UMLS:C0038454 - FACTA Search

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Query: UMLS:C0038454 (stroke)
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Increased arterial blood pressure following a pyrogenic reaction has been reported in previous studies, however the mechanism of this hypertension has not been examined in detail. The present study investigated the effects of both intravenous (IV) and intracerebroventricular (ICV) injection of lipopolysaccharide (LPS) from E. coli on body temperature (Tb), mean arterial pressure (MAP), heart rate (HR), cardiac output (CO), calculated total peripheral resistance (CTPR), stroke volume (SV) and plasma levels of adrenocorticotropin (ACTH) and arginine vasopressin (AVP) in conscious, chronically instrumented sheep. IV injection of LPS (1 microgram) increased Tb in a biphasic manner from 38.7 +/- 0.1 to 39.5 +/- 0.2 degrees C after 50 min and to 39.9 +/- 0.2 degrees C after 130 min, and MAP increased biphasically from 64 +/- 1 to 70 +/- 4 mmHg after 40 min and to 78 +/- 3 mmHg after 130 min. CO initially decreased from 4.4 +/- 0.1 to 3.5 +/- 0.1 after 40 min followed by a secondary rise to 4.8 +/- 0.1 l/min after 100 min. This occurred together with a large, biphasic increase in CTPR from 14.5 +/- 1.0 to 22.0 +/- 2.0 mmHg/l/min at 40 min, and to 18.1 +/- 0.1 mmHg/l/min at 120 min. HR increased from 68 +/- 4 to 97 +/- 4 b/min and SV decreased from 65 +/- 2 to 41 +/- 4 ml/beat during the first phase of activation. Plasma ACTH increased from 22 +/- 9 to 1043 +/- 175 pg/ml after 80 min, and plasma AVP increased from 0.7 +/- 0.2 to 12 +/- 4.0 pg/ml after 60 min. ICV injection of LPS produced a long-lasting increase in Tb and MAP, but had no effect on HR or plasma AVP. Plasma ACTH increased from 30 +/- 12 to 427 +/- 110 pg/ml. These changes suggest that intravenous pyrogenic infection produces a potent vasoconstrictor action in sheep to increase blood pressure, possibly mediated by the actions of AVP within the CNS, or other pyrogenically released vasoconstrictor factors. Furthermore, the duration of activation of the cardiovascular system following peripheral and central LPS administration is different, which together with the contrasting effects on ACTH and AVP, indicate the involvement of several hypertensive mechanisms.
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PMID:Pyrogenic stimulation of vascular resistance in conscious sheep. 762 27

The ATP-sensitive potassium channels (KATP) are activated either by a decrease in intracellular ATP content or by a lowering of the ATP-ADP ratio such as during stroke. We studied the role of cerebral KATP on arterial pressure during acute reduction of cerebral blood flow in 12-week-old male Wistar rats anesthetized with urethane by recording arterial pressure and heart rate continuously. After bilateral ligation of the common carotid arteries, glibenclamide, a specific blocker of KATP, was injected intracerebroventricularly into the cerebral lateral ventricle. Glibenclamide elicited a sustained vasopressor response in a dose-dependent manner in rats with bilateral carotid artery ligation (10 nmol, +15 +/- 2 mm Hg; 1 nmol, +5 +/- 1 mm Hg, P < .01 versus vehicle), but hemodynamic alterations were barely recorded with glibenclamide in sham-operated control rats. The abdominal sympathetic discharge was not increased significantly enough to explain the pressor mechanism. Similarly, pretreatments with intravenous injections of bunazosin, an alpha 1-adrenoceptor antagonist, did not affect the pressor response of intracerebroventricular glibenclamide. To investigate the vasopressor mechanism further, we measured plasma and pituitary concentrations of arginine vasopressin and determined the effects of vasopressin receptor antagonists. The intracerebroventricular injections of glibenclamide significantly increased the plasma concentration of vasopressin (P < .05) and significantly decreased the pituitary concentration of vasopressin (P < .05) in rats with bilateral carotid artery ligation. Intravenous pretreatment with the vasopressin V1 receptor antagonist OPC-21268 abolished the vasopressor response to intracerebroventricular glibenclamide (+16 +/- 2 versus +1 +/- 1 mm Hg, P < .01).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cerebral ATP-sensitive potassium channels during acute reduction of carotid blood flow. 773 18

Neurohypophysial arginine vasopressin (AVP) concentrations were determined by RIA in 9 patients with cerebral infarction, 11 patients with intracerebral hemorrhage, 5 patients with subarachnoid hemorrhage and 5 control subjects. The results showed that neurohypophysial AVP concentration in patients with cerebral infarction increased by 225.8% as compared with the control subjects (P < 0.05), and the AVP concentrations in patients with intracerebral and subarachnoid hemorrhage did not change significantly. Brain herniation as a result of intracranial hypertension, gastrointestinal bleeding and hyperglycemia (two clinical manifestations of stress) was seen more frequently in hemorrhagic stroke patients than in ischemic stroke patients. These findings suggest that the ischemic brain damage may contribute to the elevation of neurohypophysial AVP concentration in patients with cerebral infarction.
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PMID:Neurohypophysial AVP concentration in stroke patients. 778 11

The hypothesis was tested that carotid baroreflex gain is increased after 20% hemorrhage. The baroreceptor reflex responses to changes in carotid sinus pressure (CSP) were measured in control, 20% hemorrhage, and reinfusion conditions in three experimental groups: conscious intact (n = 7), anesthetized intact (n = 8), and anesthetized vagotomized (n = 8) dogs. Mean arterial pressure (MAP), heart rate (HR), cardiac output (CO), stroke volume (SV), and calculated total peripheral resistance (TPR) responses to changes in CSP were measured. At any given CSP, MAP, CO, and SV all decreased significantly with the 20% hemorrhage, as reflected by a downward shift in the reflex characteristic curve with no change in overall reflex range or gain. In contrast, TPR and HR responses to CSP were not significantly altered by 20% hemorrhage; reflex curves and gains were comparable to control conditions. In the conscious intact dogs, the maximal reflex gain, Gmax, for the MAP response was -1.365 +/- 0.25, -1.298 +/- 0.33, and -1.324 +/- 0.25 in control, 20% hemorrhage, and reinfusion conditions, respectively, and was not significantly altered by hemorrhage. In the same group, the Gmax for the HR response was -1.792 +/- 0.65, -1.709 +/- 0.33, and -1.986 +/- 0.67 in control, 20% hemorrhage, and reinfusion conditions, respectively; baroreflex gain on HR was not increased with hemorrhage. Plasma arginine vasopressin (AVP), an increase in which has been proposed to augment baroreflex gain, increased from a control level of 0.98 +/- 0.27 to 9.66 +/- 2.67 pg/ml during 20% hemorrhage in the conscious intact dogs; despite the increase in plasma AVP during hemorrhage, augmentation of baroreflex gain was not observed.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Carotid baroreflex control during hemorrhage in conscious and anesthetized dogs. 834 87

The hemodynamic effect of combined V2/V1 arginine vasopressin (AVP) antagonist in conscious rats with acute 24 hour streptozotocin (STZ)--induced diabetes was studied using the microsphere technique. The rats were made diabetic with a single intravenous injection of STZ (60 mg/kg). One day after STZ administration the hemodynamic parameters in the experimental animals were measured before and 10 minutes after AVP antagonist injection (50 mg/kg, i.v.). The hemodynamic alterations observed post-antagonist included: 1) an increase in the total peripheral resistance (1.84 +/- 0.15 vs. 1.31 +/- 0.12 mm Hg/ml/min per 100 g before antagonist administration, p < 0.05), 2) a decrease in the cardiac index (49.0 +/- 3.1 vs. 68.7 +/- 5.2 ml/min/100 g before antagonist administration, p < 0.05) and stroke volume (0.40 +/- 0.03 vs. 0.57 +/- 0.06 ml before antagonist administration, p < 0.05), 3) a significant (p < 0.05) decrease in the blood flow to the skin, skeletal muscle, stomach, small intestine and kidneys. The mean arterial pressure and heart rate remained unchangeable post-antagonist. These data suggest that AVP is responsible, at least in part, for prominent hemodynamic alterations observed in conscious rats with 24 hour STZ-induced diabetes.
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PMID:[Hemodynamic changes in waking rats with acute streptozotocin diabetes after administration of the combined V2/V1 vasopressin antagonist]. 837 33

We assessed the effect of arginine vasopressin (AVP) on left ventricular (LV) performance in eight conscious dogs. Five minutes after AVP infusion (6 microns.kg-1 x min-1 for 2 min) the plasma AVP was elevated from 3.9 +/- 0.9 to 14.7 +/- 4.6 pg/ml (P < 0.05). With all reflexes intact, AVP caused significant increases in LV end-systolic pressure (P) (112 +/- 8 vs. 122 +/- 7 mmHg, P < 0.05) end-systolic volume (V) (30 +/- 5.8 vs. 38 +/- 7.7 ml, P < 0.05), total systemic resistance (6.2 +/- 1.8 vs. 10.6 +/- 4.0 mmHg.dl-1 x min, P < 0.01) and arterial elastance (Ea) (6.8 +/- 3.0 vs. 8.6 +/- 3.9 mmHg/ml, P < 0.05), while the heart rate (110 +/- 6 vs. 82 +/- 10 beats/min, P < 0.05) and stroke volume (16.5 +/- 4.3 vs. 14.2 +/- 3.9 ml, P < 0.05) were decreased. There was no significant change in the coronary sinus blood flow (82 +/- 19 vs. 78 +/- 22 ml/min, P = not significant). AVP decreased the slopes of LV end-systolic P-V relation (10.7 +/- 1.1 vs. 8.1 +/- 1.9 mmHg/ml, P < 0.05), the maximal first derivative of LV pressure (dP/dtmax)-end-diastolic volume (VED) relation (135.2 +/- 18.7 vs. 63.1 +/- 7.7 mmHg.s-1 x ml-1, P < 0.05), and the stroke work-VED relation (81.1 +/- 4.1 vs. 66.7 +/- 2.8 mmHg, P < 0.05) and shifted the relations to the right, indicating a depression of LV performance. A similar increase in Ea produced by methoxamine did not depress LV performance.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of vasopressin on left ventricular performance. 843 Aug 61

The hypothesis was tested that narrowing of arterial pulse pressure (PP) is a determinant of arginine vasopressin (AVP) release in humans. Six normal males completed a two-step lower body negative pressure (LBNP) protocol of -20 and -50 mmHg, respectively, for 10 min each. None of these subjects experienced presyncopal symptoms. Arterial plasma AVP and plasma renin activity (PRA) (at 2-min intervals) only increased subsequent to a decrease in PP (invasive brachial arterial measurements) and stroke volume (ultrasound Doppler technique, n = 4). Simultaneously, mean arterial pressure did not change. A selective decrease in central venous pressure and left atrial diameter (echocardiography, n = 4) at LBNP of -20 mmHg did not affect AVP or PRA, whereas arterial plasma norepinephrine increased (n = 4). During LBNP, significant (P < 0.05) intraindividual linear correlations were observed between log(AVP) and PP in four of the subjects with r values from -0.75 to -0.99 and between log(PRA) and PP in all six subjects with r values from -0.89 to -0.98. In conclusion, these results are in compliance with the hypothesis that narrowing of PP in humans during central hypovolemia is a determinant of AVP and renin release.
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PMID:Arterial pulse pressure and vasopressin release in humans during lower body negative pressure. 849 90

Adrenomedullin (ADM) is a 52 amino-acid peptide which is a potent vasodilator in rats, and suppresses basal and CRF-induced ACTH release from cultured pituitary cells. The present study examines the hemodynamic and hormonal actions of human ADM (1-52) infusion in conscious, chronically instrumented sheep. Five sheep were infused intravenously (IV) or intracerebroventricularly (ICV) with ADM at 100 micrograms/h for 60 min, and mean arterial pressure (MAP), heart rate (HR), cardiac output (CO), stroke volume (SV), total peripheral conductance (TPC), coronary blood flow (CF), coronary conductance (CC), peak aortic flow (Fmax), and left ventricular dF/dt were monitored by a computer-based data collection system every 2 min. Plasma concentrations of adrenocorticotropin (ACTH), arginine vasopressin (AVP) and renin were measured after 60 min of infusion. IV ADM produced a small fall in MAP of 3 +/- 1 mmHg, associated with a reflex increase in HR of 14 +/- 3 b/min. CO increased by 1.3 +/- 0.3 l/min, whereas SV remained unchanged. TPC was markedly increased by 20 +/- 3 ml/min/mmHg. Changes in CF were also seen with an increase of 10 +/- 2 ml/min, and CC increased in parallel by 0.15 +/- 0.02 ml/min/mmHg. Fmax and dF/dt showed small increases of 2.1 +/- 0.5 l/min and 85 +/- 20 l/min/sec respectively. Plasma concentrations of ACTH and cortisol were reduced by 58% and 55% respectively, whereas plasma renin concentration increased by 106%. There was no change in plasma levels of AVP. ICV infusion of ADM had no effect on any parameter measured. These data suggest that systemic ADM produces a sustained vasodilator action to lower blood pressure in sheep, and this is the first study to report the ACTH-suppressor action of ADM in conscious animals. ADM may therefore be an important hormone involved in the regulation of pituitary/adrenal function, in addition to its cardiovascular and fluid regulatory actions in mammals.
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PMID:ACTH-suppressive and vasodilator actions of adrenomedullin in conscious sheep. 874 70

Objective: The number and types of surgical procedures being preformed using laparoscopic technique is increasing due to technological advances. Recent studies suggest the carbon dioxide pneumoperitoneum and patient positioning causes hemodynamic alterations, respiratory acidosis, and a release of stress hormones. However, to date, no studies have investigated the physiological effect of laparoscopic procedures lasting more than 60 minutes on the stress response and the effect of Trendelenburg positioning. The purpose of this study was to identify the physiological effect of pneumoperitoneum and positioning during prolonged laparoscopy on hemodynamic (cardiac index, mean arterial pressure, heart rate, systemic vascular resistance, and stroke volume), metabolic (arterial blood gases), and hormone (arginine vasopressin, aldosterone, and plasma renin activity) parameters. We hypothesized that pneumoperitoneum and patient positioning will alter the hemodynamic, hormone, and metabolic parameters.Methods: The study was longitudinal in design and sampled a total of 31 healthy subjects having a gynecologic oncologic laparoscopic procedure at Hurley Medical Center, Flint, Michigan. The subjects were randomly assigned one of three groups receiving an initial insufflation pressure of either 10, 15, or 18 mmHg. After obtaining informed consent hemodynamic, metabolic, and hormone measurements were obtained at the following times: 1) pre-induction, 2) post-induction, 3) post-insufflation, 4) post-Trendelenburg 5 minutes and at 30, 60, 90, and 120 minutes post-insufflation. The results were analyzed using multivariate analysis of variance for repeated measures with a P <.05. A power of 0.9 was obtained to identify changes over time.Results: During the time course of the study the hemodynamic, metabolic, and hormonal parameters showed significant alterations. The most dramatic hemodynamic changes occurred post-insufflation characterized by a decrease in cardiac index and stroke volume with a concurrent increase in systemic vascular resistance. The metabolic parameters showed a significant decrease in pH and corresponding increase in PaCO(2). However, the pH and PaCO(2) remained within normal limits through the study. As part of the study's protocol the investigators increased minute volume to control for a rise in PaCO(2) during the procedure. A significant increase was noted in aldosterone and arginine vasopressin at post-insufflation and Trendelenburg positioning. Plasma renin activity showed a dramatic increase following post-insufflation. None of the subjects developed any post anesthetic complications.Conclusion: Our study demonstrated that pneumoperitoneum and Trendelenburg positioning cause statistically significant elevations in the stress hormones and concurrently cause a decrease in hemodynamic parameters. A healthy patient may tolerate these changes but a patient with cardiovascular disease or pulmonary problems may not be able to compensate as efficiently.
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PMID:Hemodynamic and hormonal changes during pneumoperitoneum and trendelenburg positioning for operative gynecologic laparoscopy surgery. 1083 88

Our long-term objective is to identify genes whose expression results in hypertension and in phenotypic changes that may contribute to hypertension. The purpose of the present study was to describe evidence for the heritability of hypertension-related phenotypes in hypertensive, hyperlipidemic black sib pairs. Outpatient anthropomorphic measurements were obtained in >200 affected sib pairs. In addition, 68 of these sib pairs were studied under controlled, standardized conditions at an inpatient clinical research center while off both antihypertensive and lipid-lowering medications. Heritability was estimated on the basis of sib-sib correlations and with an association model. Higher heritability estimates for blood pressure were observed with multiple measurements averaged over 24 hours than with measurements at a single time point, and heritability estimates for nighttime blood pressures were higher than those for daytime blood pressures. Heritability estimates for several of the phenotypes were augmented by obtaining measurements in response to a standardized stimulus, including (1) blood pressure responses to the assumption of upright posture, standardized psychological stress, and norepinephrine infusion; (2) plasma renin, aldosterone, epinephrine, and cAMP and cGMP responses to the assumption of upright posture; (3) para-aminohippurate and inulin clearances in response to norepinephrine infusion; and (4) plasma arginine vasopressin in response to NaCl infusion. High heritability estimates were also observed for various measures of body size and body fat, left ventricular size, cardiac index, stroke volume, total peripheral resistance, and serum concentrations of LDL and HDL cholesterol and leptin. These heritability estimates identify the hypertension-related phenotypes that may facilitate the identification of specific genetic determinants of hypertension in blacks with hyperlipidemia.
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PMID:Genetic determinants of hypertension: identification of candidate phenotypes. 1090 5

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