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 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hemodynamic and oxygen transport effects of dopamine and dobutamine were studied in a series of 25 critically ill postoperative general surgical patients by a prospective, randomized crossover design after maximal response to fluids had been obtained. Dopamine increased MAP, HR, CI, PvO2, DO2, and Qsp while decreasing PaO2. Dobutamine increased HR, CI, SI, stroke work, DO2, VO2, and Qsp while decreasing PAWP and SVRI and PVRI. In general, the effects of the two drugs were greater in patients in the first 72 hours after surgery. The effects of dobutamine on flow and oxygen transport were greater than those of dopamine, especially in the early postoperative period. The effects were smaller and not significant in patients more than three days after surgery, as well as in those with sepsis, respiratory failure, renal failure, age over 65 years, and hyperdynamic states, in part because of the small number of patients in each group. These data are consistent with the hypothesis that the beta 2-adrenergic action of dobutamine vasodilates the previously constricted peripheral circulation, enhances tissue perfusion by improving micro-circulatory flow distribution, and improves DO2 and VO2.
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PMID:Comparison of hemodynamic and oxygen transport effects of dopamine and dobutamine in critically ill surgical patients. 273 68

In our previous work thyroidectomy significantly improved survival in canine hemorrhagic shock. This finding, coupled with the reported beneficial hemodynamic effects of thyrotropin-releasing hormone (TRH) in circulatory collapse, led to the present study. Anesthetized, heparinized dogs were bled rapidly into a reservoir until MAP = 40 mm Hg. After 60 min of hypotension (E60) the reservoir line was clamped for 30 min (E90). In 10 dogs three doses of TRH (2 mg/kg) were administered iv at 10-min intervals during clamping. In 11 other animals equivalent volumes of saline were given. At E90 the reservoir line was unclamped, and shed blood was reinfused over 30 min. After 1 hr of monitoring (E180) the dogs were returned to the kennel and observed for at least 3 days. Among 11 control dogs, 6 died. In the TRH group only 1 of 10 dogs died (P less than 0.05). During uncompensated shock (E60-E90), TRH-treated dogs had significantly higher mean arterial pressure, cardiac index, stroke index, and right and left ventricular stroke work indexes, and arterial pH than control animals. At the conclusion of the acute experiment (E180) there were few intergroup hemodynamic-metabolic differences. The significant enhancement of 3-day survival by TRH in canine hemorrhagic shock might be related to hemodynamic improvement at a critical stage of circulatory collapse (E60-E90). Direct or indirect neuromodulatory actions of TRH on the CNS could also explain our results. These findings lend further support to the potentially key role of hypothalamic-pituitary-thyroid interrelationships in shock.
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PMID:Thyrotropin-releasing hormone increases survival in canine hemorrhagic shock. 307 47

Three groups of 11 male subjects with the same mean age were studied: normotensives (group I), patients with sustained essential hypertension (group II) and patients with borderline hypertension (group III). M-mode echocardiography provided a measure of aortic root systolic diameter (D) and left ventricular mass index (LVMi, g/m2). We have used a 4 MHz pulsed doppler velocity meter with spectral analysis to measure instantaneous ascending aortic blood velocity. Measurements values were averaged during 10 s and included: stroke volume (SV, cm3 = integrated velocity over one cardiac cycle.aortic cross sectional area (3.14D2/4)), cardiac output (CO, cm3 = SV.heart rate), systemic vascular resistance (SVR, mmHg/cm3.s-1 = MAP/co) and maximal aortic acceleration (MA, cm/s2). (Table: see text). Stroke volume and cardiac output were similar in three groups. SVR was higher in group II than in group I. The myocardial contractility appreciated from the maximal aortic acceleration (Bennett et al, Cardiovasc Res 1984; 18: 632-8) was increased in patients with borderline hypertension and remained within the normal range in patients with sustained essential hypertension despite and increase in cardiac mass.
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PMID:[Non-invasive measurement by Doppler pulse of cardiac output and maximal aortic acceleration in essential arterial hypertension]. 314 28

Verapamil (1 mg/kg, i.v.) and nifedipine (0.3 mg/kg, i.v.) were tested at equi-antihypertensive doses for systemic hemodynamic responses in conscious spontaneously hypertensive rats (SHR) using the Fick method. Systemic hemodynamic effects of these agents were also evaluated in areflexic, spinal cord-transected and vagotomized SHR using the electromagnetic flowmetry technique. Both verapamil and nifedipine lowered mean arterial pressure (MAP:verapamil = -24%; nifedipine = -28%) in conscious SHR by decreasing total peripheral resistance (TPR:verapamil = -48%; nifedipine = -59%) with a concomitant rise in cardiac output (CO: verapamil = 48%; nifedipine = 86%) and stroke volume (SV:verapamil = 54%; nifedipine = 65%), but verapamil prevented tachycardia, whereas nifedipine increased heart rate (HR:13%). Verapamil and nifedipine also altered systemic hemodynamics in the areflexic SHR; verapamil reduced MAP (-31%) by reducing CO (-18%) with associated bradycardia (-25% HR), whereas nifedipine also lowered MAP (-21%) by decreasing TPR (-18%) without changes in CO and HR. It is concluded that, firstly, the antihypertensive action of verapamil and nifedipine in conscious SHR is due to systemic vasodilation that is associated with reflexly increased CO; secondly, that verapamil has a direct negative chronotropic effect, but nifedipine appears to be devoid of such an effect, and finally that the ability of verapamil to decrease TPR may depend upon resting sympathetic tone.
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PMID:Effects of verapamil and nifedipine on systemic hemodynamics in spontaneously hypertensive rats. 322 Oct 97

The effect of induction of epidural analgesia with 0.5 per cent bupivacaine on maternal haemodynamics was investigated in 21 patients with uncomplicated full-term pregnancies in early labour. Stroke volume, heart rate, and cardiac output (SV, HR, and CO) were measured by transcutaneous aortovelography (TAV). Systolic, diastolic, and mean arterial blood pressures (SBP, DNP, and MAP) were measured by indirect automatic oscillometry. Measurements were made with the patient in the left lateral decubitus position before and after an intravenous bolus of 500 ml of lactated Ringer's solution preceding induction of epidural analgesia, and again 30 and 45 minutes after induction. The 500 ml bolus of lactated Ringer's solution did not prevent fall of CO and BP measured 30 minutes after induction, when there were statistically significant decreases in CO and cardiac index (-10.2 and -10.6 per cent, p less than 0.05), and in SBP, DBP, and MAP (-9.7, -12.5, and -11.9 per cent, p less than 0.005, p less than 0.005 and p less than 0.01 respectively). At 45 minutes after induction, CO and cardiac index had returned to baseline values. Although the decreases in SDP and DBP persisted, the change in MAP was not statistically significant.
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PMID:Haemodynamic effects of induction of epidural analgesia in labour. 334 53

Six healthy males were exposed to 20 mm Hg lower body negative pressure (LBNP) for 8 min followed by 40 mm Hg LBNP for 8 min. Naloxone (0.1 mg.kg-1) was injected intravenously during a 1 h resting period after which the LBNP protocol was repeated. Systolic, mean, and diastolic arterial blood pressures (SAP, MAP, DAP), and central venous pressure (CVP) were obtained using indwelling catheters. Cardiac output (CO), forearm blood flow (FBF), heart rate (HR), left ventricular ejection time (LVET), and electromechanical systole (EMS) were measured non-invasively. Pulse pressure (PP), stroke volume (SV), total peripheral resistance (TPR), forearm vascular resistance (FVR), systolic ejection rate (SER), pre-ejection period (PEP), PEP/LVET and indices for the systolic time intervals (LVETI, EMSI, PEPI) were calculated. During the second LBNP exposure, only two parameters differed from the pre-injection values: DAP at LBNP = 40 mm Hg increased from 60.0 +/- 4.8 mm Hg to 64.8 +/- 4.1 mm Hg (N = 4, p less than 0.02) and LVETI at LBNP = 20 mm Hg increased from 384.4 +/- 5.2 ms to 396.8 +/- 6.2 ms (N = 6, p less than 0.02).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Human cardiovascular reactions to simulated hypovolaemia, modified by the opiate antagonist naloxone. 339 65

Two primary predictor variables, age and supine plasma norepinephrine, were studied with respect to their influences on supine hemodynamic variables in 52 white men with essential hypertension who were 23 to 67 years of age and had been off active therapy for at least 4 weeks. Plasma norepinephrine was related to age (r = 0.39, p less than 0.01), correlated closely with mean arterial pressure (MAP; r = 0.54, p less than 0.0002) and systemic vascular resistance (r = 0.49, p less than 0.0005), and was related inversely to cardiac output (r = -0.26, p less than 0.06) and stroke volume (r = -0.31, p less than 0.05). Age correlated weakly with MAP (r = 0.31, p less than 0.05) and more strongly with systemic vascular resistance (r = 0.46, p less than 0.005) but was negatively related to cardiac output (r = -0.41, p less than 0.005) and heart rate (r = -0.33, p less than 0.05). Weight did not correlate with any of the hemodynamic variables. Partial regression techniques yielded significant residual correlations between age-adjusted plasma norepinephrine and MAP (r = 0.42, p less than 0.005) or systemic vascular resistance (r = 0.38, p less than 0.005). Residual correlations with cardiac output (r = -0.34, p less than 0.05), heart rate (r = -0.36, p less than 0.02), and systemic vascular resistance (r = 0.33, p less than 0.05) remained after adjusting age for the corresponding plasma norepinephrine values. These correlations demonstrate the independent effects of sympathetic nervous activity and the aging process on the systemic vasoconstriction and decreased cardiac function observed in essential hypertension.
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PMID:Plasma norepinephrine and age as determinants of systemic hemodynamics in men with established essential hypertension. 355 6

The hemodynamic effects of dobutamine (2.5-20 micrograms/kg per min) were studied in six elderly patients with septic shock which was refractory to dopamine (15 micrograms/kg per min). Dobutamine infusion resulted in significant increases in cardiac index (CI), stroke index (SI) and left ventricular stroke work index (LVSWI) and similar declines in heart rate (HR), mean pulmonary artery pressure (MPAP), pulmonary capillary wedge pressure (PCWP), systemic vascular resistance (SVR) and total pulmonary resistance (TPR). Dose response curves demonstrated a linear rise in CI with increasing doses of dobutamine and parallel decreases in HR and PCWP. MAP was unchanged. These data indicate that dobutamine may be a useful adjunct to dopamine therapy in the management of elderly patients with septic shock.
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PMID:Dobutamine in elderly septic shock patients refractory to dopamine. 355 31

The purpose of this study was to investigate the effects of plasma volume expansion on the cardiac and peripheral components of the baroreceptor reflex. Nine male Rhesus monkeys were chronically instrumented to measure arterial pressure and aortic blood flow. The aortic arch was denervated at the time of surgery. Bilateral carotid artery occlusion (BCO) was used to elicit the carotid sinus reflex both before and after 25% plasma volume expansion with an iso-osmotic dextran solution. The BCO elicited significant increases in heart rate (HR, 29.8 +/- 5.3 bpm) mean arterial pressure (MAP, 55.0 +/- 8.2 mm Hg) and total peripheral resistance (TPR, 0.076 +/- 0.01 mm Hg/ml/min) coupled with a significant reduction in mean aortic flow (AF, -246.9 +/- 55.3 ml/min) and stroke volume (SV, -2.86 +/- 0.36 ml). Volume expansion significantly attenuated the HR (15.2 +/- 5.8 bpm), MAP (30.4 +/- 4.4 mm Hg) and TPR (0.036 +/- 0.006 mm Hg/ml/min) response to carotid sinus hypotension. The changes in mean AF and SV elicited by BCO, however, were not significantly different between the control and volume expansion conditions. These data suggest that plasma volume expansion significantly attenuates the baroreceptor reflex control of circulation with a similar reduction in both the peripheral resistance and heart rate components of the response.
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PMID:The effect of plasma volume expansion on the response to carotid occlusion in the non-human primate. 359 48

The influence of triglycyl-lysine-vasopressin (TGLVP) on cardiovascular responses to orthostatic stress was studied. Arterial pressures, heart rate (HR) and stroke volume (SV) were measured in eight healthy males subjected to 20 min 70 degrees head-up tilt. On different days they received either 0.01 mg/kg b.w. of TGLVP or a corresponding volume of 0.9% saline i.v. after 15 min supine rest. After the drug injection, in supine subjects, HR had decreased from 58 to 50 beats min-1, total peripheral resistance (TPR) was elevated by 29%, systolic (SAP) and diastolic pressure (DAP) had increased by 7 and 8 mmHg, respectively. During tilt, values for HR and SAP were similar with and without TGLVP whereas DAP and MAP were elevated 8 and 7 mmHg, respectively, by the drug. 4-8 min into the tilt, TGLVP caused an 8% sustained curtailment of SV. Both with and without the drug TPR increased by about 30% in response to head-up tilt. Thus, the marked peripheral arteriolar constriction after vasopressin in the supine position was not affected by head-up tilt. Tilting also abolished the drug-induced elevation in SAP, most likely explained by the reduction in SV. Although TPR was markedly increased by TGLVP during head-up tilt, reflected in the behaviour of DAP, the response of SV speaks against any beneficial effect of this drug on orthostatic tolerance in healthy subjects.
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PMID:Effects of triglycyl-lysine-vasopressin on cardiovascular responses to orthostatic stress. 362 70


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