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

This study determined the physiologic responses to prolonged functional neuromuscular stimulation (FNS) leg-cycle exercise in seven quadriplegic and seven paraplegic subjects. Each subject completed 30 minutes of continuous FNS leg cycling during which open-circuit spirometry, impedance cardiography, auscultation, and fingertip capillary blood sampling were used to assess metabolic and hemodynamic responses. Compared with resting values, oxygen uptake, carbon dioxide production, respiratory exchange ratio (RER), pulmonary ventilation, heart rate (HR), left ventricular stroke volume (SV), cardiac output (Qt), and blood lactate (La) concentration were significantly (p less than .05) elevated, whereas plasma volume, bicarbonate concentration, and pH were significantly decreased in both groups during prolonged FNS leg-cycle exercise. Mean arterial pressure remained unchanged in quadriplegic and paraplegic subjects during the prolonged FNS leg-cycle exercise bout. Persons with quadriplegia elicited significantly lower MAP and tended to have lower SV and Qt responses than persons with paraplegia, probably due to a higher degree of sympathetic dysfunction and circulatory hypokinesis during FNS leg-cycle exercise. All other physiologic variables responded similarly between groups. We speculate that the relative increases observed for HR (33% to 60%), SV (45% to 69%), and Qt (113% to 142%) during prolonged FNS leg-cycle exercise create a sufficient cardiac-volume load to promote central cardiovascular conditioning in persons with both quadriplegia and paraplegia. The La accumulation (4.7 to 5.2 mmol.L-1) in the spinal cord injured during prolonged FNS leg cycling is unusually high for the power output attained (5.2W and 6.1W for quadriplegia and paraplegia, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Physiologic responses to prolonged electrically stimulated leg-cycle exercise in the spinal cord injured. 222 53

The Nimbus pump is an indwelling, electromagnetic powered left ventricular (LV) assist device inserted transfemorally. The inflow cannula (7 mm) is positioned across the aortic valve and the pump in the descending aorta. Indications for insertion include cardiogenic shock despite maximal medical support and PCWP greater than 18 mmHg, MAP less than 90 mmHg, and Cl less than 2 L/min/m2. Twelve patients underwent the attempt at surgical insertion of the Nimbus pump. Diagnoses included eight acute myocardial infarctions (AMI), two ischemic cardiomyopathy, one postpartum cardiomyopathy, and one transplanted heart rejection. Eight (67%) of twelve patients had successful insertion. One patient had peripheral vascular disease preventing passage, and three had femoral vessels too small for insertion (less than 7.5 Hagar dilator). Five patients with the diagnosis of AMI had successful insertion and three (60%) underwent sufficient LV recovery for removal of the device; the other two patients died of stroke and ventricular arrhythmias, respectively. Three patients with the diagnosis of cardiomyopathy had progression of the disease process, and their needs exceeded the capabilities of the pump and they died of multiorgan failure. The Nimbus pump is an attractive LV assist device because of its pumping capacity (3.5 L/min) and minor surgical procedure for insertion. However, its application is limited because of access route and size. The device appears to work well for patients in cardiogenic shock after AMI (60% recovery) but does not appear indicated for patients with cadiomyopathy.
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PMID:Clinical experience with the Nimbus pump. 225 70

Because of the growing interest in the use of coronary artery ligation (CAL) in rats as a model for studies on heart failure, we have investigated the acute hemodynamic changes following CAL in conscious rats. Animals were equipped for measurement of cardiac output (CO), arterial pressure (MAP), and central venous pressure (CVP). These parameters were measured before CAL, immediately after, and 24 h after. Furthermore, peak CO, obtained by rapid infusion of 12 ml Ringer's solution (in 1 min) was measured 2 days before and 1 day after CAL. CAL resulted in immediate reduction of CO, because of reduced stroke volume (SV). CO as well as SV were inversely correlated with infarct size as determined 24 h after CAL. Heart rate (HR) and MAP did not change. Twenty-four hours later, CO was still reduced. MAP was now reduced, possibly as a result from resetting of nervous reflex mechanisms. Before CAL, peak CO and SV were similar in CAL and sham animals. At 24 h after CAL, these parameters were greatly reduced in CAL rats. Peak values were strongly correlated to infarct size. Results indicate that CAL in rats leads to hemodynamic changes similar to the ones observed following myocardial infarction in man. Cardiac function is related to infarct size and is altered both at rest and during maximal stimulation.
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PMID:Acute hemodynamic effects of coronary artery ligation in conscious rats. 232 51

At 31 critically ill surgical patients who on clinical grounds required fluid therapy, hemodynamic and oxygen transport, responses were measured after volume expansion with 500 ml 6% HES 450/0,7. There were statistically significant increases in cardiac index (CI) from 3,5 +/- 2,1 to maximal values of 4,4 +/- 0,2 (l/min/m2) and in wedge pressure (WP) from 9,3 +/- 0,7 to maximal values of 13,6 +/- 0,8 (mm Hg) and a significant reduction of systemic vascular resistance index (SVRI) from 2018 +/- 128 to 1641 +/- 102 (dynsec/cm5 m2). There were also observed statistically significant maximal increases of left ventricular stroke work index (LVSWI) from 41 +/- 3,1 to 53 +/- 3,2 (gm/m2) of oxygen delivery (DO2) from 489 +/- 24 to 587 +/- 29 (ml/min/m2) and of oxygen consumption (VO2) from 111 +/- 6 to 130 +/- 7 (ml/min/m2) which took place at the time of the maximum CI-increase. Moreover MAP-, CI- and VO2-responses of patients were stratified according to clinical conditions like time of operation, age, prognosis, ARDS, sepsis, hyperdynamic- and blood volume status.
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PMID:[Reactions of critically ill patients to volume therapy with hydroxyethyl starch (6% HES 450/0.7)]. 242 57

The hemodynamic responses of atrial (AP), atrioventricular sequential (AVP) and ventricular pacing (VP) were compared to sinus rhythm (SR) in seventeen anesthetized dogs with intact AV conduction. The atrium and/or ventricle were paced at fixed rates above the control sinus rate. An AV interval shorter than normal conduction was selected to capture the ventricle. The changes of pulmonary capillary wedge pressure (PCWP, mmHg), mean aortic pressure (MAP, mmHg), cardiac output (CO, L/min), systemic vascular resistance (SVR, dynes/s/cm-5), left ventricular stroke work index (SWI) and mean systolic ejection rate (MSER, ml/s) during sinus rhythm, atrial pacing and atrioventricular sequential pacing (expressed in percentages of the individual values during ventricular pacing) were: (Chart: See text) The importance of atrial systole for cardiac performance was clearly demonstrated in dogs with normally compliant hearts. In both atrial and atrioventricular sequential pacing compared to ventricular pacing there was a reduction of pulmonary capillary wedge pressure (PCWP) (p less than 0.01) and systemic vascular resistance (SVR) (p less than 0.01) despite an increase in cardiac output (CO). The lesser mean systolic ejection rate (MSER) found during atrioventricular sequential pacing compared to sinus rhythm and atrial pacing may be explained by the abnormal ventricular depolarization in this pacing mode; nevertheless, the mean systolic ejection rate was still greater than that found during ventricular pacing (p less than 0.05).
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PMID:Hemodynamic findings during sinus rhythm, atrial and AV sequential pacing compared to ventricular pacing in a dog model. 243 56

The pharmacodynamics of felodipine were analyzed in patients with congestive heart failure in a randomized, double-blind, placebo-controlled study. Felodipine at a dose of 1 mg (n = 11) or placebo (n = 12) was given intravenously during a 60-min period. Hemodynamic measurements and plasma samples were obtained every 15 min during a 2-hour period. An increase in heart rate (HR, +8%, p less than 0.01) and cardiac output (CO, +36%, p less than 0.001), and a decrease in mean arterial pressure (MAP, -24%, p less than 0.001) and systemic vascular resistance (SVR, -46%, p less than 0.001), were found. Pulmonary artery, right atrial, wedge pressure, and stroke-work index did not change. Linear regression analysis showed a significant correlation between felodipine plasma levels and changes in HR (r = 0.71, p less than 0.05), MAP (r = 0.94, p less than 0.01), CO (r = 0.73, p less than 0.05), and SVR (r = 0.88, p less than 0.01). A strong hyperbolic correlation was demonstrated between individual plasma levels and changes in MAP (r = 0.97, p less than 0.001). Hysteresis analysis showed that plasma levels are directly related to the concentration at the receptor site. A clockwise hysteresis was found in HR, CO, and SVR, but not in MAP. It is concluded that changes in flow and resistance are based on a physiological adjustment, a baroreflex-mediated response to vasodilation induced by felodipine, resulting in MAPs that remain closely related to felodipine plasma levels over a wide range.
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PMID:Plasma concentration-effect relationship of felodipine intravenously in patients with congestive heart failure. 247 24

The effects of a moderate dose of sufentanil (1 microgram.kg-1 + 0.015 micrograms.kg-1.min-1) plus nitrous oxide (30% O2/70% N2O) anesthesia (group I; n = 8) and of high-dose sufentanil/O2 anesthesia (10 micrograms.kg-1 + 0.15 micrograms.kg-1.min-1) without N2O (group II; n = 8) on cardiovascular dynamics, myocardial blood flow, myocardial oxygen consumption, myocardial lactate balance, and hypoxanthine release were studied in two groups of male patients scheduled for elective coronary artery bypass surgery. All patients were on maintenance doses of calcium channel blockers and nitrates with the last doses of medications given the morning of operation. All patients were premedicated with flunitrazepam (2 mg orally), piritramide (7.5 mg IM) and promethazine (25 mg IM). Measurements were performed before the induction of anesthesia with the patients premedicated but awake; 20 min after induction of anesthesia with sufentanil plus pancuronium 0.1 mg.kg-1 for muscle relaxation before surgery; and during sternotomy and sternal spread. Sufentanil at either dose decreased mean arterial pressure, as well as cardiac and stroke volume index while heart rate remained unchanged. Following the induction myocardial blood flow and myocardial oxygen consumption decreased 23% (79 ml.min-1.100 g-1 to 61 ml.min-1.100 g-1 and 28% (9.2 ml O2.min-1.100 g-1 to 6.6 ml O2.min-1.100 g-1) in group I and 14% (78 ml.min-1.100 g-1 to 67 ml.min-1.100 g-1 and 18% (8.7 ml O2.min-1.100 g-1 to 7.1 ml O2.min-1.100 g-1) in group II. Myocardial ischemia was seen in one patient of group II (patient No. 4), as indicated by a hypoxanthine release into the coronary sinus, when after the induction MAP decreased from 93 to 67 mm Hg and heart rate increased from 56 to 71 min-1. During sternotomy 8 of 16 patients (50%) developed hypertension and 9 of 16 patients (56%) showed signs of myocardial ischemia, i.e., a lactate and hypoxanthine release.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Sufentanil does not block sympathetic responses to surgical stimuli in patients having coronary artery revascularization surgery. 252 78

The hemodynamic effects of ketamine, 1.5 mg/kg, or sufentanil, 3.4 +/- 0.3 micrograms/kg, were studied prospectively for the anesthetic induction of 20 patients with cardiomyopathies undergoing cardiac transplantation. Plasma epinephrine (EPI), norepinephrine (NE), and sufentanil levels were also obtained. Measurements were taken at various times before induction and following intubation. Following ketamine, progressive increases (P less than 0.05) in mean arterial pressure (28%, MAP), mean pulmonary artery pressure (56%, PAP), central venous pressure (109%, CVP), and pulmonary capillary wedge pressure (84%, PCWP) occurred over time, whereas the cardiac index (CI), stroke volume index (SVI), and stroke work index (SWI) remained unchanged or decreased. The use of sufentanil was associated with no significant changes in MAP, PAP, CVP, PCWP, CI, SVI, or SWI. The heart rate (HR) did not significantly change in either group. Plasma NE significantly increased (31%) in the ketamine group, peaking at 10 minutes; whereas EPI levels did not significantly change in either group. Plasma sufentanil did not reflect the microgram/kg or microgram/BSA administered dose, suggesting individualized distribution kinetics. Since perioperative morbidity and mortality did not differ between groups, both ketamine and sufentanil are acceptable drugs for the anesthetic induction for cardiac transplantation. However, the dissimilar hemodynamic effects caused by ketamine and sufentanil suggest that this conclusion may not be applicable to the patient with a cardiomyopathy undergoing noncardiac surgery.
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PMID:Cardiac transplantation: a prospective comparison of ketamine and sufentanil for anesthetic induction. 253 97

Cerebral autoregulation is impaired in ischaemic regions. We hypothesized that pre-existing STA-MCA bypass would be superior to delayed revascularization in maintaining ipsilateral rCBF and preserving cerebral autoregulation following experimental stroke. Two series of dogs were tested to evaluate this hypothesis, but which was disproved for the chosen experimental conditions. In the first, eight dogs underwent craniotomy, STA-MCA bypass, and radiolabeled microsphere rCBF determinations. Blood pressure was manipulated with intravenous adenosine and levarterenol. Ischaemic zone rCBF was measured at MAP 60 mm Hg (97.2 ml.min-1.100 g-1) and MAP 140 mm Hg (113.6) (p = NS), in the intact arterial system with the patent bypass in place. An hemispheric ipsilateral ischaemic lesion was then created, and three further microsphere rCBF determinations were made at MAP 60 mm Hg (41.7 ml.min-1.100 g-1), MAP 100 mm Hg (52.6) and MAP 140 mm Hg (58.3). There were no significant differences between these measurements (ANOVA p = NS). In a second series of five animals the bypass was placed and the stroke lesion created first. Ischaemic zone rCBF was then measured at MAP 60 mm Hg (35 ml.min-1 . 100 g-1) and MAP 140 mm Hg (44 ml.min-1 . 100g-1) (p = NS), with the patent bypass in place. The bypass was then clamped for 15 minutes and profound ischaemia confirmed (5 ml.min-1 . 100 g-1, p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cerebral autoregulation following prophylactic and delayed experimental STA-MCA bypass. 260 72

In rats with incomplete cerebral ischemia the effects of 70% N2O alone, isoflurane alone (0.5 and 1 MAC), and the combination of N2O + isoflurane on neurologic outcome, neurohistopathology, and EEG were compared. Moderate and severe ischemia were produced by right carotid artery occlusion combined with hemorrhagic hypotension (moderate ischemia, MAP = 30 mmHg, FIO2 = 0.30; severe ischemia, MAP = 25 mmHg, FIO2 = 0.20). Neurologic outcome was evaluated using a graded deficit score from 0 to 5 (0 = normal, 5 = death associated with stroke), and neurohistopathology was evaluated using a 40-point scale from 0 = normal to 40 = total hemisphere infarct at the level of the caudate nucleus in coronal section. Compared with N2O alone, isoflurane (0.5 and 1 MAC) improved neurologic outcome following moderate ischemia (P less than 0.05). Isoflurane also decreased histopathologic damage following moderate ischemia (N2O control = 33 +/- 1 vs. 0.5 MAC isoflurane = 11 +/- 4 and 1 MAC isoflurane = 12 +/- 3, P less than 0.05), whereas only 0.5 MAC isoflurane decreased histopathologic damage following severe ischemia (N2O control = 38 +/- 1 vs. 0.5 MAC isoflurane = 25 +/- 5; P less than 0.05) Adding N2O to 0.5 MAC isoflurane attenuated the neurologic protective effect of isoflurane alone and increased histopathologic damage following both moderate and severe ischemia (moderate = 23 +/- 5, severe = 37 +/- 2; both P greater than 0.05 compared with N2O controls). The effect of adding 70% N2O to isoflurane on cerebral blood flow (CBF) and cerebral oxygen consumption(CMRO2) was also evaluated.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The interaction of nitrous oxide and isoflurane with incomplete cerebral ischemia in the rat. 271 9


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