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

Lateral (L) cilia of freshwater mussel (Margaritana margaritifera and Elliptio complanatus) gills can be arrested in one of two unique positions. When treated with 12.5 mM CaCl2 and 10(-5) M A23187 they arrest in a "hands up" position, ie, pointing frontally. When treated with approximately 10 mM vanadate (V) they arrest in a "hands down" position, ie, pointing abfrontally. L-cilia treated with 12.5 mM CaCl2 and 1 mM NaN3 also arrest in a "hands down" position; substitution of 20 mM KCl and 1 mM NaN3 causes cilia to move rapidly and simultaneously to a "hands up" position. The observations suggest that there are two switching mechanisms for activation of active sliding in ciliary beat one at the end of the recovery stroke and the other at the end of the effective stroke; the first is inhibited by calcium and the second by vanadate or azide. This is consistent with a model of ciliary beating where microtubule doublet numbers 1, 2, 3, and 4 are active during the effective stroke while microtubule doublets numbers 6, 7, 8, and 9 are passive, and the converse occurs during the recovery stroke.
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PMID:Effect of vanadate on gill cilia: switching mechanism in ciliary beat. 12 Sep 5

Of 410 consecutive patients undergoing cardiopulmonary bypass, 13 (3.2%) required pressor and inotropic support beyond volume replacement with whole blood and administration of CaCl2 to discontinue bypass. In 4 patients, isoproterenol was ineffective in maintaining cardiac output and systemic arterial pressure. In 12 patients addition and/or substitution of dopamine permitted discontinuation of cardiopulmonary bypass. In 7 patients who had serial hemodynamic measurements, mean systemic arterial pressure increased by 26%; cardiac index increased by 36%; stroke volume increased by 31%; and stroke work index increased by 83% (all p less than 0.005). There were no significant changes in central venous and mean pulmonary arterial wedge pressures, heart rate, or pulmonary and peripheral vascular resistances. Eleven of the 13 patients survived. We conclude that dopamine is an effective pressor and inotropic agent in the management of left ventricular dysfunction immediately after cardiopulmonary bypass.
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PMID:Favorable influence of dopamine on left ventricular performance in patients refractory to discontinuation of cardiopulmonary bypass. 92 19

To determine whether ephedrine or CaCl2 improves hemodynamics in cardiac surgery patients emerging from cardiopulmonary bypass, three sequential doses of either CaCl2 (200 mg/dose; n = 12), ephedrine (5 mg/dose; n = 12), or placebo (n = 12) were administered in a prospective, randomized, double-blind fashion. Thermodilution volumetric catheters were used to calculate right ventricular (RV) volumes and ejection fraction. The first dose of ephedrine improved RV stroke volume from 57 +/- 3 to 63 +/- 4 mL/beat (P < 0.05) and ejection fraction from 44 +/- 2% to 49 +/- 2% (P < 0.05). Subsequent doses maintained this improvement but without further change. In contrast, placebo and CaCl2 had minimal effects on RV end-systolic volume, stroke volume, and ejection fraction. After the third injection of ephedrine, mean arterial pressure had significantly increased from 78 +/- 2 to 93 +/- 4 mmHg (P < 0.05) in contrast to insignificant increments with placebo and CaCl2. Serum ionized calcium increased by 6% to 8% after each CaCl2 bolus but remained stable in the ephedrine and placebo groups. CaCl2 failed to improve RV performance in mildly hypocalcemic patients during separation from cardiopulmonary bypass. In patients with normal preoperative ventricular function, ephedrine more effectively improved RV performance and arterial blood pressure than placebo or CaCl2, and is a suitable short-acting drug to assist separation from cardiopulmonary bypass.
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PMID:Is calcium or ephedrine superior to placebo for emergence from cardiopulmonary bypass? 142 Oct 63

To assess the hemodynamic interactions when combining verapamil, acute changes in extracellular ionized calcium concentration [Ca2+] and enflurane (2.5%), halothane (1.2%) or isoflurane (1.6%), seven dogs were chronically instrumented to measure heart rate (HR), aortic, left atrial and left ventricular (LV) pressures, and cardiac output (CO). [Ca2+] was lowered 0.35 mmol.l-1 by citrate infusion and then increased 0.35 mmol.l-1 above control level by CaCl2 infusions. Verapamil was infused at 3 micrograms.kg-1 x min-1 (loading dose 200 (awake), 150 (isoflurane) or 100 (enflurane and halothane) micrograms.kg-1), giving mean verapamil concentrations around 75 (range of means: 66-84 ng.ml-1). Verapamil produced mostly minor changes in the cardiovascular effects of changing [Ca2+] in both awake and anesthetized dogs, indicating mostly additive effects. Verapamil induced a decrease in HR at high [Ca2+] and abolished an increase in mean aortic pressure at both low and high [Ca2+] awake. Verapamil exaggerated the decrease in CO and stroke volume (SV) induced by low [Ca2+] during enflurane anesthesia and abolished the increase in CO induced by low [Ca2+] and exaggerated the increase in SV and LV dP/dtmax induced by high [Ca2+] during halothane anesthesia.
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PMID:Hemodynamic interactions when combining verapamil, acute changes in extracellular ionized calcium concentration and enflurane, halothane or isoflurane in chronically instrumented dogs. 146 19

Binding of iodine-125-labeled thrombin to fibrin clots from two siblings with juvenile stroke was 30% of normal, and abnormally high amounts of the radioligand (not adsorbed by fibrin) were found in the supernatant. In concordance with this finding, supernatants from the patients' fibrin clots caused abnormal enhancement of platelet aggregation, ATP secretion, and binding of 125I-fibrinogen to platelets exposed to subthreshold concentrations of ADP or epinephrine. Hirudin suppressed the enhancing effect of the patients' supernatants, and substitution of gamma-thrombin for alpha-thrombin led to normalization of platelet responses. Under some experimental conditions, degradation of the patients' fibrinogen by plasmin was impaired. However, the euglobulin lysis time, the rate of fibrin degradation by plasmin, and the lysis of the patients' plasma clots by human melanoma tissue-type plasminogen activator were normal. Patients' plasmas, as well as purified fibrinogen, showed a prolonged thrombin time (partially corrected by 10 mM CaCl2) and an impaired release of fibrinopeptide A in response to thrombin. However, the release in response to reptilase was normal, and the reptilase, ancrod, and thrombin coagulase times were within control (normal) values. In addition, the patients' fibrinogen showed normal polymerization of preformed fibrin monomers, normal sialic acid content, and normal binding to ADP or epinephrine-stimulated platelets. Our studies support the concept that thrombin and platelets play an important role in the occurrence of stroke in these patients and suggest a direction to be followed to identify the mechanism(s) contributing to thrombosis in subjects with abnormal fibrinopeptide release.
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PMID:A role for platelets and thrombin in the juvenile stroke of two siblings with defective thrombin-adsorbing capacity of fibrin(ogen). 182 31

Calcium antagonists have a protective effect on postischemic myocardial function when included in normothermic cardioplegia solutions. This effect varies with the calcium antagonist, but is generally lost under hypothermic conditions. The hypothesis tested was that a calcium antagonist would increase postischemic myocardial performance if given before the onset of hypothermic arrest. Isolated working rat hearts were used with an oxygenated modified Krebs-Henseleit buffer solution as a perfusion media. Rats were pretreated with 1 of 9 doses of a nicardipine solution (0 to 100 micrograms/kg, intraperitoneally) 20 minutes before excision of the heart. Nicardipine is a light-stable, water-soluble calcium antagonist with minimal myocardial depressant effects. The hearts were arrested for 25 minutes at 37 degrees C or 93 minutes at 24 degrees C with 20 mL of cardioplegia solution containing 0.05 mmol/L CaCl2. Postischemic performance and adenosine triphosphate content were used as determinants of efficacy. Eighty-three percent of 101 treated hearts recovered in contrast to a mortality of 50% in the 24 nontreated hearts. Pretreatment with 25 micrograms/kg significantly increased (p less than 0.05) the percent recovery (compared with the nontreated group) of the following variables of cardiac function: systolic pressure, 74% to 96% (37 degrees C), 76% to 90% (24 degrees C); cardiac output, 61% to 90% (37 degrees C), 62% to 84% (24 degrees C); stroke work, 49% to 95% (37 degrees C), 50% to 92% (24 degrees C); and adenosine triphosphate, 76% to 87% (37 degrees C), 58% to 68% (24 degrees C). Progressive increases in postischemic function at 37 degrees and 24 degrees C were seen as the dose of nicardipine was increased from 0 to 25 micrograms/kg and decreased function was seen with a pretreatment dose greater than 25 micrograms/kg of nicardipine. Pretreatment with nicardipine significantly improved postischemic myocardial performance under hypothermic conditions and should be administered or at least not discontinued before cardiac operations.
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PMID:Pretreatment with nicardipine preserves ventricular function after hypothermic ischemic arrest. 202 76

To study the cardiovascular effects of low blood ionized calcium ion concentrations [Ca2+] induced by citrate infusion followed by high [Ca2+], induced by CaCl2 infusion awake and during enflurane (2.5% ET), halothane (1.2% ET), and isoflurane (1.6% ET) anesthesia, dogs were chronically instrumented to measure heart rate, aortic, left atrial, and left ventricular (LV) blood pressures, and cardiac output. In conscious dogs low [Ca2+] (decreased 0.35 mM); increased heart rate (HR) and mean aortic pressure (MAP) and decreased stroke volume (SV) and LV dP/dtmax. Low [Ca2+] increased HR during all three anesthetics and decreased LV dP/dtmax except during isoflurane anesthesia. Low [Ca2+] produced more hemodynamic depression during enflurane anesthesia than during anesthesia with halothane or isoflurane increasing left atrial pressure and decreasing MAP and SV. The differences seen were partially related to decreased systemic vascular resistance during halothane and isoflurane anesthesia. In conscious dogs following high [Ca2+] (increased 0.37 mM); only MAP and LV dP/dtmax increased. LVdP/dtmax was also increased by high [Ca2+] during all three anesthetics without a change in MAP. Cardiac output increased during halothane and isoflurane anesthesia but was unchanged during enflurane. It would appear that the hemodynamic sensitivity for the effects of changing [Ca2+] was enflurane greater than halothane greater than isoflurane greater than awake. The results suggest that the effects of changes in [Ca2+] induced by citrate and CaCl2 infusion are modified by the three volatile anesthetics.
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PMID:Cardiovascular effects of acute changes in extracellular ionized calcium concentration induced by citrate and CaCl2 infusions in chronically instrumented dogs, conscious and during enflurane, halothane, and isoflurane anesthesia. 229 13

Both Mg2+ and Ca2+ have been implicated as having roles in the pathomechanisms of cerebral ischemia. To further study the effects of these ions on postischemic histologic outcome, fasted rats were given one of three intravenous infusions: 5.0 mmol/kg MgCl2, 5.0 mmol/kg MgCl2 + 0.035 units/kg regular insulin, or 1.0 mmol/kg CaCl2. This resulted in elevated plasma Mg2+ or Ca2+ concentrations in the corresponding groups. A fourth group received 0.9% NaCl (saline). Preinfusion plasma glucose concentration was similar for all groups and was unchanged after infusion in rats receiving either saline or MgCl2 + insulin. In contrast, postinfusion glucose concentration was increased in the MgCl2 group (p less than 0.001) and decreased in the CaCl2 group (p less than 0.001) relative to saline-treated rats. Following respective infusions, all rats underwent 10 minutes of reversible forebrain ischemia (bilateral carotid artery occlusion and systemic hypotension) followed by 7 days' recovery. Six of 12 CaCl2-treated rats died 2-3 days after ischemia; all other rats remained neurologically indistinguishable, without gross neurologic deficits. Histologic injury in the neocortex and caudate was moderate in all groups. In the hippocampus, MgCl2 + insulin resulted in 66 +/- 6% (mean +/- SD) dead CA1 pyramidal cells, which was similar to the amount in saline-treated rats (68 +/- 10%). Injury was increased in the MgCl2 group (79 +/- 4% dead cells), while in surviving CaCl2-treated rats, injury was decreased (54 +/- 13%). We conclude that the increased injury in MgCl2-treated rats and the decreased injury noted in surviving rats receiving CaCl2 are due to the plasma glucose concentrations present prior to ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)
Stroke 1989 Apr
PMID:Effects of elevated plasma magnesium versus calcium on cerebral ischemic injury in rats. 264 53

The side effects associated with recombinant interleukin 2 administration, including systemic hypotension and a vascular leak syndrome, may limit therapy before reaching maximum doses of this innovative and promising treatment for cancer. In an attempt to reverse this hypotension without decreasing cardiac output and systemic oxygen delivery (DO2), we studied several inotropic agents, dobutamine, dopamine, amrinone, CaCl2, and a pure alpha-adrenergic vasoconstrictor, methoxamine. These were administered singly or in combination to sheep with chronically implanted arterial and pulmonary artery catheters following 24 h of 3 x 10(5) units/kg recombinant interleukin 2. Compared to baseline values, 24 h of recombinant interleukin 2 infusion caused a significant increase in cardiac output from 4.4 +/- 0.9 (SD) to 5.0 +/- 0.6 liters/min, a significant fall in systemic vascular resistance (SVR) from 21 +/- 7 to 15 +/- 5 units, a decrease in mean systemic blood pressure (SBP) from 88 +/- 9 to 78 +/- 6 mm Hg, and a decrease in left ventricular stroke work from 51.5 +/- 8 to 49 +/- 6 gram meters (P less than 0.05) without any change in DO2. Dopamine, dobutamine, and CaCl2 returned SBP to baseline values by increasing cardiac output without increasing SVR. Methoxamine increased SBP by increasing SVR, but cardiac output decreased significantly. A combination of 12 micrograms/kg/min of dopamine and 2 to 3 mg of methoxamine infused over 15 min resulted in an increase in SBP, cardiac output, and SVR to baseline values while maintaining DO2 and oxygen consumption (VO2). We suggest that this latter combination would be appropriate for clinical use since it returns physiological parameters to normal.
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PMID:Inotropic and vasoactive drug treatment of interleukin 2 induced hypotension in sheep. 278 5

The protective effects of a perfluorocarbon emulsion (FC-43) against the physiological sequelae of selective coronary air embolism (CAE) were examined in dogs. Animals were randomly assigned to two groups: group 1 received 20 mL/kg of 6% hetastarch in 0.9 normal saline solution with 280 mg/L of CaCl2; group 2 received 20 mL/kg of FC-43 (Oxypherol, Alpha Therapeutic Corp, Los Angeles). Infusion time for both groups was 30 minutes. Following a ten-minute stabilization period, a 0.02-mL/kg bolus of air was injected into the left anterior descending coronary artery distal to the first branch. Surface and epicardial ECGs, systemic BP, pulmonary artery pressure, central venous pressure, left ventricular pressure, left ventricular end-diastolic pressure (LVEDP), dP/dtmax, and Vmax were recorded continuously. Cardiac output (by thermodilution technique), myocardial creatine phosphokinase levels and the lactic acid concentration were measured. The study revealed a significantly lower systemic mean arterial pressure (MAP), LVEDP, left ventricular stroke work index (LVSWI), and right ventricular stroke work index (RVSWI) in the group receiving the FC-43 prior to receiving CAE. Possible causes of the differences are a species-specific direct vasodilating effect of FC-43 or histamine release. Following CAE, myocardial function as measured by dP/dtmax, Vmax, and MAP was lower in group 1 during the first five minutes following CAE. ECG tracings showed all of the ten group 1 dogs had ST-T changes (greater than 2 mm), and six of the ten had ventricular dysrhythmias or conduction defects. Only one of the group 2 dogs showed ST-T wave changes (P = .0006, Fisher's exact test), and none had dysrhythmias (P = .005, Fisher's exact test).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Protection from coronary air embolism by a perfluorocarbon emulsion (FC-43). 297 96


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