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

Hemorrhagic shock was induced in 20 spontaneously breathing adult greyhounds by lowering the mean arterial pressure to 40 millimeters of mercury. In the first group of six dogs, reinfusion was carried out without delay; in a second group of six dogs, hypovolemia was continued for two hours, during which time the arterial pressure was permitted to rise in response to intact cardiovascular reflexes; in a third group of eight dogs, the mean arterial pressure was artificially maintained at 40 millimeters of mercury for two hours, initially by further bleeding. In all dogs in the latter group, take-up of blood from the reservoir was required during the second hour to maintain the arterial pressure, this being indicative of irreversible shock. In two of this group, fatal arrhythmias developed during reinfusion. All three groups showed evidence of ventricular dysfunction during and immediately after reinfusion, as indicated by disproportion between left ventricular stroke work and left ventricular end diastolic pressure, these data being used to construct ventricular function curves. Measurement of dP/dt maximum suggested that this dysfunction was due to impairment of myocardial contractility. The first two groups recovered normal function within one hour; the third group failed to have such a recovery. Evidence indicates that generalized tissue hypoxia, in addition to myocardial hypoxia, is important in the cause of cardiac dysfunction in irreversible shock.
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PMID:Ventricular function in experimental hemorrhagic shock. 23 1

Local application of prostacyclin (PGI2) to cerebral (pial) microvessels, inhibited the aggregation of platelets induced in the vessels by exposing them to a filtered mercury light source following intravenous sodium fluorescein. The inhibition was consistantly observed in venules rather than arterioles and was manifest by a lengthening of the time required for the noxious stimulus to produce an initial aggregate, and/or by a lengthening of the time required for enlarging aggregates to totally block the venule. The consistency of the inhibition diminished at doses below 100 microgram/ml. Inhibition was observed whether or not alcohol was used as the vehicle for PGI2 and whether or not the body temperature of the anesthetized mouse was permitted to fall.
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PMID:Topical prostacyclin (PGI2) inhibits platelet aggregation in pial venules of the mouse. 38 37

To determine the sequence of changes in segmental myocardial function, regional lactate metabolism and global left ventricular function induced by mild regional ischemia, blood flow in the left anterior descending coronary artery of 10 dogs was reduced by 10 percent decrements with use of a screw clamp. At each level of flow, segmental mechanical function and regional metabolism were assessed, the former with use of a mercury-in-Silastic length gauge and the latter with transmyocardial lactate balance measurements obtained with sampling from the anterior interventricular vein. Coronary arterial flow at the onset of regional lactate production was 48 +/- 4 percent (mean +/- standard error of the mean) of the control value. The onset of segmental mechanical dysfunction coincided with the onset of lactate production. Epicardial S-T segment abnormalities over the ischemic zone usually could not be detected until coronary flow was further reduced. After the onset of regional ischemia there was a linear correlation between coronary arterial flow and regional lactate production. At the onset of mild regional ischemia, defined as the onset of regional lactate production, no significant or directionally consistent changes were noted in standard measurements of global left ventricular performance, including heart rate, mean aortic pressure, left ventricular end-diastolic pressure, cardiac output, stroke volume, stroke work and peak positive dP/dt (maximal rate of rise of pressure). However, peak negative dP/dt (maximal rate of pressure decrease) decreased from 99 +/- 2 to 89 +/- 3 percent of the control value (P less than 0.0005) coincident with the onset of ischemia. It is hypothesized that dyssynchronous wall motion in the ischemic zone during isometric relaxation accounts for this decrease in peak negative dP/dt.
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PMID:Early changes in regional and global left ventricular function induced by graded reductions in regional coronary perfusion. 84 38

Acute myocardial infarction with shock (AMI/S) was produced in 46 anesthetized "closed-chest" dogs by catheter injection of metallic mercury into the circumflex coronary artery. Twenty-four dogs were kept normothermic and 22 were maintained at 32 degrees C. Nine of the latter were rewarmed to 37 degrees C. and the experiments then were terminated, so that true survival time was arbitrarily shortened. Including these dogs, the survival time was three times longer than in the normothermic series (p less than 0.001). Hypothermia reduced heart rate (HR) by 34 percent, oxygen consumption by 38 percent, and myocardial oxygen consumption by an estimated 30 to 40 percent, while cardiac output (CO), stroke volume, and stroke work were unchanged. Left ventricular end-diastolic pressure (LVEDP) was reduced by 40 percent during hypothermia (p less than 0.05) and increased by 60 percent on rewarming. HR during rewarming increased substantially more than CO and thereby significantly reduced stroke volume.
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PMID:Induced hypothermia in dogs with acute myocardial infarction and shock. 88 82

Platelet aggregation was produced in pial arterioles by exposing them to appropriately filtered light from a mercury lamp, following intravascular injection of sodium fluorescein. The dye acted as a target for the radiant energy and initiated a sequence of events resulting in the platelet aggregation. The aggregates adhered to the vessel in which they first appeared. When a microneedle punctured the brain adjacent to a subsequently irradiated arteriole, platelet aggregation was inhibited, even though the arteriole was not touched by the microneedle. Inhibition was manifested by prolongation of the exposure time required for the light-dye stimulus to initiate an adherent aggregate and by lengthening the time required for the aggregate to grow and totally block erythrocyte flow in the affected vessel. It is suggested that a material(s) diffuses from the zone of brain puncture, to and through the arteriolar wall, with a resultant inhibition of aggregation. It is noted that the inhibiting effect is reduced as the distance between puncture and wall increases.
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PMID:Effects of combined parenchymal and vascular injury on platelet aggregation in pial arterioles of living mice: evidence for release of aggregate-inhibiting materials. 92 58

The mechanism of elevation of left ventricular end-diastolic pressure during acute global ischemia was evaluated by examiniation of the relative contributions of a decrease in contractility and an alteration of the pressure-volume relationship. The external circumference (mercury-in-silastic gauge) pressure relationship, as an index of the pressure-volume relationship, was studied in beta adrenergic and ganglionic blocked, open chest dogs on right heart bypass at constant heart rate ane aortic pressure. Ischemia of one and two hours' duration was produced by reducing total coronary blood flow in cannulated left and right coronary arteries until left ventricular end-diastolic pressure rose significantly. At a constant stroke work, left ventricular end-diastolic pressure rose from 5.0 +/- 0.5 to 15.0 +/- 0.5 cm H2O in the experiments of one hour of ischemia, and from 7.0 +/- 1.0 to 17.0 +/- 1.0 cm H2O in experiments of two hours of ischemia. Ischemia was followed by one hour of restoration of coronary blood flow. Ischemia produced a marked depression of ventricular function: stroke work, considered at a left ventricular end-diastolic pressure of 15 cm H2O, decreased from 21.0 +/- 3.0 to 3.5 +/- 0.5 gm-m, and from 15.0 +/- 2.0 to 2.5 +/- 0.5 gm-m, in the experiments of one and two hours, respectively. Neither ischemia nor reflow changed the pressure-volume relationship. Thus, the elevation of left ventricular end-diastolic pressure during ischemia in an otherwise normal canine myocardium is due to a decrease in systolic performance of the heart rather than to an alteration of the pressure-volume relationship.
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PMID:Left ventricular end-diastolic pressure volume relationships with experimental acute global ischemia. 108 86

Most frequently encountered causes of intractable pain and intractable medical problems, including headache, post-herpetic neuralgia, tinnitus with hearing difficulty, brachial essential hypertension, cephalic hypertension and hypotension, arrhythmia, stroke, osteo-arthritis, Minamata disease, Alzheimer's disease and neuromuscular problems, such as Amyotrophic Lateral Sclerosis, and cancer are often found to be due to co-existence of 1) viral or bacterial infection, 2) localized microcirculatory disturbances, 3) localized deposits of heavy metals, such as lead or mercury, in affected areas of the body, 4) with or without additional harmful environmental electro-magnetic or electric fields from household electrical devices in close vicinity, which create microcirculatory disturbances and reduced acetylcholine. The main reason why medications known to be effective prove ineffective with intractable medical problems, the authors found, is that even effective medications often cannot reach these affected areas in sufficient therapeutic doses, even though the medications can reach the normal parts of the body and result in side effects when doses are excessive. These conditions are often difficult to treat or may be considered incurable in both Western and Oriental medicine. As solutions to these problems, the authors found some of the following methods can improve circulation and selectively enhance drug uptake: 1) Acupuncture, 2) Low pulse repetition rate electrical stimulation (1-2 pulses/second), 3) (+) Qi Gong energy, 4) Soft lasers using Ga-As diode laser or He-Ne gas laser, 5) Certain electro-magnetic fields or rapidly changing or moving electric or magnetic fields, 6) Heat or moxibustion, 7) Individually selected Calcium Channel Blockers, 8) Individually selected Oriental herb medicines known to reduce or eliminate circulatory disturbances. Each method has advantages and limitations and therefore the individually optimal method has to be selected. Applications of (+) Qi Gong energy stored paper or cloth every 4 hours, along with effective medications, were often found to be effective, as Qigongnized materials can often be used repeatedly, as long as they are not exposed to rapidly changing electric, magnetic or electro-magnetic fields. Application of (+) Qi Gong energy-stored paper or cloth, soft laser or changing electric field for 30-60 seconds on the area above the medulla oblongata, vertebral arteries or endocrine representation area at the tail of pancreas reduced or eliminated microcirculatory disturbances and enhanced drug uptake.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Common factors contributing to intractable pain and medical problems with insufficient drug uptake in areas to be treated, and their pathogenesis and treatment: Part I. Combined use of medication with acupuncture, (+) Qi gong energy-stored material, soft laser or electrical stimulation. 135 50

To determine if an isolated right ventricular wall infarct (RVI) alters right ventricular diastolic function (RVDF), 6 mongrel dogs were studied before and after a right ventricular wall infarct was produced by ligating the right coronary artery and embolizing the distal right coronary artery with mercury. Right ventricular diastolic function was assessed by prior instrumentation of the animals with an RV Millar catheter and segment length crystals attached to the infarct (I) and non-infarct (NI) territory of the right ventricle. The time constant of RV isovolumic relaxation (Tau) was assessed by fitting right ventricular pressure decline after minimum dp/dt to the equation 1nP = At + B, where A represents the slope of the relationship, a negative number, tau = -1/A. The right ventricular diastolic pressure segment length relationship (RVD PSR) was analyzed using a multiple linear regression model whereby the independent effects of heart rate, segment length, and right ventricular wall infarct could be assessed. Right ventricular wall infarct reduced stroke volume to 63% of baseline values largely by increases in RV-I end-systolic segment length. Tau was significantly prolonged. However, there was no significant upward shift in RVDPSR in any animal. These data suggest that in this model RV diastolic relaxation is impaired. However, the degree of this impairment is not significant enough to shift the right ventricular diastolic pressure segment length relationship, as long as the pericardium remains open.
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PMID:Right ventricular diastolic function after experimental right ventricular infarction: effects independent of the pericardium. 178 33

In order to evaluate the antihypertensive action of intravenous (i.v.) nicardipine, a calcium channel blocker, we included 28 patients (20 women and 8 men) aged from 71 to 93 years (mean age: 80.4 yrs) poorly controlled by their normal antihypertensive treatment, which had not consisted of a calcium channel blocker. These patients had past histories of a variety of cardiovascular disorders: valve disease (n = 4), disorders of cardiac rhythm (n = 3), paced or unpaced disorders of cardiac conduction (n = 8), and cerebrovascular accident (n = 12). On inclusion, their systolic blood pressure (SBP) was greater than or equal to 180 mmHg and/or their diastolic blood pressure (DBP) greater than or equal to 100 mmHg. Blood pressure recordings (SBP, DBP, MBP) and heart rate (HR) were simultaneously taken every 3 minutes for a period of 140 minutes by an automatic apparatus and a mercury manometer, before and after i.v. administration of nicardipine at 3 increasing dosages, respectively 1.25 mg (20 th min), 2.5 mg (32 th min) and 5 mg (44 th min), each injected over a period of 6 minutes. With a cumulative dose of 8.75 mg nicardipine i.v., the SBP decreased significantly from 192.6 to 138.8 mmHg (p less than 0.001); similarly, the DBP fell from 93.9 to 65.8 mmHg (p less than 0.001) and the MBP from 126.2 to 90.1 mmHg (Hg manometric measurement). In addition, after the final dose of nicardipine, the blood pressure progressively rose to reach levels, by the end of the trial, of 172.1 mmHg (SBP) and 91.1 mmHg (DBP).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Antihypertensive effects of intravenous nicardipine in arterial hypertension in the elderly]. 267 76

We studied pial vessels in vivo in mice, examining under mercury light the permeability of these vessels to sodium fluorescein. Topical application of hypertonic solutions of NaCl caused leakage of fluorescein. However, putative chemical mediators of leakage, such as histamine, serotonin, arachidonic acid, and bradykinin, all failed to increase permeability to the dye. Apparent increases in permeability only accompanied endothelial damage caused by the dye + light combination, as indicated by production of local platelet aggregates. The technique is useful, provided inadvertent endothelial injury is recognized and avoided. The data in mice suggest that pial vessels may not participate in the permeability changes reportedly produced in parenchymal brain vessels by several of the mediators we tested. Therefore, studies of pial vascular permeability are not expected to provide reliable data concerning the actions of agents that might mediate cerebral edema.
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PMID:In vivo studies of pial vascular permeability to sodium fluorescein: absence of alterations by bradykinin, histamine, serotonin, or arachidonic acid. 312 Mar 61


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