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Query: DrugBank:APRD00627 (
MAP
)
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document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Cardiovascular responses have been studied in baboons, after total exchange transfusion with hemoglobin solutions having various P50 values. At the end of the exchange transfusion, the hematocrit was 1.5%, the mean hemoglobin concentration was 4.4 g/dl, and the P50 varied between 12 and 26 mm Hg. Cardiac output did not change during the study, although heart rate increased, and
stroke
volume and
MAP
decreased. Hemoglobin concentration, per se, does not appear to be the critical stimulus for an increase in cardiac output with hemoglobin solution. In addition, the position of the hemoglobin-oxygen dissociation curve does not appear to influence these hemodynamic responses. The physiological response to anemia in the presence of hemoglobin solution appears different from that observed in the absence of plasma O2 carriers.
...
PMID:Cardiac output response to extreme hemodilution with hemoglobin solutions of various P50 values. 11 94
Maximal changes in haemodynamics and segmental wall motion were seen 2 min after coronary occlusion and were examined in relation to the loading conditions of the left ventricle before occlusion in 20 open chest dogs. There was a significant inverse relationship between the preligation mean aortic pressure and the percentage decrease in
stroke
volume following ligation. This relationship was observed whether afterload was distributed randomly (mean aortic pressure ranging from 9.7 to 17.6 kPa [73 to 132 mmHg]) between all dogs (r = 0.65; P less than 0.001) or altered by methoxamine (+4 kPa [+30 mmHg]) and nitroprusside (-3.2 kPa [-24 mmHg]) within the same dog (r = 0.82; P less than 0.001; n = 8). Although occlusion of the anterior descending artery caused a small (+5.5%) but significant increase in end-diastolic length of the non-ischaemic epicardial segment, the capacity for compensatory ventricular dilatation was not dependent on preligation afterload. However, the capacity of the ischaemic segment to undergo systolic expansion was significantly greater (+30.2% of end-systolic segment length) in those dogs with the lowest preligation
MAP
(8 to 12 kPa [60 to 90 mmHg]) compared with systolic lengthening of only 15.8% in the high afterload group (15 to 18 kPa [112 to 135 mmHg]). These data indicate that the loading conditions of the left ventricle predetermine the extent of global and segmental left ventricular dysfunction during the early phase of acute ischaemic injury.
...
PMID:Afterload as a predeterminant of haemodynamics and segmental wall motion following coronary artery occlusion. 47 39
The systemic hemodynamic effects of deep hypotension (
MAP
: 38 +/- 6 mm Hg) induced by sodium nitroprusside (S.N.) were studied in 20 patients who underwent surgery for cerebral aneurysm. The hemodynamic measurements were performed four times.: (1) during the preoperative period, (2) during stable anesthesia just before hypotension, (3) during stable hypotension, (4) 20 minutes after stopping nitroprusside. All patients were mechanically ventilated with a constant tidal volume and rate. Parameters for acid-base balance and Pa O2 were also recorded. Nitroprusside produces arterial and venous dilatation which results in a decrease of afterload and preload. The mean dosage of S. N. was 18 mcg/kg/mn. Systemic vascular resistances decreased by 62 p. cent. Mean arterial pressure decreased by 53 p. cent; it reached 40 mm Hg. Fall in preload resulted in a decrease in pulmonary wedge pressure by 28 p. cent. This fall in preload produced a decrease in
stroke
index according to Frank-Starling's mechanisms. However tachycardia allowed a rise in cardiac index by 20 p. cent. Increase of pulmonary wedge pressure at 8-10 mm Hg by blood volume expansion maintains
stroke
index at control level. Under these conditions the elevation of cardiac index is due to tachycardia. Cardiac rhythm disorders (wandering pace-maker, nodal rhythm) are observed in 5 patients after having stopped nitroprusside.
...
PMID:[Deep hypotension induced by sodium nitroprusside in neurosurgery. I.--Systemic hemodynamic effects (author's transl)]. 48 87
Hypotensive episodes occur frequently during hemodialysis; they are often sudden and difficult to prevent despite careful clinical control. Their etiology was studied by investigating the hemodynamic response of five patients submitted to ultrafiltration during their three first dialyses. A Swan Ganz catheter was inserted and left in position for 5 days. Simultaneous determination of cardiac output, mean pulmonary artery (PAP) and capillary and systemic arterial pressures were recorded. 10 hypotensive episodes were observed. In 3 patients in whom the first hypotensive episode occurred 10 minutes after the start of dialysis, there was a significant drop in PAP, cardiac index and
stroke
index while heart rate and peripheral resistance remained unchanged. Paradoxical bradycardia was observed. In 4 patients hypotension was observed more than one hour after initiation of dialysis. Before the hypotensive episode there was moderate elevation of heart rate and peripheral resistance and an insignificant reduction in PAP. Cardiac index and
stroke
index were diminished. The decrease in
MAP
was only 2 mm Hg. Hypovolemia is the most important factor in hemodialysis-induced hypotension but other factors such as vagal stimulation, autonomic neuropathy and osmotic disequilibrium can interfere with blood pressure control and trigger hypotension. Methods of preventing hypotension during dialysis, including the infusion of low molecular weight dextran, are discussed.
...
PMID:Hemodynamic evaluation of hypotension during chronic hemodialysis. 88 13
Cardiac and circulatory function (cardiac output,
stroke
volume, heart rate, mean arterial pressure =
MAP
, total peripheral resistance = TPR), further renal function (PAH- and inulin clearance, filtration fraction, urinary excretion, renal sodium- and potassium excretion) were measured on 15 patients undergoing cardiac surgery to whom Dopamine and Orciprenaline were administered in increasing doses of 100 mug - up to 500 mug/min (Dopamine) and 10 mug - to 20 mug/min (Orciprenaline). An infusion of Dopamine up to 250 mug/min caused a dosis-related increase of the cardiac output up to 31% (2P less than 0.001) without essential increasing of the
MAP
and of the heart rate. Dopamine caused a decrease of the TPR up to 24%. Doses of Dopamine over 250 mug/min cause an increase of the
MAP
and of the heart rate without a real increase of the cardiac output. Renal function improved under increasing doses of Dopamine, effective renal plasma flow (ERPF) up to 74%, urinary excretion up to 130%, sodium and potassium excretion up to 60% respectively. After administering Orciprenaline in a dosis of 20 mug/min cardiac output increases up to 28%,
MAP
and heart rate up to 12% and 17% respectively. After the administration of Orciprenaline (20 mug/min) and Dopamine (500 mug/min) frequent extra systoles were observed without any increase of the cardiac output;
MAP
increased by 12%, TPR decreased by 16% after 20 mug/min of Orciprenaline. ERPF decreased slightly after Orciprenaline. Urinary excretion was reduced by a half.
...
PMID:[Comparing studies on the influence of dopamine and orciprenaline on cardiac and renal function of patients after cardiac surgery (author's transl)]. 108 62
1. The effects of epinine or dopamine (both 1-10 micrograms kg-1 min-1) on systemic haemodynamics and plasma concentrations of catecholamines and prolactin were studied in conscious pigs before and after combined non-selective alpha- and beta-adrenoceptor blockade. 2. The plasma concentrations of the two compounds did not differ from each other over the entire dose-range. 3. Epinine increased aortic blood flow (AoBF, 24 +/- 6%), which was due to an increase in heart rate (HR) for doses less than 10 micrograms kg-1 min-1. At 10 micrograms kg-1 min-1, HR decreased slightly (10 +/- 3%, as compared to the value obtained at 5 micrograms kg-1 min-1) and
stroke
volume increased up to 15% (P < 0.05). Mean arterial pressure (
MAP
, 99 +/- 3 mmHg at baseline) decreased dose-dependently (14 +/- 2%, P < 0.05) up to the infusion rate of 5 micrograms kg-1 min-1, but increased by 4.0 +/- 1.8 mmHg during infusion of 10 micrograms kg-1 min-1. Systemic vascular resistance (SVR) decreased up to 23 +/- 3% for doses less than 10 micrograms kg-1 min-1, but did not change further during infusion of the highest dose. LVdP/dtmax increased during the two highest infusion rates up to 22 +/- 6% (P < 0.05). After the infusion was stopped there was an abrupt increase in HR (18 +/- 4%, P < 0.05) and a further decrease in SVR before all parameters returned to baseline.4. Dopamine caused increases in AoBF (27 +/- 3%) similar to epinine, the only difference being that HR continued to increase (32 +/- 5%) and
MAP
(13 +/- 3%) and SVR continued to decrease (31 +/- 3%) over the entire dose-range. The increase in LVdP/dt,,,, at the highest dose (48 +/- 4%, P <0.05) was more pronounced than with epinine.5. Adrenoceptor blockade inhibited all epinine-induced changes, but did not affect the dopamineinduced changes in AoBF, SVR and
MAP
, but attenuated the increases in HR and LVdP/dtmax.6. Noradrenaline (NA) and adrenaline (Ad) concentrations did not change during infusion of epinine or dopamine, but NA increased by 50% within 2.5 min after stopping the infusion of epinine. After adrenoceptor blockade NA and Ad concentrations did not change during infusion of dopamine, which contrasted with a decrease of 55 +/- 5% (P<0.05) in NA during infusion of epinine.7. Prolactin concentrations decreased gradually from 480 +/- 40 pg ml-' to 270 +/- 50 pg ml1' (P<0.05) during infusion of epinine, but did not change significantly during dopamine infusion.8. The differential effects of epinine and dopamine on
MAP
, SVR, plasma NA (before and after adrenoceptor blockade) and prolactin, leads us to conclude that in conscious pigs, epinine is a more potent a, P2 and D2-receptor agonist, but a weaker D,-receptor agonist than dopamine.
...
PMID:Differential cardiovascular and neuroendocrine effects of epinine and dopamine in conscious pigs before and after adrenoceptor blockade. 133 Jan 72
The impact of esmolol infusion on hemodynamics, ventricular performance, venous admixture, sympathoadrenal, and renin-angiotensin system responses during sodium nitroprusside (SNP)-induced hypotension was studied in 11 patients undergoing lymph node dissection during general anesthesia with 60% nitrous oxide and fentanyl. Radial arterial and thermistor-tipped pulmonary catheters were employed for hemodynamic monitoring. Arterial and mixed venous blood gas tensions, arterial plasma renin activity (PRA), and plasma catecholamine levels were measured. Derived hemodynamic parameters and venous admixture (Qs/Qt) data were obtained from standard equations. Transesophageal echocardiography (6 patients) was used to assess left ventricular performance using the relationship between end-systolic wall stress (ESWS) and velocity of circumferential shortening (VCFC). After surgical incision, arterial hypotension was induced with SNP alone. Esmolol was infused at each of the following rates in sequence: 200, 300, and 400 micrograms/kg/min. Each esmolol infusion lasted 20 minutes and the SNP dose was adjusted to maintain
MAP
at 55 to 60 mm Hg. The mean dose of SNP required to induce hypotension was 5.5 micrograms/kg/min +/- 0.5 SE. Compared to prehypotension values, SNP induced significant increases in Qs/Qt and reductions in PaO2, systemic vascular resistance (SVR), and
stroke
volume index (SVI). Esmolol infusion caused dose-dependent (highest with 400 micrograms/kg/min) reductions in the SNP requirement, heart rate (HR), SVI, Qs/Qt, and PRA, and also led to significant increases in SVR and left ventricular (LV) internal diameter in diastole as well as systole. Furthermore, esmolol infusion was associated with a dose-dependent downward and leftward shift of the ESWS versus VCFC relationship, implying diminished contractility.(ABSTRACT TRUNCATED AT 250 WORDS)
...
PMID:Esmolol infusion during nitroprusside-induced hypotension: impact on hemodynamics, ventricular performance, and venous admixture. 134 63
This study investigated the cardiorespiratory (CR) responses at rest and during submaximal (0-W) functional electrical stimulation (FES)-induced leg cycle ergometer (LCE) exercise prior to and following a progressive intensity FES-LCEa exercise training program in spinal cord injured (SCI) subjects. Seven quadriplegics and six paraplegics participated in FES-LCE training three sessions per week for approximately 12 weeks (36 sessions). Monitored CR responses, including oxygen uptake (VO2), pulmonary ventilation (VE), respiratory exchange ratio (RER), arteriovenous O2 difference (a-vO2), blood pressure (BP), heart rate (HR),
stroke
volume (SV), total peripheral resistance (TPR), and cardiac output (Q), were determined before and after training. Power output (PO) increased significantly (p < .05) over the duration of the training program, indicating increased in strength and endurance of the paralyzed muscles used. Respiratory responses were not significantly altered by training in both groups. FES-LCE training significantly increased resting HR and SBP in quadriplegics and lowered SBP, DBP, and
MAP
in paraplegics. In both groups, HR and BP during submaximal exercise significantly decreased and SV and Q significantly increased after completion of the training program. These results suggest that FES-LCE training improves peripheral muscular and central cardiovascular fitness in SCI subjects. Posttraining HR and BP may also be more stable in quadriplegics and alleviate hypotension. This therapeutic exercise may ultimately lead to improved rehabilitation outcome and reduced stress during activities of daily living, and possibly reduce the risks for secondary CR disabilities.
...
PMID:Functional electrical stimulation leg cycle ergometer exercise: training effects on cardiorespiratory responses of spinal cord injured subjects at rest and during submaximal exercise. 144 77
Administration of fentanyl or lidocaine alone often insufficiently suppresses the haemodynamic reaction to laryngoscopy and intubation. We therefore evaluated the combination of both substances in patients with good ventricular performance (EF > 60%) undergoing coronary bypass surgery. 20 patients were randomly assigned to Group 1 (G1) or Group 2 (G2). As induction agents flunitrazepam (0.025 mg/kg), fentanyl (6-7 micrograms/kg) and pancuronium (0.1 mg/kg) were used. 3 minutes prior to intubation G1-patients received saline (0.1 cc/kg) while in G2 patients lidocaine (1 mg/kg) was administered. 10 minutes after termination of the preparations for induction (M1), prior to (M2), during (M3) and 10 minutes after the end of intubation (M4) heart rate (HR), blood pressure (
MAP
), pulmonary artery pressure (PAP) pulmonary capillary wedge pressure (PCWP) and cardiac output (CO) were measured. From these values we calculated rate-pressure product (RPP), total peripheral resistance (TPR), pulmonary vascular resistance (PVR), cardiac index (CI),
stroke
volume (SV) and
stroke
index (SI). Whitney-Mann test (U-test) served for statistical evaluation. If compared to baseline (M1), induction of anaesthesia caused in both groups a significant decrease of
MAP
(G1: 109 to 81 mmHg; G2: 97 to 77 mmHg), CO (G1: 6.2 to 5.2 l/min; G2: 6.6 to 5.2 l/min), CI (G1: 3.3 to 2.8 l/min m2; G2: 3.5 to 2.7 l/min m2) and RPP (G1: 12701 to 10201 mmHg min-1; G2: 11309 to 8070 mmHg min-1).(ABSTRACT TRUNCATED AT 250 WORDS)
...
PMID:[Lidocaine plus fentanyl for controlling cardiovascular reactions to laryngoscopy and intubation]. 145 Mar 10
Hypertension is a common phenomenon in patients undergoing aortocoronary bypass grafting. This hypertension increases myocardial oxygen consumption and can be prevented by application of vasodilators. A possible cause is activation of the renin angiotensin system. Magnesium is a potent vasodilator and has a beneficial effect after myocardial ischaemia. The study was performed to analyse the influence of magnesium infusion on the haemodynamic status and plasma renin activity in patients undergoing aortocoronary bypass grafting. METHODS. Eighteen patients (NYHA classification II-III) undergoing bypass surgery were divided into two groups, a magnesium and a control group. The magnesium group (n = 9) received 0.8 mEq/kg per h magnesium aspartate as an infusion for 15 min while still awake. After induction of anaesthesia, the magnesium infusion was reduced to 0.2 mEq/kg per h and stopped after aortic cannulation was completed. Plasma magnesium levels and concentrations within erythrocytes were measured. Anaesthesia was induced by flunitrazepam (0.01 mg/kg), fentanyl (0.005 mg/kg) and pancuronium (0.1 mg/kg). After intubation, patients were normoventilated with N2O/O2 = 1:1 and isoflurane (0.5-1.0 vol%). Additional doses of fentanyl (0.0025 mg/kg) were injected before the incision and before sternotomy. Mean arterial pressure, heart rate, cardiac index, total peripheral resistance, pulmonary vascular resistance, mean pulmonary arterial pressure, pulmonary capillary wedge pressure, left ventricular
stroke
work index, right ventricular
stroke
work index, intrapulmonary shunt and plasma renin activity were evaluated at five predefined points: (1) prior to magnesium infusion; (2) after magnesium infusion; (3) 10 min following induction of anaesthesia under steady-state conditions; (4) after sternotomy; (5) after aortic cannulation. RESULTS. Concerning the haemodynamic parameters (
MAP
, RAP, PAP, PCWP) no significant difference between the two groups could be demonstrated. In the control group peripheral resistance (TPR) was higher following sternotomy and aortic cannulation than in the magnesium group. Magnesium prevented decrease of the cardiac index (CI) under steady-state conditions, during sternotomy and following aortic cannulation. Left and right ventricular
stroke
work indexes (LVSWI and RVSWI) were higher in the magnesium group. Plasma renin levels were not significantly different between the two groups. CONCLUSION. Patients undergoing cardiac surgery benefit from magnesium administration in the pre-bypass phase. Due to its vasodilating effect, magnesium lowers the output impedance of the left ventricle and improves cardiac pumping function. It opposes detrimental cardiovascular responses to sternotomy and following aortic cannulation. Also of importance is the advantageous effect of magnesium on cardiac arrest elicited by cardioplegia and for reactivation of the ischaemic myocardium.
...
PMID:[Hemodynamics of coronary surgery patients following magnesium aspartate infusion]. 148 73
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