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

In the present study, we examined whether antihypertensive treatment of young and adult hypertensive rats with the angiotensin-converting enzyme (ACE) inhibitor perindopril could restore the baroreflex vagal deficit and whether this was related to prevention of cardiac or vascular hypertrophy. Spontaneously hypertensive (SHR), stroke-prone spontaneously hypertensive (SHR-SP), and Wistar-Kyoto (WKY) rats were untreated or treated with perindopril (3 mg/kg/day) in the drinking water from 4-9 and from 14-20 weeks of age. Steady-state sigmoidal mean arterial pressure (MAP)-heart rate (HR) reflex curves were obtained in the conscious rats by the injection of pressor and depressor agents before and after atenolol (vagal component). Increased left ventricle to bodyweight ratio (LV/BW) indicated cardiac hypertrophy. After ganglion blockade, the minimum MAP produced by nitroprusside and the maximum produced by methoxamine were used as indications of vascular hypertrophy. Perindopril treatment reduced cardiac and vascular hypertrophy to different extents in SHR and SHR-SP. The 4-9 and 14-20 week treatments reduced MAP and both minimum and maximum blood pressure of the SHR to the levels of the untreated WKY. However, only in the older animals was LV/BW restored. In the SHR-SP, early treatment had a much greater effect on vascular hypertrophy than on LV/BW. The reverse occurred for the 14-20 week animals. In untreated hypertensive animals the baroreflex curves were shifted to the right with reduced vagal HR range. Perindopril treatment shifted the baroreflex curves back towards the WKY curves. Vagal HR range was strongly correlated with the LV/BW, whereas vagal HR range was less well related to the level of vascular hypertrophy or blood pressure. These results suggest that antihypertensive treatment can restore cardiac baroreflex function and that it is related to the reduction in cardiac hypertrophy. Although the mechanism of this relationship remains to be elucidated, these findings suggest that cardiac vagal afferents may be important.
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PMID:Importance of cardiac, but not vascular, hypertrophy in the cardiac baroreflex deficit in spontaneously hypertensive and stroke-prone rats. 153 47

Maximum heart rates (HR) of three soricine shrews and six other small mammals were measured in response to a single supramaximal dose of isoproterenol (Iso) under urethan anesthesia. The highest HR, 1,043 +/- 66 (SD) beats/min (n = 3), was in least shrew (Sorex minutus, mean body mass 3.02 +/- 0.81 g). Maximum HRs of common shrew (Sorex araneus, 7.16 +/- 1.54 g) and water shrew (Neomys fodiens, 12.80 +/- 1.54 g) were 938 +/- 29 (n = 7) and 887 +/- 21 (n = 6), respectively. In general, maximum HRs of soricine shrews and other small wild mammals followed the common mammalian pattern, fHmax/Iso = 443 x Mb-0.14, determined by body size. The exponent for this equation is smaller than that of resting HR (-0.25) (Stahl, J. Appl. Physiol. 22: 453-460, 1967), predicting crossover at approximately 3 g body mass. However, resting HRs of small mammals were clearly lower than expected on the basis of body mass. Lowering resting HR below the common mammalian level, with concomitant increase in stroke volume, seems to be a prerequisite for small mammals to regulate cardiac output against the ceiling of maximum HR. Electrophoretic analysis showed that the myosin of shrew ventricles is different from those of rodent species. In native conditions, shrew myosin, designated V1', migrated faster than the V3 and V1 forms of rat heart. On SDS gradient gel the single heavy chain of shrew myosin migrated slower than the alpha- or beta-chains of rat ventricle. Differences in the molecular weight of light chains were also noted between small mammals. Despite the notable differences in myosin composition, myosin-ATPase activity of the shrew hearts was similar to that of mouse and rat heart. Because duration of isometric contraction was inversely related to resting and maximum HRs, it was concluded that in the small mammals rate and duration of contraction are determined mainly by the release and uptake rate of myoplasmic Ca2+ and less by myosin-ATPase activity.
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PMID:Maximum heart rate of soricine shrews: correlation with contractile properties and myosin composition. 153 6

The goal of the current study was to determine whether treatment of hypertension reduces cerebral infarction after occlusion of the middle cerebral artery in stroke-prone spontaneously hypertensive rats (SHRSPs). Three-month-old SHRSPs received untreated drinking water or drinking water containing cilazapril, an angiotensin converting enzyme inhibitor, or hydralazine and hydrochlorothiazide. After 3 months of treatment, the left middle cerebral artery was occluded and neurological deficit was evaluated. Infarct volume was measured 3 days after occlusion using computer imaging techniques from brain slices. Cilazapril and hydralazine with hydrochlorothiazide were equally effective in reducing systolic blood pressure in SHRSPs. One day after occlusion of the middle cerebral artery, neurological deficit was decreased by both cilazapril and hydralazine with hydrochlorothiazide compared with untreated SHRSPs, and the deficit 3 days after occlusion was decreased significantly only by cilazapril. Infarct volume was 178 +/- 7 mm3 (mean +/- SEM) in untreated SHRSPs, and it was significantly reduced to 117 +/- 15 mm3 by hydralazine with hydrochlorothiazide and to 101 +/- 17 mm3 by cilazapril. Infarct volume in Wistar-Kyoto rats was 27 +/- 16 mm3. Thus, reduction in arterial pressure by hydralazine with hydrochlorothiazide or an angiotensin converting enzyme inhibitor is protective against focal cerebral ischemia in SHRSPs.
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PMID:Effect of antihypertensive treatment on focal cerebral infarction. 153 16

Even during adequate general anesthesia, hypertension is a common phenomenon in patients undergoing aortocoronary bypass grafting (CABG). In such cases application of vasodilators is recommended in order to decrease myocardial oxygen consumption. This study was performed to compare two commonly used substances, i.e., nitrates and nifedipine, with regard to their influence on hemodynamics, renal blood flow, kidney function, and the requirement for homologous blood transfusions. METHODS. Forty-four patients gave their informed consent to the study. They were randomly divided into 2 groups: group 1 received nitroglycerin (3.0 micrograms/kg.min), group 2 nifedipine (Adalat, 0.5 microgram/kg.min) in order to prevent hypertension in the phase before onset of cardiopulmonary bypass (CPB). Anesthesia was induced by etomidate and succinylcholine and maintained as a modified neuroleptanalgesia with fentanyl (up to 50 micrograms/kg), midazolam (0.3 mg/kg.h), and pancuronium (0.1 mg/kg). Systolic blood pressure was kept within the range of 120-160 mm Hg; in case of higher values boluses of either 0.25 mg nitroglycerin or 0.5 mg nifedipine were administered. Cardiac index, stroke volume index, rate-pressure product, intrapulmonary shunt, and pulmonary and total peripheral resistances were evaluated at five predefined points: (1) after induction of anesthesia; (2) before incision; (3) before cannulating the aorta; (4) after decannulating the aorta; and (5) at the end of operation. Creatinine and free-water clearances as well as sodium and potassium excretion were calculated for three phases of the operation: (A) induction of anesthesia--onset of CPB; (B) during CPB; and (C) end of CPB--end of operation. CPB was performed using a membrane oxygenator (Sorin 51) and a nonpulsatile blood flow of 2.5 1/min.m2, which was reduced during mild hypothermia of 30-32 degrees C to 1.7 l/min.m2. Mean arterial pressure in both groups was kept at approximately 70 mm Hg. In case of lower pressures norepinephrine (50-100 micrograms/bolus) was administered; higher pressures were treated as described above. Volume substitution was performed initially by 500 ml hydroxyethyl starch and continued, if necessary, by homologous blood or 5% human albumin in order to keep the hematocrit greater than 30 in the phases before and after CPB. RESULTS. Group 2 showed significantly higher values of cardiac index and stroke volume index at point 3 while the rate-pressure product was clearly lower, indicating better myocardial performance and lower oxygen consumption than in group 1. Creatinine and free-water clearances in all three phases did not differ. However, sodium excretion during CPB was significantly higher in the nifedipine group while potassium excretion showed no differences. The average requirement for blood and blood substitutes was lower in group 2, but the difference could not be confirmed statistically because of the large dispersion of values. Nevertheless, 4 patients in the nifedipine group but no patient in group 1 did not need homologous blood transfusion. CONCLUSION. In comparison to nitrates, nifedipine showed some advantages in the treatment of hypertension during CABG: (1) it provided better myocardial performance; (2) it had a more reliable but not too long-lasting effect on elevated total peripherial resistance, leading to better hemodynamic stability; and (3) by not affecting the capacitance vessels it may necessitate fewer homologous blood transfusions.
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PMID:[Nifedipine versus nitroglycerin in aortocoronary bypass surgery. The effect on hemodynamics, kidney function and homologous blood requirement]. 153 39

To determine what role duodenal clearance plays in the resistance that the duodenum generates to gastric emptying, duodenal output in vitro was assessed under a variety of preload and after-load conditions. In the presence of an outflow resistance, duodenal output occurred in pulses related to contractions of the duodenum. Stroke volume (incremental output during a single contraction) and cumulative output increased both with the degree of duodenal filling and with pharmacological stimulation. Cumulative output decreased as outflow resistance was increased from 0.5 to 5.0 cm water pressure; there was no further decrease on raising outflow resistance to 10.0 cm water pressure. Output volume was similar from the proximal and the distal duodenum. The stroke volume produced by individual duodenal contractions remained stable over a wide range of load conditions. The threshold volume and the luminal pressure at which output from the duodenum started were higher with retrograde perfusion of the duodenum than with antegrade perfusion. Also, the contraction rate of the duodenum decreased markedly with retrograde perfusion, and the powerful contractions occurring in this setting often involved the entire segment simultaneously. The findings suggest that the duodenum responds to load and to flow conditions so that luminal clearance is maintained; clearance is achieved by both antegrade and retrograde displacement of contents from the lumen at the contraction site.
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PMID:Clearance patterns of the isolated guinea pig duodenum. 153 22

Two-dimensional 1H spectroscopic imaging and magnetic resonance imaging were used to study focal ischemia induced by middle cerebral artery occlusion in rats. A water suppressing spin-echo sequence was used at 4.7 T. Phase encoding during the spin-echo delay (TE = 272 ms) yielded an 8 x 8 array of 35 microL voxels. The injured area of the brain had a higher lactate level and markedly lower N-acetyl aspartate, creatine and choline levels than did the non-ischemic regions. The spectroscopic imaging data clearly showed the localization of the infarct, which agreed well with both magnetic resonance imaging and the histological data obtained post-mortem. This study demonstrates the potential usefulness of combining magnetic resonance imaging and 1H spectroscopic imaging for studying animal models of stroke, and indicates the suitability of the technique for further pharmacological approaches.
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PMID:Two-dimensional 1H spectroscopic imaging for evaluating the local metabolic response to focal ischemia in the conscious rat. 155 Jul 5

Traumatic brain injury suppresses spontaneous cardiovascular compensation for hemorrhage, prompting us to examine the possibility that trauma to the brain modifies hemodynamic response to therapy in hemorrhage. Thirty rats that were anesthetized were randomly assigned to four groups--hemorrhagic shock (H), hemorrhagic shock after brain trauma (TH), hemorrhagic shock treated with lactated Ringer's (LR) solution (HR), and hemorrhagic shock after brain trauma treated with LR (THR). After hemorrhage, group TH had significantly lower mean arterial pressure (MAP), cardiac index (CI) and stroke volume index (SVI) than group H. Throughout the postresuscitative period, group HR had significantly higher MAP, CI, SVI and central venous pressure than group H. At 50 and 70 minutes after the start of hemorrhage, group THR showed significantly lower MAP, CI and SVI than group HR. This difference in hemodynamics is not because of transcapillary refill effect, because brain trauma did not cause changes in hematocrit and plasma protein levels. As heart rate, preload and afterload were not significantly different between groups THR and HR, the attenuation of fluid resuscitation can be attributed mainly to a depressed cardiac function. Furthermore, neither brain trauma nor fluid replacement altered the content of water in the brain in hemorrhaged rats. These data indicate that brain trauma not only suppresses spontaneous hemodynamic recovery from hemorrhage, but also impedes the efficacy of LR resuscitation. The results of the current study suggested that a more aggressive fluid replacement may be needed to treat hemorrhagic shock in individuals with brain injury.
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PMID:Traumatic brain injury attenuates the effectiveness of lactated Ringer's solution resuscitation of hemorrhagic shock in rats. 155 10

To define the optimal and safe storage period in the use of the University of Wisconsin Solution (UWS) for extended heart preservation, 34 adult canine hearts were preserved under static and hypothermic conditions for 6, 12, 18, and 24 hours. A group of 10 hearts were used as a control of the preparation used in the study. Left ventricular functions were assessed in an isolated heart preparation equipped with a computerized servo-pump to measure the pressure-volume relationship. The systolic, diastolic and total ventricular performance were derived from the end-systolic pressure-volume relationship, end diastolic pressure-volume pressure relationship, and the stroke work-end diastolic volume relationship, respectively. Myocardial water content and coronary resistance during reperfusion were also analyzed. The study revealed that UWS was able to maintain normal levels of systolic and diastolic functions, and consequently normal level of total ventricular performance after 6 hours of storage. There was a reduction of diastolic function while the systolic function was still well maintained after 12 hours of preservation. The results after 12 hours were poor. There was no increase in the myocardial water content for up to 24 hours of storage; however, the coronary resistance during reperfusion significantly increased in the 18-hour group and the 24-hour group. The findings suggest that UWS may extend the safe period of myocardial preservation beyond the traditional 4 hours of storage closer to 12 hours of storage.
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PMID:Optimal storage period for extended heart preservation with the University of Wisconsin Solution. A study of the left ventricular pressure-volume relationship. 157 80

Clinical practice and laboratory studies have demonstrated the efficacy of cold crystalloid cardioplegia for donor heart protection. Efforts to increase the margin of safety for protection led us to compare unmodified University of Wisconsin (UW) solution to the dextrose, mannitol-based Stanford (ST) solution. A canine model of heart transplantation with antegrade hypothermic cardioplegic arrest and 6 hours of 4 degrees C ischemic storage was used. An oxygenated blood-primed isolated heart preparation was used for reperfusion and myocardial mechanics and energetics studies of the working heart. Six of 6 UW and 4 of 6 ST hearts reached the working phase. Computer-assisted analysis of pressure-volume loops generated at varying flows measured by tri-axial sonomicrometry and high-fidelity micromanometry showed no significant differences in function between the ST and UW groups by maximum elastance (UW, 4.2 +/- 1.1; ST, 4.0 +/- 0.7), preload recruitable stroke work (UW, 43.7 +/- 7.3; ST, 43.4 +/- 8.7), or slope of log-linear end-diastolic pressure-volume curve (UW, 0.057 +/- 0.01, ST, 0.061 +/- 0.01). Specimens for determination of myocardial water content were taken after cardioplegic arrest, after storage, after reperfusion, and after the working phase. There was a significant increase in tissue water after reperfusion in both groups (UW, 75.7% +/- 0.5% to 81.6% +/- 0.2%, p = 0.0001; ST, 76.5% +/- 0.4% to 83.4% +/- 0.3%, p = 0.0002), which persisted after the working phase (UW, 81.5% +/- 0.9%, p = 0.0002; ST, 82.6% +/- 0.1%, p = 0.0003). Both groups exhibited postreperfusion increase in myocardial water content, but this edema was significantly less marked in the UW group (p = 0.0001).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cardioplegia for heart transplantation: unmodified UW solution compared with Stanford solution. 157 41

Outcome following stroke is difficult to measure because the behavioral response to infarction is variable. We hypothesized that cognitive function, such as spatial learning, may be a reproducible and sensitive outcome variable. We developed an animal model of multifocal cerebral ischemia in order to study the effects of infarction on learning. To cause ischemia, several hundred microspheres were injected into the internal carotid arteries of rats. After ischemia, behavior was measured using a global rating and a Morris water maze. Postmortem serial brain sections were stained and the size of the infarctions was measured. We found that intracerebral microspheres caused cortical infarction and an impairment of spatial learning. This impairment was not due to occlusion of the internal carotid artery and was not found in animals who received a sham injection of saline. The degree of learning impairment was not correlated with the volume density of the infarctions or with the volume density of the remaining cerebral hemisphere. The learning impairment clearly differentiated normal from lesioned animals, and the impairment was probably due to a delay in acquisition of spatial information rather than a defect in retention or retrieval. Measurement of learning deficit after cerebral ischemia is an efficient and sensitive method for evaluating new stroke treatments and possibly for exploring structure function relationships.
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PMID:Quantitative effects of cerebral infarction on spatial learning in rats. 157 20


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