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

The purpose of this study was to determine the role of the autonomic nervous system's control of the heart in fitness-related differences in blood pressure regulation. The cardiovascular responses to progressive lower-body negative pressure (LBNP) were studied during unblocked (control) and full blockade (experimental) conditions in 10 endurance-trained (T) and 10 untrained (UT) men, aged 20-31 yr. The experimental conditions included beta 1-adrenergic blockade (metoprolol tartrate), parasympathetic blockade (atropine sulfate), or complete blockade (metoprolol and atropine). Heart rate, blood pressure, forearm blood flow, and cardiac output were measured at rest and -16 and -40 Torr LBNP. Forearm vascular resistance, peripheral vascular resistance, and stroke volume were calculated from these measurements at each stage of LBNP. Blood pressure was maintained, primarily by augmented vasoconstriction, equally in T and UT subjects during complete and atropine blockade. The fall in systolic and mean pressure from 0 to -40 Torr was greater (P less than 0.05) in the T subjects during the unblocked and metoprolol blockade conditions. This reduced blood pressure control during unblocked condition was attributable to attenuated vaso-constrictor and chronotropic responses in the T subjects. We hypothesize that an autonomic imbalance (elevated base-line parasympathetic activity) in highly trained subjects restricts reflex cardiac responses, which accompanied by an attenuated vasoconstrictor response, results in attenuated blood pressure control during a steady-state hypotensive stress.
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PMID:Blood pressure regulation during cardiac autonomic blockade: effect of fitness. 284 97

In rats with chronically implanted intrathecal catheters, high concentrations of morphine (3 microliters of 50 mg/ml: 150 micrograms) yielded a reliable and striking syndrome of pain behavior that involved intermittent bouts of biting and scratching at the dermatomes innervated by levels of the spinal cord proximal to the catheter tip. In addition, during intervals between bouts of agitation, the animals displayed a clear, marked hyperesthesia where an otherwise innocuous stimuli (brush stroke) evoked significant signs of discomfort and consequent aggressive behavior. These effects were exaggerated rather than reversed by high doses of naltrexone. The effect, perfectly mimicked by a considerably lower dose of morphine-3-glucuronide (15 micrograms) or the glycine antagonist strychnine (30 micrograms), was not produced by equimolar concentrations of sodium sulfate, glucuronide, methadone, or sufentanil. In halothane-anesthetized cats, light brushing of the hindpaw and tail or low-intensity stimulation of the sciatic nerves resulted in prominent elevations in blood pressure and pupil diameter following the intrathecal administration of high concentrations (50 mg/ml; 0.1 ml) of morphine sulfate. This effect, exaggerated by naloxone, was produced by a lower concentration of intrathecal morphine-3-glucuronide (5 mg/ml; 0.1 ml) but not by intrathecal saline. These results suggest the possibility that the effects of high doses of morphine may be characterized by a nonopiate receptor-mediated effect that alters the coding of sensory information in the spinal cord. The authors speculate that high concentrations of spinal opiates, as may be employed in tolerant terminal-cancer patients, could exert an action that physiologically antagonizes the analgesic effects otherwise mediated by the action of morphine on the spinal opiate receptor.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:High dose of spinal morphine produce a nonopiate receptor-mediated hyperesthesia: clinical and theoretic implications. 293 24

The hemodynamic and renal excretory responses to 150-min atriopeptin II (AP II) infusion (330 ng X kg-1 X min-1) were assessed in five chronically instrumented rats with (FR protocol) and without (NR protocol) replaced urinary fluid losses. The observed changes were compared with those obtained by vehicle in the same rats. The hypotension seen with AP II infusion (120-min value: -27 +/- 2%, FR and NR responses combined) was due solely to a decreased cardiac output (CO; 120-min combined value: -34 +/- 3%). Total peripheral resistance remained unchanged or slightly elevated. A drop in stroke volume plus a later-developing (by 75-90 min) decrease in heart rate contributed to the CO decline. This latter bradycardic component, the opposite response to that typically produced reflexly by hypotension, was reversed by atropine sulfate treatment at 120 min and may thus be neural in origin. The finding of similar hemodynamic changes in the FR and NR rats and the lack of a significant effect of AP II on hematocrit suggest that volume depletion or a plasma extravasation were not contributors to the cardioinhibitory effect of the peptide.
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PMID:Cardioinhibitory effect of atrial peptide in conscious rats. 295 Jul 78

The canine gastric response to acute dilatation, its correlation with selected systemic cardiovascular changes, and preliminary study of its modulation by membrane-stabilizing agents were studied in 21 Beagle dogs. Gastric mucosal damage and adverse cardiovascular sequelae were induced by inflation of an intragastric balloon to 60 mm of Hg in each anesthetized dog for 2.5 hours. At this time, dogs were given 1 of 4 treatments: control; lidocaine HCl, 2.2 mg bolus + 66 micrograms/min, IV; prednisolone succinate, 6.6 mg, IV; and zinc sulfate, 2.2 mg bolus + 66 micrograms/min, IV. After treatments were given, there was a 4-hour deflation period. Throughout the 6.5 hours, continuous measurements were made of stroke volume, arterial blood pressure, PaO2, PaCO2, and plasma HCO3- concentration. Gastric lesions, assessed by planimetric analysis of ulcer indices, were limited to the fundus and corpus and were significantly decreased by lidocaine administration. As seen by histopathologic examination, a sharply delineated transverse area bordering the corporeal-antral junction near the lesser curvature demonstrated minimal resistance to ulceration and showed mucus depletion. Plasma HCO3- concentration, base excess, and CO2 values were negatively correlated with development of gastric damage, indicating that plasma HCO3- concentration has a key role in mucosal resistance to ulcerogenesis.
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PMID:Topographic localization of gastric lesions and key role of plasma bicarbonate concentration in dogs with experimentally induced gastric dilatation. 310 3

The purpose of our study was to investigate the effect of hypermagnesemia on spinal metabolic rate. The 2-[14C]deoxyglucose technique was used to measure regional glucose utilization in the lumbar spinal cord of paralyzed, mechanically ventilated rats receiving 70% nitrous oxide and an intravenous infusion of either saline (n = 5) or magnesium sulfate (n = 5). Plasma magnesium concentrations were 6.75 +/- 0.5 and 0.9 +/- 0.5 mM (p less than 0.01) in hypermagnesemic and control rats, respectively. Hypermagnesemic rats were hypotensive (88 +/- 1 vs. 130 +/- 4 mm Hg, p less than 0.01) but blood pressure remained within the autoregulatory range. Glucose utilization was reduced 26-45% in spinal gray matter and 53-63% in spinal white matter during hypermagnesemia. We conclude that magnesium is a potent spinal metabolic depressant and that this action, which is unusually prominent in spinal white matter, is a plausible explanation for the recently reported beneficial effect of magnesium therapy during spinal cord ischemia.
Stroke 1988 Jun
PMID:Effect of profound hypermagnesemia on spinal cord glucose utilization in rats. 337 67

We evaluated the hypothesis that increased endogenous opioid activity mediates part or all of the left ventricular contractile and pump dysfunction previously demonstrated in HCl-induced metabolic acidemia. Eighteen Western newborn lambs were catheterized and instrumented; pacing wires were sutured to the right atrial appendage; a catheter mounted micromanometer pressure transducer was inserted into the left ventricle; and a 2.5 F thermistor was inserted into the distal abdominal aorta. The lambs were studied 3 days after surgery. Metabolic acidemia was produced with an infusion of 0.5 N HCl into the inferior vena cava. Inhibition of endogenous opioids was achieved with a bolus of 2 mg/kg of intravenous naloxone, which was demonstrated to inhibit morphine sulfate-induced myocardial dysfunction. The effects of opioid inhibition were contrasted with our previously published results after restoration of a normal arterial pH with intravenous sodium bicarbonate. In agreement with our previous study, we found that reducing the arterial pH from 7.41 +/- 0.01 to 6.97 +/- 0.04 was associated with a 45% reduction in cardiac output which resulted from a 50% reduction in stroke volume. These changes in turn were mediated by a 35% reduction in the maximal first derivative of left ventricular pressure and/or a 63% increase in systemic vascular resistance which we used to estimate contractility and afterload, respectively. Left ventricular end diastolic pressure increased during acidemia. Although opioid inhibition produced a consistent increase in the maximal first derivative of left ventricular pressure, this increase was relatively small and was not associated with a significant change in cardiac output, stroke volume, or systemic vascular resistance.
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PMID:Endogenous opioids do not mediate HCl-induced myocardial dysfunction. 339

The hemodynamic and respiratory effects of intravenous nalbuphine hydrochloride and morphine sulfate were compared in a randomized fashion in 20 patients (age 65 +/- 11 years) with acute myocardial infarction and elevated pulmonary artery wedge pressure. Titration of the nalbuphine dose to lower pulmonary artery wedge pressure by greater than or equal to 25% resulted in a decrease of this parameter from 22 +/- 3 to 15 +/- 4 mm Hg, and was associated with a reduction in heart rate from 106 +/- 20 to 96 +/- 19 beats/min (p less than 0.05) and decreases in mean blood pressure (78 +/- 8 to 70 +/- 12 mm Hg, p less than 0.05) and mean pulmonary artery pressure (31 +/- 4 to 22 +/- 5 mm Hg, p less than 0.05), without any remarkable change seen in cardiac index (2.21 +/- 0.43 to 2.22 +/- 0.50 liter/min/m2, difference not significant), stroke volume index (22 +/- 7 to 23 +/- 4 ml/m2, difference not significant), stroke work index (17 +/- 7 to 18 +/- 7 g.m/m2), or systemic and pulmonary vascular resistances (1,675 +/- 333 to 1,513 +/- 508 and 191 +/- 78 to 170 +/- 109 dynes.s.cm-5 respectively, all differences not significant). Nalbuphine also significantly reduced respiratory rate (32 +/- 8 to 26 +/- 8 resp/min, p less than 0.05) and pH (7.45 +/- 0.04 to 7.41 +/- 0.03, p less than 0.05) and increased arterial PCO2 (32 +/- 6 to 35 +/- 6 mm Hg, p less than 0.05) without any major change in arterial PO2 (63 +/- 13 to 66 +/- 17 mm Hg, difference not significant).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Comparison of nalbuphine hydrochloride versus morphine sulfate for acute myocardial infarction with elevated pulmonary artery wedge pressure. 341 46

Controversy exists as to whether intraaortic (IA) administration of protamine sulfate has less adverse effects than the intravenous (IV) route. The effect of protamine on contractility is not well established. Therefore, 9 dogs underwent chronic instrumentation to monitor aortic pressure (AP), left ventricular (LV) pressure, central venous pressure, cardiac index (CI), heart rate, stroke volume index (SVI), systemic vascular resistance index, and LV volume. The end-systolic LV pressure-volume relationship was used as a load-independent measure of contractility. Each dog was administered IV and IA protamine on separate occasions after pretreatment with heparin. Studies were performed with and without anesthesia. In the awake studies, analysis of variance showed greater decreases in mean AP (p less than .03), CI (p less than .05), and SVI (p less than .02) with IA protamine infusion. In the anesthetized animals, there were no significant differences between IA and IV administration of protamine. Protamine did not decrease contractility in any group. We conclude that IA administration of protamine offers no advantage over IV administration in the dog. Protamine does not decrease contractility when given by either route.
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PMID:Comparison of the cardiovascular effects of intravenous and intraaortic protamine in the conscious and anesthetized dog. 372 12

The hemodynamic effects of lumbar epidural anesthesia (LEA) were evaluated in 11 patients with severe preeclampsia. All patients were receiving magnesium sulfate upon entry into the study. Hemodynamic measurements were obtained before and after LEA, at delivery, and 2 hr postpartum. Lumbar epidural anesthesia significantly reduced mean arterial pressure from 121.4 mm Hg to 97.7 mm Hg, without altering cardiac index, pulmonary vascular resistance, central venous pressure (CVP), or pulmonary capillary wedge pressure (PCWP). There was a slight but statistically insignificant decrease in systemic vascular resistance from 1078 to 900.7 dynes X sec X cm-5. Cardiac index and left ventricular stroke work index were elevated in these patients, suggesting hyperdynamic left ventricular function. There was poor correlation between PCWP and CVP in several patients. We conclude that LEA may be used safely in severe preeclamptic patients and that pulmonary arterial catheters may help guide appropriate therapy in preeclamptic patients with cardiac failure or oliguria refractory to modest fluid challenges.
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PMID:Severe preeclampsia: hemodynamic effects of lumbar epidural anesthesia. 394 Apr 67

Changes in haemodynamic, inotropic state, and myocardial oxygen consumption were investigated in a total of eight patients with coronary artery disease after intravenous injection of 0.07 mg/kg amezinium methyl sulfate (LU 1631, Supratonin). It was demonstrated, that the principal effects of amezinium are consistent with those of a sympathomimetic agent which stimulates vascular alpha- and beta 1-adrenoreceptors. Amezinium (0.07 mg/kg) increased cardiac index, mean arterial pressure and total systemic resistance and dp/dtmax, while there were only minor changes in stroke index, mean pulmonary pressure and total pulmonary vascular resistance. In accordance with the changes in haemodynamics there was a 21.5% increase in myocardial oxygen consumption. But there were no signs of imbalance between oxygen supply and oxygen demand.
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PMID:[Cardiocirculatory effects of a new sympathomimetic, amezinium methyl sulfate. Results of human pharmacological studies]. 398 3


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