remained depressed for at least 50 min in Group 1a. However, MBF increased after verapamil injection. After compression to 5 bar (500 kPa), Plvt, dP/dt, Pasys, VO2, and MBF were markedly elevated (Group 1b). No change in HR, SV, or Q was found in either of the groups. In Groups 2a (control group; 1 bar) and 2b (test group; 1-5 bar), quinidine (5 mg x kg(-1)), infused over a period of 10 min, reduced Plvt, +dP/dt, -dP/dt, MAP, Pasys, VO2, Q, stroke volume (SV), TPVR and MBF at 1 bar (100 kPa). These parameters remained depressed for almost the whole experimental period in Group 2a, while Plvt, +/-dP/dt, Pasys, MAP and VO2 were enhanced during exposure to 5 bar (500 kPa) in Group 2b. The HR was unchanged by quinidine in Group 2a, but was increased at elevated ambient pressure in Group 2b, whereas the MBF was unchanged in both groups. The present results show that verapamil and quinidine have a depressant effect on cardiac function, arterial pressure and VO2 at normal atmospheric pressure, whereas MBF was enhanced only in the verapamil group. During exposure to elevated ambient pressure, cardiac function, arterial pressure and VO2 increased despite adequate inhibition of slow Ca2+ and fast Na+ channels.

Air Pressure↗

PubMed2000

Effects of SCH 42495, a neutral endopeptidase inhibitor, on cardiac function and mass in rats after repeated hyperbaric exposures.

The aim of the present study was to investigate the effects of inhibition of neutral endopeptidase on left ventricular hypertrophy (LVH), myocardial necrosis and haemodynamic changes, previously shown in rats after repeated hyperbaric exposures to 5 bar, by using the novel neutral endopeptidase inhibitor SCH 42495. Ten test rats underwent chamber dives daily for 40 consecutive days, and 10 control rats were exposed in the same chamber for an equivalent period of time, but in air at 1 bar. The rats received SCH 42495 orally (30 mg/kg twice a day) for 40 days. After 40 days, the body mass was identical in the two groups. Test rats and control rats had equal heart mass (both totally and left ventricular myocardium, including the ventricular septum/100 g), thus indicating that long-term treatment with SCH 42495 inhibits hyperbarically induced LVH. The left ventricular pressure (LVP) and the maximal velocity of LVP increase and decrease (+/- dP/dt) were similar in the test rats compared to the control rats at 1 bar. Previously, we found a higher LVP and dP/dt in non-treated test rats in otherwise identical experiments. This indicates that SCH 42495 "normalizes" the cardiac function of test rats after repeated hyperbaric exposures. The systolic arterial pressure, heart rate (HR) and respiratory frequency (RF) were similar in the two groups throughout the experiments. However, treatment with SCH 42495 lowered the blood pressure compared to previously non-treated rats. In conclusion, long-term administration of the neutral endopeptidase inhibitor SCH 42495 prevented previously shown changes in cardiac function as well as myocardial mass after 40 consecutive exposures to 5 bar.

Adaptation, Physiological↗

PubMed2000

Doppler-echocardiographic findings in professional divers.

To determine if professional diving leads to morphologic and/or functional cardiologic changes, Doppler-echocardiography was performed in 20 professional saturation divers (average 15 yr diving experience) and compared to 20 control persons (policemen) who were matched for age (35-45 yr) and number and duration of training sessions. The policemen were taller than the divers, therefore the echocardiographic dimensions but not the functional variables were normalized for body surface area. The groups were comparable for resting and maximal treadmill exercise heart rate, blood pressure, oxygen uptake, and respiratory exchange ratio. Thickness of left ventricular (LV) anterior and posterior wall in end diastole and end systole, and left ventricular mass were similar in the two groups. The systolic functional parameters, LV ejection fraction, and fractional shortening were on average normal in both groups, although one of the divers had low values. Their LV chamber dimensions, wall thickness, diastolic parameters, and exercise capability were normal. The diastolic functional parameters were equal in the two groups. These results suggest that professional divers have normal size and mass of the heart, no diastolic functional changes, and a normal average systolic function.

Adult↗

PubMed1997

The effect of Losartan, an angiotensin II antagonist, on cardiac function, mass and morphology in rats after repeated hyperbaric exposures.

Previously, we have found development of left ventricular hypertrophy (LVH), myocardial necrosis and haemodynamic changes in rats after repeated hyperbaric exposures to 5 bar. Exactly the same rat model and experimental set-up was applied in the present study. The purpose of this study was to investigate if angiotensin II (Ang-II) plays a role in the development of these cardiac changes. Losartan, a recently developed non-peptide Ang-II receptor antagonist, was administrated (20 mg kg-1 day-1) to each rat for 40 days. Nine test rats underwent chamber dives daily for 40 consecutive days, and 10 control rats were exposed in the same chamber for an equal period of time, but in air at 1 bar. After 40 days, test rats and control rats had equal right and left ventricular myocardial mass/100 g-1 body mass, thus indicating that Losartan inhibits hyperbarically induced LVH. Microscopic examination revealed no changes in the left ventricle, indicating that Losartan prevents myocardial necrosis. The left ventricular pressure (LVP) and the maximal velocity of LVP increase and decrease (+/-dP/dt) were similar in the test rats compared to the control rats at 1 bar. Previously we found a higher LVP and dP/dt in non-treated test rats in otherwise identical experiments. This indicates that Losartan "normalizes" the cardiac function of test rats after repeated hyperbaric exposures. The systolic arterial pressure, heart rate (HR) and respiratory frequency (RF) were similar in the two groups at 1 bar. However, treatment with Losartan lowered the blood pressure compared to previously non-treated rats. In conclusion, long-term Ang-II receptor blockade prevented previously shown changes in cardiac function and morphology, as well as myocardial mass, after 40 consecutive exposures to 5 bar.

Adaptation, Physiological↗

PubMed1994

Effect of beta 1-adrenoceptor blockade in rats at 5 bar ambient pressure.

Conscious rats exposed to 5 bar (500 kPa) ambient pressure show increased total myocardial blood flow (TMBF) and enhanced cardiac contractility in spite of unaltered mean arterial pressure (MAP), heart rate (HR), and cardiac output (CO). Four groups of awake, adapted rats were given injections of atenolol at 1 bar air or 5 bar normoxic N2, or both. Atenolol injected at 1 bar caused a marked reduction of HR, MAP, peak left ventricular pressure (LVP), and rate of LVP rise (+dP/dt) and fall (-dP/dt). In spite of beta 1-adrenoceptor blockade, ambient pressure rise increased HR, LVP, +dP/dt, -dP/dt, TMBF, and calculated cardiac O2 consumption (P < 0.05). A second atenolol injection at 5 bar caused a brief reduction in HR but did not affect cardiac contractility. Rats receiving the first atenolol injection at 5 bar demonstrated unchanged TMBF. We conclude that beta 1-adrenoceptor blockade does not annual the increase in cardiac contractility associated with hyperbaria.

Animals↗

PubMed1994

Systemic hemodynamics during hyperbaric oxygen exposure in rats.

The effect of 1-5 bar O2 on left ventricular pressure (LVP), maximal velocity of LVP rise (+dP/dt) and fall (-dP/dt), systolic arterial pressure (APsys), pulse pressure (delta AP), heart rate (HR), and respiratory frequency (RF) was studied in anesthetized and conscious rats. At 1 bar O2, all blood pressure parameters increased significantly (9-56%) in both groups of rats, while RF fell (11-12%). HR fell only in conscious rats, while arrhythmias occurred in both groups. Compression to 5 bar O2 induced a significant further increase in all blood pressure parameters. HR fell further in the conscious rats. Arrhythmias were observed in increasing number during compression and at 5 bar O2. Elevation in estimated oxygen-consumption of the heart was found both during compression and at 5 bar O2. We conclude that O2 exposure markedly stimulates the myocardium by elevating the LVP, +dP/dt, and -dP/dt, thus elevating APsys and delta AP. Arrhythmias developed in both groups, while bradycardia occurred only in conscious rats.

Anesthesia↗

PubMed1993

Repeated normoxic hyperbaric exposures induce haemodynamic and myocardial changes in rats.

The effect of repeated exposure to ambient pressures of 5 bar (500 kPa), in atmospheres comprising normal partial pressures of oxygen [0.2 bar (20 kPa)] and nitrogen [0.8 bar (80 kPa)] and 4 bar (400 kPa) helium, on cardiac function and morphology was assessed in conscious rats. Ten test rats underwent chamber dives daily for 40 consecutive days, and ten control rats were exposed in the same chamber for an equal period of time, but in air at 1 bar (100 kPa). Cardiac output (Qc) and myocardial blood flow (Qmyocardial) were determined by the microsphere method. After 40 days, the body mass was 7% greater in the control than in the test rats (P < 0.05), although they were given exactly the same amount of standard food. The test rats had a significantly higher (7% absolute, 12% ventricular mass to body mass, P < 0.05) heart mass (left ventricular myocardium, including the ventricular septum) than the control rats. The percentage tissue dry mass of the right and left ventricles was equal in the two groups. Microscopic examination revealed a number of small focal necroses in the left ventricle of the test rats but none in the control rats. The left ventricular pressure (LVP) and the maximum velocity of LVP increase (contractility) and decrease were significantly increased (25%-96%, P < 0.001) in the pre-exposed compared to the control rats at 1 bar (100 kPa). The systolic arterial pressure, heart rate and respiratory frequency were similar in the two groups at 1 bar (100 kPa).(ABSTRACT TRUNCATED AT 250 WORDS)

Adaptation, Physiological↗

PubMed1991

Inotropic and chronotropic effects of isoprenaline in rats exposed to 30 bar.

Inotropic and chronotropic responses to the beta-agonist, isoprenaline (ISO) were studied with a transducer located in the left ventricle and a catheter placed in the left femoral artery in anesthetized rats at 1 and 30 bar. The hemodynamic control values were equal in both series. During ISO infusion the chronotropy increased equally (34%) at 1 and 30 bar. The inotropy increased by 38% during ISO infusion at 1 bar (Series 1). Increased inotropy (44%), and unchanged chronotropy were found during compression to 30 bar (Series 2). The ISO evoked inotropic responses in absolute values were greater at 30 bar than at 1 bar. Nevertheless, an equal relative (%) increase in inotropy was found during ISO infusion at 30 bar compared to 1 bar. The cardiac oxygen consumption was estimated to be 65% higher at 30 bar during ISO infusion compared to that at 1 bar.

Animals↗

PubMed1990

Cardiovascular changes in anesthetized rats during exposure to 30 bar.

The effect of exposure to 30 bar (PHe = 29.0 bar, PN2 = 0.8 bar, PO2 = 0.2 bar) on left ventricular pressure, cardiac contractility, heart rate (HR), and arterial pressure was studied in anesthetized rats. During compression there was a progressive increase in maximal left ventricular pressure (LVPmax), maximal velocity of LVP rise (+ dP/dtmax) and fall (- dP/dtmax), systolic pressure (APsys), and pulse pressure (delta AP). The greatest increase in contractility per bar was found between 1 and 5 bar. Immediately after 30 bar was reached, LVPmax (19%), + dP/dtmax (60%), and - dP/dtmax (22%). APsys (19%), and delta AP (43%) were significantly increased from predive values, with an additional increase detected for all these variables after 60 min at 30 bar. An increase in estimated oxygen consumption (work load) of the heart was also found during compression to and at 30 bar. No changes in HR, mean arterial pressure, and end-diastolic pressure were observed during the high-pressure exposure, indicating that the inotropic changes were not due to changes in peripheral hemodynamics.

Anesthesia↗

PubMed1989

Increased cardiac contractility in rats exposed to 5 bar.

The left ventricular pressure, arterial blood pressure and heart rate were studied in three series of pentobarbital-anaesthetized rats exposed to 5-bar normoxic (PO2 = 0.2 bar) environments: nitrogen-oxygen (15 and 60 min) and helium-oxygen (15 min). The maximal left ventricular pressure (LVP max) and the maximal velocities of LVP rise (+ dP/dt max) and fall (- dP/dt) were significantly (P less than 0.01) increased immediately after reaching normoxic 5 bar (He, 13-28%; N2, 13-23%) and during the exposure at 5 bar (He, 22-44%; N2, 13-18%). The pulse pressure increased significantly (He, 50-62%; N2, 30-34%; P less than 0.01) during the hyperbaric exposure. No changes in heart rate or end-diastolic and mean arterial pressure were detected. The present findings indicate an enhanced cardiac contractility (+ dP/dt max) at 5 bar, with the greatest increase found when He was used as inert gas. The increased contractility was of significant duration (at least 60 min), and was not completely reversed until 5-10 min after decompression.

Animals↗