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

Two young patients with extensive ulcerative colitis were treated with oral steroids and developed seizures between 36 and 72 h after emergency colectomy. These cases highlight the problem of postoperative seizures, related to previous steroid administration, fluid overload, postoperative hypertension and biochemical abnormalities.
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PMID:Postoperative seizures. 159 Jul 12

Recent studies about renal function and volume regulating hormones in obstructive sleep apnea (oSAS) indicate complex disturbances in volume homeostasis. Increased nocturnal secretion of atrial natriuretic peptide (ANP) and decreased renin secretion during apnea looks similar to a situation seen during hypervolemia or increased cardiac volume load. Increased venous return induced by pathologically high negative intrathoracic pressure during obstructive apnea may be the cause. Since during wakefulness no true hypervolemia is present, a "pseudohypervolemia" or "central hypervolemia" must exist caused by volume shift from the peripheral to the central compartment during apnea. Since volume homeostasis and blood pressure regulation are complexly connected the question arises whether disturbances in volume homeostasis play a role in the pathogenesis of arterial hypertension in sleep apnea. In a subgroup of hypertensive patients hypertension is salt-sensitive and volume dependent; it is called volume-expanded or low-renin hypertension. An inhibitor of the Na+/K(+)-ATPase acting via the digitalis receptor - called digitalis like factor (DLF) - is regarded as the causative agent for the development of hypertension in these cases. From this background, we were interested in the question whether DLF may be the linkage between disturbances in volume homeostasis and the pathogenesis of hypertension in sleep apnea. We could demonstrate a decrease of nocturnal urinary excretion of DLF during nasal continuous positive air pressure (nCPAP) therapy. Since a positive correlation between changes in diuresis respectively natriuresis and DLF excretion was found, we suggested DLF to be involved in changes of renal function in sleep apnea besides ANP. In 3 patients we measured nocturnal plasma levels of DLF and renin.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Disturbances in volume regulating hormone system--a key to the pathogenesis of hypertension in obstructive sleep apnea syndrome? 165 Sep 45

In the past several years great progress has been made in the understanding of the (patho) physiology of ANP. Because an inhibitor of ANP is not available for human use, there is still discussion about the physiological role of ANP. Nevertheless, from the studies described above the evidence is accumulating that ANP has a role in protecting against fluid overload and hypertension by means of inducing natriuresis, inhibition of the renin-angiotensin-aldosterone system and vasopressin and by vasodilation. The therapeutic potential of modulation of the ANP system seems promising, but must await further research.
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PMID:Atrial natriuretic peptide. 183 64

Basic parameters of central and intracardiac hemodynamics were studied in 49 urological patients 24 of which with urolithiasis entered group I, 13 with hypertension-group II and 12 with varicocele-group III. The patients' age averaged 46.4, 41.6 and 28.6 years, respectively. The data were provided by routine clinical and laboratory examinations, ECG, one-passage radionuclide cardiography with 132I-albumin using a radiocirculographer of Hungarian manufacture and radiocardioanalyzer RKAZ-01 made in this country. Neither marked ischemic disturbances of the myocardium nor valvular defects were revealed. Ambiguous group-specific shifts presented in central and intracardiac hemodynamics. Total peripheral vascular resistance exhibited a moderate increase while left ventricular circulation time grew 1.5-2-fold. The greater resistance can be attributed to activation of renin-angiotensin system in prolonged ischemia of renal parenchyma due to nephrolithiasis. Group II patients demonstrated parallel elevation of arterial pressure, peripheral resistance, left ventricular performance and output suggesting myocardial functional stress. In group III there was a rise in blood volume, left ventricular performance and output, cardiac index, stroke volume. This myocardial overloading may result from changes in intravascular volumetric relations characteristic of hypervolemia. These hemodynamic changes reflect adaptation in urological patients and should be accounted for in treatment and operative interventions.
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PMID:[The radionuclide assessment of the central hemodynamic indices in patients with urolithiasis, arterial hypertension and varicocele]. 194 10

Hypertension is an important risk factor in hemodialysis patients. Fluid overload and increased peripheral resistance are considered the two main causes. We studied the relation between volume state and blood pressure in 18 hemodialysis patients. Actual total body water (aTBW) was measured as tritium space and "ideal" total body water (iTBW) by an anthropometric method. The difference between aTBW and iTBW was considered a measure of fluid excess or deficit. Twelve patients were overhydrated, 5%-23%. Their predialysis blood pressure was significantly correlated to their degree of fluid excess; systolic BP:r = 0.71, p = 0.03, diastolic BP:r = 0.73, p = 0.02, mean arterial BP:r = 0.76, p = 0.03. Five of these patients had multiple antihypertensive drugs instead of adequate ultrafiltration. Five patients had a fluid deficit of -3 to -13% and hypertension due to vasoconstriction. Four of these were adequately treated with antihypertensive drugs but had exaggerated ultrafiltration. TBW determination with tritium is simple to perform and gives information on the volume state and thereby on the cause of hypertension in hemodialysis patients. Based on this, appropriate treatment can be chosen.
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PMID:Hypertension profiling by total body water (TBW) determinations in patients on chronic hemodialysis. 203 45

This paper synthesizes the pathogenic steps of arterial hypertension in diabetes mellitus: hyperosmolarity due to the hyperglycemia and increased sodic tubular reabsorption accounting for the expansion of the extracellular volume with hypervolemia; abnormalities of the ionic membrane pumps leading to abnormal intracellular calcium distribution, thereby inducing an increased vascular tone; atypical vasomotor reactivity to cathecolamines; modifications of the renin-angiotension-aldosterone system. The pathophysiological derangements by which hypertension could induce nephropathy are examined: the vasodilatation which can be detected from the onset of diabetes, may be a determinant in the transmission of systemic hypertension to the glomerular microcirculation with resulting enhancement of the hydrostatic transglomerular pressure gradient (i.c. the major factor producing glomerular injury), glomerular plasmatic flow and filtration rate. The nephron hyperfiltration increases the movement of plasmatic proteins across the glomerular capillary wall with subsequent mesangial hyperactivity and sclerosis. Antihypertensive treatment in diabetes follows general guidelines and it should be instituted even in the case of microhypertension being facilitated in this setting the appearance of microalbuminuria i.e. the starting point of nephropathy. Even if experimental studies are to favor ACE inhibitors as the first-line drugs for abating glomerular hypertension by mitigation of the direct effect of angiotensin II on the efferent arteriolar tone, clinical observations suggest that, regardless of type of treatment, the normalization of systemic arterial pressure, by reversing glomerular hypertension may be effective in preventing diabetic nephropathy.
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PMID:[The pathogenesis of arterial hypertension in diabetes mellitus and its role in nephropathy]. 207 80

Ischemic cerebral edema frequently develops after aneurysm surgery and may lead to severe intracranial hypertension. Of prime importance are reducing the level of ICP and preserving oligemic areas from becoming infarcted. Besides correction of factors known to worsen intracranial hypertension, several therapeutics may be of value: external CSF drainage, perfusion of mannitol, induced arterial hypertension and use of anesthetic agents with cerebral vasoconstricting capability. Hyperventilation is not recommended. Arterial hypotension and hypovolemia certainly contribute to aggravate cerebral ischemia and must be corrected. Cerebral ischemia may be reduced by two specific approaches: by improving cerebral oxygen transport in ischemic areas using arterial hypertension and calcium blockers rather than hemodilution or hypervolemia; by reducing cerebral metabolic rates with heavy anesthesia under the cover of a complete cardiovascular monitoring. In view of the large heterogenicity in cerebral lesions and physiopathological stages, a therapeutical trial appears suitable in each individual case. Criteria allowing to know if any therapeutic, used alone or in association, is beneficial include increase in blood flow in ischemic areas, reduction of ICP level and normalizing of indices like CSF or venous jugular blood lactate.
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PMID:[Treatment of ischemic cerebral edema with intracranial hypertension after neurosurgery of intracranial aneurysms]. 212 75

The absence of a reduction in peripheral vascular resistance secondary to hypervolaemia leads to so-called volume hypertension. In order to study whether a deficient formation of the vasodilator autacoid prostaglandin E2 (PGE2) contributes to the preservation of inadequate vascular tone during extracellular volume expansion, arterial plasma PGE2 and the stable PGE2 metabolite 13,14-dihydro-15-keto-PGE2 (PGE2-M) were determined in 13 oligoanuric women on chronic haemodialysis. Prior to treatment eight of them had hypervolaemia and hypertension (mean arterial pressure (MAP) 128 +/- 3 mmHg (mean +/- SE] and five patients had hypervolaemia of a similar degree but were not hypertensive (MAP: 99 +/- 4 mmHg P less than 0.005). Before haemodialysis the arterial PGE2 and PGE2-M concentrations were less (P less than 0.05) in hypertensive (11 observations in eight patients) than in normotensive patients (ten observations in five patients). As blood pressure decreased during the course of haemodialysis of volume hypertensive patients, the concentration of PGE2 and PGE2-M increased (P less than 0.02) by 104 +/- 43% and 89 +/- 32%, respectively. In normotensive patients neither blood pressure nor the concentration of PGE2 and PGE2-M were found to change during treatment. Since volume hypertension was associated with reduced values and dialysis induced normalisation of blood pressure with increased arterial values of PGE2 and PGE2-M, we hypothesise that the development of hypertension associated with fluid overload of haemodialysed patients may be related to a decreased release of prostaglandin E2.
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PMID:Changes of arterial prostaglandin E2 during haemodialysis. 212 29

In summary, over a period of approximately four decades, an important new pathologic process was identified. There is no longer any doubt that the deposition of the subarachnoid clot in the basal cisterns can, over the course of a few days, lead to a progressive, severe vasoconstriction. This, in turn, can reduce cerebral blood flow to the distal brain, which, depending on a multitude of factors, can result in cerebral infarction. It is highly likely that the erythrocyte is the most important blood element in the pathophysiology of this process. The exact mechanism by which the blood vessel is forced into this destructive spasm remains to be elucidated. Significant steps have been taken to avoid the consequences of vasospasm by using hypertension and hypervolemia (or at the very least avoiding iatrogenic hypotension and hypovolemia). These measures have resulted in a reduced incidence of delayed ischemia. Because clot has been shown to cause vasospasm, it has seemed only logical that the early removal of clot would be efficacious in its prophylaxis. Experimental and clinical evidence to support this view has been gathered. Therapeutic measures based on it have been shown to be effective in the experimental situation but await controlled clinical evaluation. In the past decade, thanks to such trials, one of the calcium antagonist drugs has been shown to be effective in improving the outcome following subarachnoid hemorrhage, probably on the basis of reducing the frequency and extent of infarction by small vessel dilatation or neuronal protection. Although patients still die from this lethal complication of subarachnoid hemorrhage, it is difficult not to have some measure of optimism, based on the history just reviewed, that cerebral vasospasm will be a treatable disease within a few decades.
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PMID:The history of cerebral vasospasm. 213 40

Acute and rapidly progressive renal failure is caused by a number of pathogenetically distinct types of glomerulonephritis, some of which are associated with systemic vasculitis. In a given patient, accurate diagnosis of the specific type of glomerulonephritis is essential for optimum treatment. Making a specific diagnosis usually requires renal biopsy or serologic analysis. The two categories of treatment for glomerulonephritis are (1) treatment for the pathophysiologic complications of glomerulonephritis, such as hypertension, fluid overload, and uremia, and (2) treatment for the inflammatory injury, which usually employs immunosuppression with steroids and cytotoxic drugs.
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PMID:Diagnosis and management of glomerulonephritis and vasculitis presenting as acute renal failure. 219 60


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