Effect Of Acute Hypertension Research Articles

Effect of Acute Hypertension on the Extravasation

Effect of Acute Hypertension on the Extravasation

Intensive care unit variables and outcome after pediatric traumatic brain injury: A retrospective study of survivors

Traumatic brain injury is a leading cause of death and disability in children. Hypotension has been associated with poor survival and outcome in children after traumatic brain injury, but the effect of acute hypertension is less certain. The objective was to obtain acute physiologic variables during the early hospitalization period in a cohort of children prospectively enrolled in another study. Retrospective chart reviews. University-affiliated pediatric rehabilitation center. Fifty-seven survivors, 5-17 yrs of age, admitted for rehabilitation between 1992 and 1995 after sustaining a traumatic brain injury. Standard of care. Outcomes were assessed at 1 yr postinjury through cognitive testing of the child and parent interview of the child's global functional skills. Cognitive outcome was measured using the Performance IQ from the Wechsler Intelligence Scale for Children, Third Edition. Overall functional outcome was assessed using the Disability Rating Scale. This study suggests that early markers of secondary injury after moderate to severe traumatic brain injury in children may be predictive of long-term outcome. This study reinforces the need for longer term, systematic, and more precise measurements of outcomes in children with traumatic brain injury and prospective studies to examine the predictive value of acute management variables on multiple types of outcomes after traumatic brain injury in children.

The Effect of Acute Hypertension on Left Ventricular Diastolic Pressures in a Canine Model of Left Ventricular Dysfunction with a Preserved Ejection Fraction and Elevated Left Ventricular Filling Pressures

Decompensated heart failure with preserved left ventricular (LV) ejection fraction (EF) is often accompanied by hypertensive episodes. We hypothesized that acute increase in arterial pressure results in elevated early and late diastolic LV pressures as a result of further impaired LV relaxation. To test this hypothesis, we used a chronic canine model of LV systolic dysfunction with preserved LV function (LVDPEF) (EF > 50%) and elevated LV end-diastolic pressure using coronary microsphere embolization. At baseline and with LVDPEF, each dog was paced 10 beats above their baseline heart rate and high-fidelity LV pressures, echocardiographic LV volumes, and transmitral Doppler were obtained before and after methoxamine pressure loading. With normal LV function, LV pressures at peak negative dP/dt (+18 mm Hg, P < .05) and at LV pressure minimum (+3.6 mm Hg, P < .01) increased. Both tau (P < .05) and LV end-diastolic pressure increased (5 +/- 3 vs 13 +/- 4 mm Hg, P < .01). EF was unchanged, although LV end-diastolic volume increased (P < .01). Pressure loading with LVDPEF resulted in a timing delay (P < .05) and a greater increase in LV pressures at peak negative dP/dt (+45 mm Hg) and LV minimal pressure (+7.5 mm Hg) as compared with normal LV function (P < .01). LV end-diastolic pressure increased (9 +/- 2-23 +/- 5 mm Hg, P < .001), diastolic filling period shortened (288 +/- 51-204 +/- 54 milliseconds, P < .01), and tau increased (P < .001). EF declined from 54 +/- 9% to 43 +/- 9% (P < .05) and LV size increased (P < .01). Pressure loading with normal LV function and with LVDPEF results in increased LV diastolic pressures, which are further exaggerated with LVDPEF as a result of prolonged relaxation and shortened diastolic filling.

The effect of acute hypertension on blood-brain barrier permeability to albumin during experimentally induced epileptic seizures

The present study was to examine the effect on the blood-brain barrier function of a rapid blood pressure elevation and the duration of this pressure during bicuculline and pentylenetetrazol-induced seizures. The experiments were carried out on Wistar rats. Evans blue was used as a blood-brain barrier tracer. Our results showed that the presence of blood pressure increase does not always result in blood-brain barrier leakage during convulsions. Besides the rate of increase in the pressure, the duration of this increased pressure was the important factor in the disruption of blood-brain barrier during bicuculline or pentylenetetrazol-induced seizures.

Ultrastructural study of the effect of acute hypertension on the stria vascularis and spiral ligament.

The effect of acute hypertension, induced in rats by intravenous injection of methoxamine chloride (Mexan), on the stria vascularis and spiral ligament was studied electronmicroscopically with the tracer method of horseradish peroxidase (HRP). Considerable extravasation of HRP occurred in the stria vascularis, due to the increased vesicular transport. The leaked HRP spread into intercellular spaces, but was prevented from spreading towards the endolymph by zonulae occludentes between marginal cells and towards the perilymph by zonulae occludentes between basal cells. The reaction product was occasionally found between basal cells. No leakage of HRP from capillaries was observed in the spiral ligament, although some labelled micropinocytotic vesicles were present in the endothelium. It is suggested that, under acute hypertensive conditions, areas of zonulae occludentes bordering the stria vascularis play an important role as a barrier to HRP, whereas capillaries in the spiral ligament themselves act as a barrier to it.

Effects of Experimental Acute Hypertension on the Blood-Labyrinthine Barrier

With intraperitoneal injection of 0.16mg/kg methoxamine hydrochloride, experimental acute hypertension was made in guinea pig. Blood pressure was measured with a physiological pressure transducer. The initial mean blood pressure was 50-60mmHg and methoxamine caused a rapid increase of 50-60mmHg in about 15-20 minutes.For the first experiment, Kanamycin was used as a tracer. Four hundred mg/kg Kanamycin was injected intraperitoneally, and 20min. after injection, acute hypertension was created.Inner ear fluids were collected with micro-glass capillaries 10min., 40min., and 3 hours 40min. after inducing acute hypertension. Kanamycin concentrations in the inner ear fluids were measured with the bioassay technique.The results showed that Kanamycin went into the inner ear fluids rapidly at a higher dose with acute hypertension, and excretion from inner ear fluids were rapid compared with the normal group. This result indicates that the permiability of Kanamycin through the blood-labyrinthine barrier seems to be increased by acute hypertension.The ion concentrations of the inner ear fluids under the effect of acute hypertension were measured with an atomic absorption spectro photometer (Japan Jarrell Ash AA 855). Fifteen minutes after injection of methoxamine, the inner ear fluids were taken and K+ and Na+ ion concentrations were analysed. The results show that in the case of perilymph, the K+ ion concentration in the scala tympani was increased; the Na+ ion in the scala vestibuli was decreased; and in the endolymph, K+ was decreased and Na+ was increased.From these two experiments, we concluded that the function of the blood-labyrinthine barrier was affected by acute hypertension and the ion concentrations in the inner ear fluids were also changed.Because of the relationship between the perilymph and endolymph, which changes of ion concentrations are primary is not known and the meaning of these changes is not clear.The osmotic pressure between the endolymph and perilymph may be changed and if these unbalances in the ion concentrations are continued, histological and functional disturbances of the inner ear can occur.

Effects of acute hypotension and hypertension on serum TSH concentrations in male rats

The effect of acute hypertension and hypotension on serum TSH concentration was studied in anesthetized male rats. I.v. infusions (10 and 30 min) of Na-nitroprusside and dihydralazine induced a profound hypotension, and angiotensin amide and noradrenaline increased blood pressure, but none of the treatments significantly modified serum TSH concentrations. Also clonidine and noradrenaline, when given i.p., caused hypertension, but again the increase of serum TSH levels was not consistent. When the whole material was analysed, there was a scarcely significant correlation between the change of blood pressure and the change of serum TSH level. It is inferred that the drugs affecting TSH secretion, do not exert their action solely by changing the blood pressure.

Some factors influencing the damaging effect of acute arterial hypertension on cerebral vessels in rats.

1. Abrupt increase of arterial blood pressure can give rise to multifocal areas of protein extravasation in the brain due to overstretching of the vessels. 2. The vascular tone of the resistance vessels is of importance for the occurrence of the increased permeability. 3. Vasodilatation aggravates the damaging effect of acute hypertension whereas vasoconstriction induced by hyperventilation reduces the incidence of areas of increased permeability. 4. Ligation of a carotid artery prevents lesions in the ipsilateral hemisphere.

Effect of acute hypertension on the natriuretic response to saline loading.

ARTICLESEffect of acute hypertension on the natriuretic response to saline loadingM Raeder, P Omvik Jr, and F KillM Raeder, P Omvik Jr, and F KillPublished Online:01 Apr 1974https://doi.org/10.1152/ajplegacy.1974.226.4.989MoreSectionsPDF (2 MB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformation Cited ByEffect of acute salt ingestion upon core temperature in healthy men14 April 2011 | Hypertension Research, Vol. 34, No. 6Effect of indomethacin on modest pressure natriuresis in chloralose-anesthetized, non-laparotomized dogsLife Sciences, Vol. 42, No. 15Effects of digitalis on renal tubular sodium reabsorptionHypothesis Discrepancy Between Intra- and Interpopulation Studies of the Relationship Between Dietary Salt and Blood Pressure: Fact or Fiction?3 July 2009 | Clinical and Experimental Hypertension. Part A: Theory and Practice, Vol. 6, No. 4Lack of stimulation of renal (Na+ + K+)-ATPase by thyroid hormones in the rabbitBiochimica et Biophysica Acta (BBA) - General Subjects, Vol. 717, No. 1PRESSURE NATRIURESIS IN HYPERTENSION.24 April 2009 | Acta Medica Scandinavica, Vol. 209, No. S646Renal response to graded intravenous hypertonic NaCl infusion in healthy and hypertensive subjects:dose-related impairment in distal NaCl reabsorptionAmerican Heart Journal, Vol. 100, No. 2Regulation of sodium balance in hypertension.Hypertension, Vol. 2, No. 4Studies on the Influence of Salt and Water Balance and Blood Pressure Regulation in Hypertensive PatientsRe-examination of the dose-response relationship for the renal effect of acetozolamide8 July 2009 | Scandinavian Journal of Clinical and Laboratory Investigation, Vol. 39, No. 4Factors limiting renal proximal tubular reabsorption at high glomerular filtration rate7 April 2011 | Scandinavian Journal of Clinical and Laboratory Investigation, Vol. 38, No. 6Renal energy metabolism and regulation of sodium reabsorptionKidney International, Vol. 11, No. 3Hypertension—The Chicken and the EggThe Lancet, Vol. 307, No. 7955 More from this issue > Volume 226Issue 4April 1974Pages 989-995 Copyright & PermissionsCopyright © 1974 by American Physiological Societyhttps://doi.org/10.1152/ajplegacy.1974.226.4.989PubMed4823064History Published online 1 April 1974 Published in print 1 April 1974 Metrics

Effect of acute hypertension on sodium transport by the distal nephron.

Effect of acute hypertension on sodium transport by the distal nephron.

The effect of acute arterial hypertension on the blood-brain barrier to protein tracers.

A study was made on the effect of acute hypertension on the blood-brain barrier to proteins. The arterial blood pressure was raised by intravenous injections of metaraminol bitartrate (Aramine) and Evans Blue was used as protein tracer. Multiple foci Evans Blue extravasation became evident in the gray matter of the brain as early as 10 min after the sudden increase of blood pressure by 90 mm Hg or higher. As observed under the fluorescence microscope, the tracer had penetrated the walls of intracerebral vessels and accumulated in numerous adjacent neurons. EEG recordings from blue stained areas of the cerebral cortex showed changes in neuronal activity.

Effect of acute hypertension on sodium reabsorption by the proximal tubule.

The effect of acute hypertension on sodium reabsorption by the proximal tubule was studied in rats by means of micropuncture methods. Hypertension was induced by bilateral carotid artery ligation and cervical vagotomy. Within a few minutes after blood pressure rose (30-60 mm Hg above control levels), a moderate natriuresis and diuresis began. Proximal sodium reabsorption, measured by two independent methods, was found to be markedly suppressed, both in absolute amount per unit length and per unit of tubular volume (C/pir(2)). The ratio between tubular volume and glomerular filtration rate (GFR) (pir(2)d/V(0)) was found to be increased. These observations indicate that the inhibition of proximal sodium reabsorption induced by hypertension cannot be explained by the tubular geometry hypothesis of sodium regulation. Several possible hormonal mechanisms were investigated. Intravenous d-aldosterone did not prevent the suppression of sodium transport due to acute hypertension, nor did chronic oral saline loading to reduce the renal content of renin. Constriction of the suprarenal aorta, with maintenance of a normal renal perfusion pressure, did prevent the inhibition of proximal transport during carotid artery occlusion, thus excluding an extrarenally produced natriuretic hormone as the mechanism. The observations are compatible with the view that sodium transport was inhibited either by an intrarenal natriuretic hormone or by an increase in the interstitial volume of the kidney produced by a transient hydrostatic pressure gradient across the peritubular capillaries. The latter seems more likely to us because of the rapidity of onset of the natriuresis, and because removing the renal capsule and releasing the surface interstitial fluid prevented the effect of hypertension on proximal sodium transport.