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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The haemodynamic and gas exchange abnormalities occurring in neurogenic pulmonary oedema (NPO) were examined retrospectively in 20 patients admitted to the Intensive Therapy Unit (ITU) over a 45-month period (February 1992 to November 1995). In 12 patients, where vasoactive therapy with dobutamine was employed, its effect on haemodynamics was examined. Cardiac index (CI median 2.2 l min-1 m-2) and left ventricular stroke work index (LVSWI 20 g.m.m-2) were markedly depressed, while pulmonary artery wedge pressure (PAWP 17 mmHg), mean pulmonary artery pressure (MPAP 30.5 mmHg), systemic vascular resistance index (SVRI 2852 dyne.s.cm-5.m2) and pulmonary vascular resistance index (PVRI 393 dyne.s.cm-5.m2) were substantially elevated above normal values. Mean arterial pressure (MAP 82.5 mmHg) and heart rate (HR 102 bpm) were within normal limits. The poor oxygenation is indicated by a median PaO2/fiO2 ratio of 18.0 kPa. Patients treated with dobutamine showed significant increases in CI and LVSWI and significant falls in SVRI and PAWP at 2 and 6 h after institution of therapy, and there was a significant rise in PaO2/fiO2 ratio to 27.8 kPa at 6 h. NPO was generally associated with severe depression of myocardial function and elevation of pulmonary vascular pressures. This dysfunction was readily reversed by dobutamine.
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PMID:Haemodynamic changes in neurogenic pulmonary oedema: effect of dobutamine. 884 33

KT3-671, a nonpeptide AT1 receptor antagonist, was administered to 20-week-old stroke-prone spontaneously hypertensive rats (SHRSP) daily for 3 weeks. Its effects on systolic, mean, and diastolic arterial blood pressure (SAP, MAP, DAP), heart rate and locomotor activity were investigated with radiotelemetry. A clear diurnal variation in blood pressure, heart rate, and locomotor activity was observed in synchrony with the light cycle. KT3-671 at a daily dose of 10 mg/kg orally (p.o), produced a significant and consistent reduction in blood pressure, preventing the development of hypertension. KT3-671 reduced SAP more than DAP, suggesting that it may affect both vascular tone and cardiac output. Although KT3-671 did not affect diurnal rhythms in heart rate and locomotor activity, it did cause a slight but significant reduction in heart rate. The MAP determined 23 h after the administration of KT3-671 showed a significant reduction from the day 2 of therapy to the day 3 after discontinuation of therapy, suggesting a long duration of antihypertensive action. There was no rebound increase in blood pressure after discontinuation of KT3-671 therapy. These results suggest that KT3-671 may be potentially useful in the therapy of hypertension.
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PMID:Effect of repeated administration of KT3-671, a nonpeptide AT1 receptor antagonist, on diurnal variation in blood pressure, heart rate, and locomotor activity in stroke-prone spontaneously hypertensive rats as determined by radiotelemetry. 890 3

This study was performed to determine the cardiovascular responses to isoflurane in euthyroid and hypothyroid dogs. Four healthy mixed-breed dogs were studied prior to thyroidectomy (PRE), 6 months after thyroidectomy (HYP), and after 2 months of oral supplementation with 1-thyroxine (SUP). Heart rate (HR), cardiac output (Q), stroke volume (SV), systolic, diastolic, mean arterial blood pressure (SAP, DAP, MAP), and total peripheral resistance (TPR) were determined in awake dogs and in the same dogs when end-tidal isoflurane concentration were 1.28%, 1.92%, and 2.56%. Ventilation was controlled in anesthetized dogs and PACO2 maintained between 38 to 42 mm Hg. Isoflurane caused significant (P < .05) dose-dependent reduction in Q, SV, SAP, DAP, and MAP in the PRE, HYP, and SUP dogs. Cardiac output was lower in the HYP dogs than in the PRE or SUP dogs during awake measurement. TPR was increased in the awake HYP dogs compared with the PRE or SUP dogs. During anesthesia, HYP dogs tended to have lower Q, SV, SAP, and MAP PRE or SUP groups, but the only significant reduction was SAP during 1.5 MAC. The cardiovascular responses to isoflurane in hypothyroid dogs are similar to euthyroid animals with a dose-dependent depression in Q, SV, and arterial pressure.
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PMID:Cardiovascular effects of 1.0, 1.5, and 2.0 minimum alveolar concentrations of isoflurane in experimentally induced hypothyroidism in dogs. 892 95

YM358 2,7-diethyl-5-[[2'-(1H-tetrazole-5-yl)biphenyl-4-yl]methyl]-5H-pyrazolo[ 1,5-b][1,2,4]-triazole potassium salt), a novel nonpeptide angiotensin AT1-receptor antagonist, was administered daily for 4 weeks to 24-week-old stroke-prone spontaneously hypertensive rats (SHRSP). Its effects on systolic, mean and diastolic arterial pressure (SAP, MAP and DAP), heart rate and locomotor activity were investigated by using radiotelemetry. A clear diurnal variation in blood pressure, heart rate and locomotor activity was observed in synchrony with the light cycle. YM358 at a daily oral dose of 10 or 30 mg/kg produced a reduction of blood pressure in a dose-dependent manner. Although a mild attenuation of the antihypertensive effect of YM358 was observed during the early stage of therapy, YM358 at 30 mg/kg per day produced a significant and consistent decrease in 24-hr MAP and DAP, and it prevented the further development of hypertension. YM358 did not affect either heart rate or locomotor activity or their diurnal variations. After the discontinuation of therapy with YM358, the blood pressure recovered promptly to the control level while there was no sign of a rebound increase in blood pressure. These results suggest that YM358 may be potentially useful for the treatment of hypertension.
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PMID:Antihypertensive effect of repeatedly administered YM358, an angiotensin AT1-receptor antagonist, in stroke-prone spontaneously hypertensive rats. 903 37

The haemodynamic effects of head-up tilt (HUT) at different tilt angles were investigated non-invasively in eight normal male subjects. Mean arterial pressure (MAP; by Ohmeda Finapres 2300), stroke volume (SV) and heart rate (HR; by BoMed NCCOM3-R7S) were continuously recorded whilst performing a series of HUTs (55 degrees, 10 degrees, 20 degrees, 30 degrees and 55 degrees) lasting 3 min each. The response to HUT was proportional to the sinc of the tilt angle. The magnitude of the response varied between subjects. HUT to 55 degrees resulted in mean (95% confidence limits) increases in MAP by 16 (+/-16)% and HR by 11 (+/-24)% and a decrease in SV by -25 (+/-22)%. These results were repeatable after 30 min. At small tilt angles, i.e. < or = 20 degrees, MAP did not change and HR decreased by -3 (+/-4)%. A detailed analysis revealed immediate dynamic (0-30 s), late dynamic (30-90 s) and plateau (after 90 s) phases in the response to HUT. In conclusion, HUT produces reproducible haemodynamic effects, although differences exist among subjects. A detailed analysis of these effects can be successfully performed using non-invasive methods.
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PMID:Non-invasive continuous arterial pressure, heart rate and stroke volume measurements during graded head-up tilt in normal man. 917 58

We studied the haemodynamic changes induced by pneumoperitoneum (PP) in elderly patients with increased cardiac risk (ASA class III; n = 10; age 72.3 +/- 8.8 years, mean +/- SD, P < 0.05; group 2) and compared the results with patients at normal risk (ASA class I, II; n = 12; age 55.6 +/- 11.8 years; group 1). Thermodilution measurements were performed after induction of general anaesthesia (T1), after onset of PP (T2, intraabdominal pressure 14 mmHg) and after additional 15 degrees head-up tilt (T3). In both groups PP, as compared with T1, induced a significant increase in mean arterial pressure (MAP, mmHg, group 1: 77 +/- 14 to 96 +/- 18, P < 0.05/group 2: 75 +/- 10 to 102 +/- 18, P < 0.01), mean pulmonary artery pressure (MPAP, mmHg: 15 +/- 5 to 22 +/- 4, P < 0.01/18 +/- 3 to 25 +/- 5, P < 0.01), central venous pressure (CVP, mmHg: 7 +/- 2 to 15 +/- 3, P < 0.01/7 +/- 2 to 12 +/- 2, P < 0.01), pulmonary capillary wedge pressure (PCWP, mmHg: 9 +/- 4 to 16.3, P < 0.01/8 +/- 2 to 15 +/- 6, P < 0.01) and in systemic vascular resistance (SVR, dynes s cm-5: 1415 +/- 375 to 1873 +/- 412, P < 0.01/ 1502 +/- 360 to 2067 +/- 647, P < 0.01). Cardiac index (CI, L min-1 m-2: 2.3 +/- 0.3 to 1.9 +/- 0.3, P < 0.05/2.2 +/- 0.4 to 2.2 +/- 0.5 P = 0.76) and oxygen delivery index (DO2I, mL min-1 m-2: 388 +/- 54 to 324 +/- 61, P < 0.05/358 +/- 69 to 353 +/- 82, P = 0.77) decreased in group 1 but not in group 2. Heart rate, stroke Index, pulmonary vascular resistance, arteriovenous oxygen content difference and oxygen consumption index were unchanged. After head-up tilt MAP (mmHg, 92 +/- 15, P < 0.05/ 101 +/- 17, P < 0.01), MPAP (mmHg, 20 +/- 3, P < 0.01/22 +/- 4, P < 0.05), CVP (mmHg, 12 +/- 2, P < 0.01/10 +/- 2, P < 0.01) and PCWP (mmHg, 12 +/- 3, P < 0.05/12 +/- 5, P < 0.05) remained elevated compared with T1 in both groups, SVR (dynes s cm-5, 1575 +/- 372, P = 0.13/1793 +/- 528, P < 0.01) in group 2 only. No complications occurred. The results indicate that PP is associated with significant but relatively benign haemodynamic changes. Anaesthesia for laparoscopic cholecystectomy may be performed safely also in elderly ASA class III patients with increased cardiac risk. An adequate haemodynamic monitoring is recommended.
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PMID:Haemodynamic effects of pneumoperitoneum in elderly patients with an increased cardiac risk. 969 12

Rats are generally believed to be insensitive for cardiac glycosides. However, like in humans, the hemodynamic effects may be related to the pathophysiological condition. Since the hemodynamic effects of cardiac glycosides have never been investigated in rats with heart failure, the aim of the present experiments was to investigate the role of the pathophysiological condition in the rat. Therefore, hemodynamic and cardiac effects of ouabain were investigated both in normal rats and rats with heart failure due to myocardial infarction (MI). Since the effects of ouabain may also depend on the treatment scheme, rats were treated either for a short-term period or a long-term period. Three weeks after sham surgery or ligation of the left coronary artery (MI), Wistar rats were treated for two weeks with ouabain (14.4 mg/kg.d s.c.), either continuously (osmotic minipumps) or intermittently (once daily). A separate group of rats was treated for 45-60 min (1-100 microg/kg.min ouabain; i.v. infusion 5 weeks after MI). Hemodynamic measurements were performed at rest and after volume loading in conscious rats, chronically instrumented with an electromagnetic flow probe and catheters. Induction of MI resulted in a significant increase in total peripheral resistance (TPR), and a significant decrease in basal and maximal cardiac output following volume loading (basal CO: sham, 92 +/- 5; MI, 74 +/- 5 ml/min; maximal CO: sham, 152 +/- 4; MI, 105 +/- 7 ml/min; n = 7-11). Chronic intermittent ouabain treatment further increased TPR in MI rats. In contrast, continuous ouabain treatment normalized TPR in rats. Only in continuously treated MI rats, basal and maximal CO improved significantly (basal: 83 +/- 4; maximal: 134 +/- 7 ml/min; n = 7). Acute treatment dose-dependently worsened the hemodynamic conditions of MI rats, since TPR and MAP increased and CO and stroke volume decreased significantly. These experiments demonstrate that ouabain can improve cardiac function in rats, although only in MI rats and strongly depending on the delivery regimen. Thus, in contrast to the general belief, the presently used rat model is suitable for investigation of cardiac glycosides in heart failure. The preferential improvement of cardiac function in MI rats continuously treated with ouabain may depend upon changes in Na+,K+-ATPase or altered neurohumoral conditions due to MI and chronic treatment.
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PMID:Ouabain improves cardiac function in vivo in rats with heart failure after chronic but not acute treatment. 927 26

This study had the purpose of documenting the hemodynamic correlates of effective arterial elastance (Ea; i.e., an accurate estimate of hydraulic load) in mitral stenosis (MS) patients. The main hypothesis tested was that Ea relates to the total vascular resistance (R)-to-pulse interval duration (T) ratio (R/T) in MS patients both before and after successful balloon mitral valvotomy (BMV). High-fidelity aortic pressure recordings were obtained in 10 patients (40 +/- 12 yr) before and 15 min after BMV. Ea value was calculated as the ratio of the steady-state end-systolic aortic pressure (ESAP) to stroke volume (thermodilution). Ea increased after BMV (from 1.55 +/- 0.63 to 1.83 +/- 0.71 mmHg/ml; P < 0.05). Throughout the procedure, there was a strong linear relationship between Ea and R/T: Ea = 1.09R/T - 0.01 mmHg/ml, r = 0.99, P = 0.0001. This ultimately depended on the powerful link between ESAP and mean aortic pressure [MAP; r = 0.99, 95% confidence interval for the difference (MAP - ESAP) from -18.5 to +4.5 mmHg]. Ea was also related to total arterial compliance (area method) and to wave reflections (augmentation index), although to a lesser extent. After BMV, enhanced and anticipated wave reflections were observed, and this was likely to be explained by decreased arterial compliance. The present study indicated that Ea depended mainly on the steady component of hydraulic load (i.e., R) and on heart period (i.e., T) in MS patients.
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PMID:Hemodynamic correlates of effective arterial elastance in mitral stenosis before and after balloon valvotomy. 933 14

We studied the response in left ventricular (LV) internal dimensions and posterior wall thickness during the performance of sudden strenuous exercise without warm-up (SSE) and sudden strenuous exercise with warm-up (SSEw) in 15 healthy, untrained college-aged males (26 +/- 5.0 yr). Measurements of left ventricular end-diastolic dimension (LVEDD), left ventricular end-systolic dimension (LVESD), stroke dimension (SD = LVEDD-LVESD), fractional shortening (FS = SD/EDD) and posterior wall thickness (PWT) were obtained from continuous 2-D targeted on M-mode echocardiography. Continuous EKG and blood pressure were obtained at rest and during the final 10 s of SSE (30 s of upright leg cycle ergometry of 400 W at 80 rpm). SSEw was preceded by warm-up exercise (6 min of graded leg cycle exercise of 2-min stages initial load 30 W, increasing in 30-W increments at 60 rpm, followed immediately by SSE). Our findings revealed that there were no significant differences in the LV internal dimensions (LVEDD, LVESD, FS, PWT), HR max, RPP max, ECG, and MAP max between SSE and SSEw. Sudden strenuous exercise without warm-up is not associated with a reduced LV function. The results of this study are contradictory to previous findings that have suggested that SSE is associated with transient global left ventricular (LV) dysfunction.
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PMID:Cardiovascular response to sudden strenuous exercise: an exercise echocardiographic study. 934 59

Cytosolic Ca2+ overload has been proposed as a main cause of neuronal injury during cerebral ischemia. SNX-111, a synthetic product of the naturally occurring omega-conotoxin MVIIA, is a novel, presynaptic N-type Ca2+ channel antagonist and has been reported to be neuroprotective against cerebral ischemia. We studied the neuroprotective effects of SNX-111 in a rabbit model of focal cerebral ischemia. New Zealand white male rabbits (2.5-3.5 kg) were given 1 mg/kg/h i.v. SNX-111 (n=8) or normal saline (n=8) 10 min after onset of a 2-h period of transient focal cerebral ischemia induced by occlusion of the left middle cerebral, anterior cerebral and internal carotid arteries followed by 4 h reperfusion. SNX-111 significantly attenuated overall cortical ischemic neuronal damage by 44% (saline, 38.7+/-3.0%; SNX-111, 21.5+/-6.0%, P<0.05) and regions of hyperintensity on T2-weighted MRI by 30% (saline, 70.6+/-4.0%; SNX-111, 49.3+/-11.0%, P<0.05). No significant difference in (regional cerebral blood flow) rCBF or MAP (mean arterial blood pressure) was found between SNX-111- and saline-treated rabbits suggesting that neuroprotection is due to a cellular effect. We conclude that SNX-111 reduces ischemic injury in this model. Its use as a clinical neuroprotective agent for cerebrovascular surgery or stroke should be investigated further.
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PMID:SNX-111, a novel, presynaptic N-type calcium channel antagonist, is neuroprotective against focal cerebral ischemia in rabbits. 945 74


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