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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The aim of the intensive care of the injured is the coupling of the availability and the requirement of the cerebral metabolic substates. The measurement of the cerebral blood flow is not currently available at the bedside and less direct monitoring is required. The cerebral perfusion can be estimated looking at the cerebral perfusion pressure (CPP), that can be easily measured using intracranial pressure (ICP) and the systemic arterial pressure (MAP) monitoring. Hundred-twenty-one consecutive head injured admitted to an Intensive Care Unit were studied assessing the severity of the neurological injury, the CT-Scan diagnosis of the intracranial lesion, the Trauma Score and the behavior of the ICP and MAP. The outcome was classified according to a modified version of the Glasgow Outcome Scale. More than 77% of the patients suffered raised intracranial pressure above 20 mmHg and 16 of them had a CPP less than 60 mmHg for more than 5 minutes. The outcome was directly related to the degree of intracranial hypertension and to the severity of insufficient CPP. The treatment of the severe head injured must be aimed at maintaining a good CPP, because of the close relationships between this value and the prognostic result. The monitoring of the ICP is a reliable and relatively safe procedure in this series, where the rate of infections complicating the intracranial recording is less than 3%.
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PMID:[Cerebral perfusion pressure in endocranial hypertension in comatose head-injured patients]. 221 79

Blood pressure (BP) becomes more sodium and body fluid sensitive as renal function deteriorates. Thus, hypertension in chronic renal failure is mostly of the sodium sensitive type. We studied whether the increased sodium sensitivity (SS) can be restored to normal on the maintenance phase of hemodialysis (HD) therapy. Body weight (BW) and BP (specifically, mean arterial pressure [MAP]) were measured after HD and before the next HD, and the body fluid sensitivity (BFS) was calculated as the ratio of changes in these factors on both introduction and maintenance phases in HD patients (n = 56) who were not taking any antihypertensive drugs (BFS = delta MAP/delta BW). In a preliminary study, the amount of interdialytic sodium intake (QNa+) was measured (n = 30), and SS was calculated as the ratio of the change in MAP to QNa+ (SS = delta MAP/QNa+). Interdialytic BW gain (3.1 +/- 0.1 kg) was correlated with the amount of sodium intake (136 +/- 17 mEq), resulting in a positive relationship between BFS and SS (r = 0.79, P less than .0001). Therefore, BFS was used as an index of SS. As a whole, BFS decreased from the introduction to the maintenance phase (6.5 +/- 1.0 to 3.5 +/- 0.6 mm Hg/L, P less than .01). This decrease was marked (6.2 +/- 1.1 to 2.9 +/- 0.6 mm Hg/L, P less than .01) in patients (n = 46) whose BP was normalized in the maintenance phase, while not significant (7.9 +/- 1.9 to 6.3 +/- 1.3 mm Hg/L) in patients (n = 10) whose BP was still high.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Normalization of increased sodium sensitivity by maintenance hemodialysis. 222 54

We evaluated the effect of acute unilateral renal denervation (DNX) on the tubuloglomerular feedback (TGF) mechanism in Inactin-anesthetized hydropenic male 8- to 10-wk-old spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY). SHR had higher mean arterial pressure (MAP, 28%) and renal vascular resistance (RVR, 35%), whereas renal blood flow (RBF), glomerular filtration rate (GFR), urine flow, and sodium excretion were similar. DNX in SHR did not change MAP but decreased RVR (26%) and increased RBF (29%), GFR (16%), urine flow (52%), and sodium excretion (431%). DNX did not affect these in WKY. Loop of Henle perfusion with Ringer solution reduced early proximal flow rate (EPFR) in SHR more than in WKY; significantly different at a loop flow of 20 nl/min (9.8 +/- 0.7 vs. 6.5 +/- 0.7 nl/min). DNX in SHR increased the nonperfused EPFR from 25.6 +/- 1.1 to 31.7 +/- 1.3 nl/min and reduced TGF responses during perfusion at both 20 nl/min (9.8 +/- 0.7 vs. 4.4 +/- 0.7 nl/min) and 40 nl/min (14.2 +/- 1.1 vs. 10.4 +/- 0.7 nl/min). TGF sensitivity was attenuated by DNX, as indicated by reduced maximum reactivity (-0.89 +/- 0.14 to -0.36 +/- 0.07) and increased turning point (16.5 +/- 0.9 to 25.2 +/- 2.9 nl/min). TGF responses in WKY were not influenced by DNX. Sham denervation did not alter renal hemodynamics and TGF. These results indicate that renal nerves exert a tonic influence on the renal vasculature and the TGF system in SHR but not in WKY. Enhanced TGF responsiveness may be involved in volume retention and in the maintenance of hypertension in SHR.
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PMID:Attenuation of enhanced tubuloglomerular feedback activity in SHR by renal denervation. 233 Sep 89

The extent of cerebral injury and edema was determined in isoflurane-anesthetized rats (n = 32) after 180 min of middle cerebral artery occlusion (MCAO) and 120 min of reperfusion. One of the following was employed during the occlusion period only: 1) control, mean arterial pressure [MAP = 131 +/- 7 (SD) mmHg] and hematocrit (43 +/- 2%) were not manipulated; 2) hemodilution, the hematocrit was reduced to 30% with 5% albumin (MAP = 104 +/- 19 mmHg); 3) hemodilution-normotension, hemodilution was established, and MAP was maintained at 131 +/- 9 mmHg with phenylephrine; 4) hemodilution-hypertension, hemodilution was established, and MAP increased to 161 +/- 2 mmHg with phenylephrine. Brain injury was determined with 2,3,5-triphenyltetrazolium chloride, and cerebral edema was assessed by microgravimetry. Brain injury and cerebral edema were less in both phenylephrine groups, compared with the control and hemodilution groups (P less than 0.05). These results are consistent with the premise that if normotension is maintained, hemodilution reduces ischemic brain injury and edema. They also indicate that the addition of phenylephrine-induced hypertension to hemodilution therapy results in a further reduction of ischemic injury without exacerbating cerebral edema.
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PMID:Hypertension and hemodilution during cerebral ischemia reduce brain injury and edema. 237 8

The effect transcutaneous oestradiol for four months supplemented by medroxyprogesterone (Perlutex) from the 12th to 26th day of every month was assessed in an open uncontrolled prospective investigation in 34 women with menopausal symptoms and follicle stimulating hormone greater than 40 international units and luteinizing hormone greater than 25 international units. A marked effect was found on sweating and hot flushes and other menopausal complaints as expressed by Kupperman's menopausal index. Serum oestradiol increased during the first two months to follicular phase values and this was followed by an unexplained decrease after the fourth month which did not, however, result in aggravation of the symptoms. No alterations were found in steroid-hormone-binding globulin, lipids and body weight. Whether the patients placed the plasters in the hip or abdominal regions was found to be of no significance. Seventeen patients had no side effects of the treatment. Nine patients had transient skin symptoms which disappeared spontaneously. Five patients had mastalgia which disappeared after reduction of the Perlutex dose. One patient developed metrorrhagia. A total of three patients abandoned the treatment: one on account of skin symptoms, one on account of high blood pressure and a third on account of psychiatric symptoms which were unrelated to the treatment. A total of 28 patients wanted to continue treatment after the fourth month.
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PMID:[Transcutaneous estradiol treatment in the climacteric]. 240 44

Relationships between changes in levels of catechols and directly recorded sympathetic nerve activity were examined using simultaneous measurements of renal sympathetic nerve activity and arterial and renal venous concentrations of norepinephrine (NE), dihydroxyphenylalanine (dopa), and dihyroxyphenylglycol (DHPG) during reflexive alterations in renal sympathetic nerve activity in anesthetized, adrenal-demedullated rats. Nitroprusside infusion increased renal sympathetic nerve activity by 90%, arterial levels of dopa by 96%, NE by 326%, and DHPG by 141%. Phenylephrine infusion increased arterial DHPG levels by 81% and decreased renal sympathetic nerve activity by 37% and NE levels by 26%; arterial dopa levels were unchanged. Ganglionic blockade by chlorisondamine (with concomitant phenylephrine infusion to maintain MAP) decreased renal sympathetic nerve activity by 65% and NE concentrations by 37%; arterial dopa concentrations were unchanged, and DHPG concentrations increased by 60%. Proportionate responses of arterial levels of NE were strongly related to proportionate changes in renal sympathetic nerve activity. Clearance of DHPG from arterial plasma was prolonged by phenylephrine-induced hypertension and by nitroprusside-induced hypotension. The results suggest that changes in arterial NE levels reflect changes in sympathetic activity; changes in dopa levels reflect changes in catecholamine biosynthesis; and changes in DHPG levels depend on reuptake of released NE and on hemodynamic factors affecting DHPG clearance.
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PMID:Plasma levels of catechols during reflexive changes in sympathetic nerve activity. 250 66

Chronic hypertension causes the lower and upper limits of CBF autoregulation to reset to higher blood pressure levels. In the present study we examined whether the theophylline derivative P-23, which had lowered blood pressure in SHR, would influence CBF autoregulation. P-23 (10 mg/kg po) was administered once daily for 4 weeks and tail systolic pressure was measured weekly in this P-23 group and in a control group of SHR. At the end of the treatment period, CBF autoregulation was studied. CBF was determined using the intracarotid 133Xe injection method in halothane/nitrous oxide anesthetised animals. The lower and upper limits of autoregulation were studied in two subgroups of rats by, either raising blood pressure (MAP) stepwise with norepinephrine or lowering MAP stepwise by controlled bleeding and measuring CBF at MAP intervals of 10 mmHg. In the P-23-treated group, blood pressure fell significantly but in the control group, blood pressure increased slightly. The lower part of the autoregulation curve was shifted towards lower pressure in the treated group and the lower limit of autoregulation was significantly different from that in the control. The upper limit of autoregulation was above 180 mmHg in both groups. The beneficial effect of P-23 on CBF autoregulation should be taken into consideration during chronic administration in clinical studies in man.
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PMID:Cerebral blood flow (CBF) autoregulation in spontaneously hypertensive rats (SHR) during chronic administration of a theophylline derivative (P-23). 251 76

The effects of a moderate dose of sufentanil (1 microgram.kg-1 + 0.015 micrograms.kg-1.min-1) plus nitrous oxide (30% O2/70% N2O) anesthesia (group I; n = 8) and of high-dose sufentanil/O2 anesthesia (10 micrograms.kg-1 + 0.15 micrograms.kg-1.min-1) without N2O (group II; n = 8) on cardiovascular dynamics, myocardial blood flow, myocardial oxygen consumption, myocardial lactate balance, and hypoxanthine release were studied in two groups of male patients scheduled for elective coronary artery bypass surgery. All patients were on maintenance doses of calcium channel blockers and nitrates with the last doses of medications given the morning of operation. All patients were premedicated with flunitrazepam (2 mg orally), piritramide (7.5 mg IM) and promethazine (25 mg IM). Measurements were performed before the induction of anesthesia with the patients premedicated but awake; 20 min after induction of anesthesia with sufentanil plus pancuronium 0.1 mg.kg-1 for muscle relaxation before surgery; and during sternotomy and sternal spread. Sufentanil at either dose decreased mean arterial pressure, as well as cardiac and stroke volume index while heart rate remained unchanged. Following the induction myocardial blood flow and myocardial oxygen consumption decreased 23% (79 ml.min-1.100 g-1 to 61 ml.min-1.100 g-1 and 28% (9.2 ml O2.min-1.100 g-1 to 6.6 ml O2.min-1.100 g-1) in group I and 14% (78 ml.min-1.100 g-1 to 67 ml.min-1.100 g-1 and 18% (8.7 ml O2.min-1.100 g-1 to 7.1 ml O2.min-1.100 g-1) in group II. Myocardial ischemia was seen in one patient of group II (patient No. 4), as indicated by a hypoxanthine release into the coronary sinus, when after the induction MAP decreased from 93 to 67 mm Hg and heart rate increased from 56 to 71 min-1. During sternotomy 8 of 16 patients (50%) developed hypertension and 9 of 16 patients (56%) showed signs of myocardial ischemia, i.e., a lactate and hypoxanthine release.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Sufentanil does not block sympathetic responses to surgical stimuli in patients having coronary artery revascularization surgery. 252 78

1. This study investigated the effect of progesterone, which, under certain circumstances, can antagonize both the mineralocorticoid and glucocorticoid activities of steroid hormones, on the development and maintenance of adrenocorticotrophic hormone (ACTH)-induced hypertension in conscious sheep. 2. Progesterone (500 mg/day) alone, for 5 days, had no effect on blood pressure, but increased urinary Na excretion by 38 +/- 10 mmol/day (P less than 0.05) during the first 24 h. 3. Infusion of ACTH (5 micrograms/kg per day), alone, for 3 days, increased arterial pressure by 21 +/- 2 mmHg (P less than 0.001) associated with hypernatraemia, hypokalaemia, urinary Na retention, and increased fasting plasma glucose concentration. 4. Progesterone (500 mg/day) concurrently with ACTH blocked the rise in mean arterial pressure and the mineralocorticoid (urinary Na retention) but not the glucocorticoid (increase in plasma glucose concentration) effects associated with ACTH administration. 5. Progesterone (500 and 1000 mg/day) failed to reverse the hypertension and hypokalaemia in sheep pretreated for 3 days with ACTH. 6. Thus, progesterone blocked the onset but did not affect established ACTH hypertension. The mechanism by which progesterone blocked the development of ACTH hypertension appears to be related to the ability of progesterone to block the essential mineralocorticoid component of the adrenocortical steroids involved in the development of ACTH hypertension.
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PMID:Progesterone antagonizes development but not maintenance of ACTH-induced hypertension in sheep. 255 50

1. Previous studies demonstrated that the combined infusion of cortisol (F), aldosterone (ALDO), deoxycorticosterone (DOC), corticosterone (B), 11-deoxycortisol (S), 17 alpha-hydroxyprogesterone (17 alpha OHP) and 17 alpha, 20 alpha- dihydroxy-4-pregnane-3-one (17 alpha 20 alpha OHP), at rates equivalent to their production during adrenocorticotrophic hormone (ACTH) treatment, reproduced the pressor and metabolic responses to ACTH administration in sheep. 2. This study examined which of these adrenocortical steroids were necessary for the initiation of the hypertension produced by these steroids in sheep. 3. Infusion of F, ALDO, 17 alpha OHP and 17 alpha 20 alpha OHP together, increased MAP by 19 mmHg, similar to both complete steroid cocktail (+25 mmHg) or ACTH administration (+21 mmHg). Infusion of F, 17 alpha OHP and 17 alpha 20 alpha OHP increased MAP by +7 mmHg. Infusion of ALDO, 17 alpha OHP and 17 alpha 20 alpha OHP had no effect on MAP. Thus F and ALDO were essential for the pressor effects of the steroid infusion. 4. To determine the role of glucocorticoid activity in the MAP rise, prednisolone, a non-pressor glucocorticoid, was substituted for cortisol. Combined prednisolone, ALDO, 17 alpha OHP and 17 alpha 20 alpha OHP infusion did not raise blood pressure. This suggested that the mineralocorticoid component rather than glucocorticoid component of cortisol's activity was involved in the pressor response. 5. Aldosterone (7 micrograms/h) was substituted for cortisol, giving a total of 10 micrograms/h aldosterone. High dose ALDO (10 micrograms/h), 17 alpha OHP and 17 alpha 20 alpha OHP infusion raised blood pressure by 18 mmHg. Thus, the essential role of cortisol appeared to be due to its occupancy of mineralocorticoid receptors, rather than glucocorticoid receptors. 6. Given that ACTH produces a transient initial increase in aldosterone secretion of up to 10 micrograms/h, it appears that aldosterone and not cortisol is essential for the pressor effects of ACTH. 7. Hypertension resulting from the combined steroid infusion in the sheep appears to be produced by a mechanism which involves a complex interaction between ALDO, F, 17 alpha OHP and 17 alpha 20 alpha OHP. Therefore, the putative 'hypertensinogenic' receptor may be multivalent with binding sites for F, ALDO and 17 alpha 20 alpha OHP, or is a site of single interactive receptors for these steroids and that F exerts its permissive action by occupying the same site as ALDO on the hypertensinogenic receptors.
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PMID:Adrenocortical steroid requirements for initiation of ACTH-dependent hypertension in sheep. 255 26


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