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

Two box jellyfish in particular cause problems in tropical Queensland waters. Chironex fleckeri inhabit calm waters close to the shore between November and May. The venom includes three major components: haemolytic dermatonecrotic and myocardial. The dermatonecrotic toxin causes a ladder pattern of whiplash lesions to the skin which ulcerate become necrotic and heal very slowly over months: Neuromuscular paralysis and cardiovascular collapse may be fatal within minutes of envenomation. Emergency treatment comprises inactivation of stinging capsules by vinegar removal of tentacles analgesia, cardiopulmonary resuscitation and the administration of the specific antivenom. Carukia barnesi ('Irukandji') are found in both coastal and open waters. A patch of erythema with papules at the sting site is characteristically followed 30 min later by the onset of a catecholamine mediated syndrome. Headache and severe abdominal and back pain are usual and may be followed by hypertension, tachyarrhythmias and cardiogenic shock.
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PMID:Marine stingers in far north Queensland. 871 6

Four women were admitted over three years because of anemia and renal failure. They had evidence of hemolytic uremic syndrome (HUS) with severe vascular involvement and glomerular collapse. Despite intensive plasma exchange, all patients developed neurologic signs (with seizures and coma in 2) and papilledema. Three developed refractory hypertension and three required dialysis. All patients had abnormal von Willebrand factor (vWF) fragmentation as reflected by decreased high molecular weight and increased low molecular weight vWF multimers in the circulation. Assuming that the disease was sustained by shear stress-induced abnormal vWF fragmentation in damaged renal microvasculature, bilateral nephrectomy was done. Surgery was followed within two weeks by complete hematologic and clinical remission consistently associated with the restoring of vWF fragmentation pathway to normal. We speculate that in HUS resistant to plasma exchange or infusion, removing the kidneys eliminates a major site of vWF fragmentation, which would limit platelet activation and protect patients from the further spreading of microvascular lesions.
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PMID:Bilateral nephrectomy stopped disease progression in plasma-resistant hemolytic uremic syndrome with neurological signs and coma. 877 Sep 81

The paper first describes the phenomenon of pituitary compression in the Turkish saddle--intracellular hypertension--which develops during stresses and morphologically appears as a volumetric conflict between abruptly (acutely) 1.5-2-fold enlargement of the brain appendage (at the expense of adenocytic hypertrophy, hyperemia, colloidal retention) on the one hand, and the poor pliable capsule and Turkish saddle), on the other. Extrapituitary factors (elevated liquor and venous pressure) that compress the pituitary outside may be involved in the formation of the phenomenon. Intracellular hypertension seems to be one of the causes that are encountered in critical conditions (shock, collapse, coma, etc.), of acute pituitary-adrenal failure episodes.
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PMID:[Compression of the appendix cerebri in the sella turcica in critical states as a possible cause of acute adrenocortical insufficiency]. 877 58

Obstructive sleep apnea (OSA) is a disorder in which there is repetitive collapse and closing of the pharynx during sleep. There is growing evidence to suggest that this disorder is a major cause of essential hypertension (EH) and that successful treatment of OSA can reduce the blood pressure (BP) significantly. In addition many other patients with EH have milder forms of sleep related breathing disorders (SRBD) like snoring, and upper airway resistance syndrome (UARS) which, while not as severe as OSA, may be severe enough to also cause systemic hypertension. We therefore propose a unifying hypothesis-that many patients with EH may have sleep related breathing disturbances (SRBD) and treatment of these disorders may improve the BP. SRBD could also explain many of the epidemiological, clinical, hereditary, biochemical, hematological and physiological characteristics seen in EH. In addition, many types of secondary hypertension (those caused by excessive alcohol intake, chronic renal failure, diabetes, hypothyroidism or acromegaly) have a higher than normal prevalence of OSA and OSA may contribute to the hypertension and organ damage found in these conditions as well. Thus SRBD may play an important role in the production of many cases of essential and secondary hypertension, and their early detection and treatment could reduce the hypertension and organ damage seen in these conditions.
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PMID:Essential and secondary hypertension and sleep-disordered breathing: a unifying hypothesis. 887 97

These cases demonstrate a few of the presentations that may occur with new onset oncologic problems. While the transport phase of these children's care was not extraordinary, the development and management of the clinical issues might have been influenced by earlier interventions. Would the outcome of Case 1 have been different if the abnormal hematologic parameters demonstrated on the preoperative laboratory results had been further investigated? Would the institution of cerebral resuscitative measures before and during transport have offered this child a better chance of survival? Would the involvement of a specialized pediatric team earlier in the process have addressed some of those issues and would it have made a difference? Should the patient in case two have had cerebral resuscitative measures instituted at the referring hospital or during transport? In hindsight, this clearly would not have been useful or beneficial to the patient. But what if the initial CT interpretation of a brain tumor and increased intracranial pressure with ventricular ablation and midline shift had been correct? Should the transport team have suggested or instituted a different level of therapy with the information that was available at the time of transport? The patient in Case 3 had a dramatic presentation of his ALL. Were there signs and symptoms that should have alerted the referring hospital, transport command physician or transport team to the likely deterioration of that patient? If this patient had presented to a hospital a further distance away, would the impending cardiovascular collapse and respiratory failure have been anticipated or occurred during the transport? Would or should the mode of transport or team configuration have been altered? If this patient had deteriorated during the transport, would the transport team have had the skills to manage this potentially difficult airway? Should the patient in Case 4 have had antihypertensive medication started at the referring hospital or during the transport process? What are the guidelines for antihypertensive intervention in this situation? If antihypertensive therapy were instituted by the transport team, should this have affected time or mode of transport, or was it more prudent not to rock the boat by instituting interventional therapy? Is hypertension a different issue with a liver mass, as suspected at the time of referral, or with a nephrogenic tumor? These cases afford us the ability to review several presentations of oncologic emergencies. The questions above are but a few of the potential areas of discussion that can arise from these cases. We should use these cases as an opportunity to review and refresh our transport teams on the many faces of oncology and potential pitfalls in the care of those patients.
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PMID:Oncology and transport. Beware of the presentation and anticipate the clinical course. 898

The As4.1 cell line was established from a mouse kidney tumor by transgene-targeted tumorogenesis. These cells express high levels of renin mRNA from their endogenous renin gene and release approximately eightfold-more prorenin than active renin in culture. Levels of renin mRNA in As4.1 cells are decreased in a dose-dependent manner by the addition of physiological concentrations of cytokine interleukin-1 to the media. Stability of renin mRNA and initial rates of release of active renin and prorenin were not significantly altered by interleukin-1. In contrast, transcription initiated from a construct that consisted of 4.1 kilobases of renin 5' flanking sequence fused to a reporter gene (chloramphenicol acetyltransferase) was markedly inhibited by interleukin-1. On the basis of our findings, we conclude that downregulation of renin synthesis caused by interleukin-1 occurs primarily at the level of transcription and that DNA sequence or sequences mediating that effect are positioned within 4.1 kilobases upstream of the renin gene. The physiological relevance of this regulation is related to the events that occur during septic shock, characterized by hypotension, cardiovascular collapse, multiple organ failure, and high mortality. Unexpectedly, hypotension associated with septic shock does not lead to activation of the renin-angiotensin system. The hypotension in septicemia is believed to be mediated by the combined action of many modulators including cytokines, and data presented here suggest direct involvement of interleukin-1 in this process.
Hypertension 1997 Aug
PMID:Downregulation of renin gene expression by interleukin-1. 926 Sep 85

Intrasellar hypertension--a phenomenon of the hypophysis compression in the sella turcica-was described 13 years ago. It develops under stressor conditions and is probably one of the causes of frequent in critical situations (shock, collapse, coma, etc.) episodes of acute hypophyseo-adrenal failure. Intrasellar hypertension morphologically manifests by the volume unbalance between a suddenly increasing, 1.5-2 times, hypophysis (due to adenocyte hypertrophy, hyperemia, colloid retention) on the one hand, and its rigid capsule and sella turcica, on the other. Extrahypophyseal factors (high liquid and venous pressure) may take part in developing of this phenomenon due to hypophysis squeezing from outside.
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PMID:[Hypophysis compression syndrome in the sella turcica: mechanisms of development, pathology]. 929 23

The pathogenesis of fibrosis and the functional features of pressure overload myocardial hypertrophy are still controversial. The objectives of the present study were to evaluate the function and morphology of the hypertrophied myocardium in renovascular hypertensive (RHT) rats. Male Wistar rats were sacrificed at week 4 (RHT4) and 8 (RHT8) after unilateral renal ischemia (Goldblatt II hypertension model). Normotensive rats were used as controls. Myocardial function was analyzed in isolated papillary muscle preparations, morphological features were defined by light microscopy, and myocardial hydroxyproline concentration (HOP) was determined by spectrophotometry. Renal artery clipping resulted in elevated systolic arterial pressure (RHT4: 178 +/- 19 mmHg and RHT8: 194 +/- 24 mmHg, P < 0.05 vs control: 123 +/- 7 mmHg). Myocardial hypertrophy was observed in both renovascular hypertensive groups. The myocardial HOP concentration was increased in the RHT8 group (control: 2.93 +/- 0.38 micrograms/mg; RHT4: 3.02 +/- 0.40 micrograms/mg; RHT8: 3.44 +/- 0.45 micrograms/mg of dry tissue, P < 0.05 vs control and RHT4 groups). The morphological study demonstrated myocyte necrosis, vascular damage and cellular inflammatory response throughout the experimental period. The increased cellularity was more intense in the adventitia of the arterioles. As a consequence of myocyte necrosis, there was an early, local, conjunctive stroma collapse with disarray and thickening of the argyrophilic interstitial fibers, followed by scarring. The functional data showed an increased passive myocardial stiffness in the RHT4 group. We conclude that renovascular hypertension induces myocyte and arteriole necrosis. Reparative fibrosis occurred as a consequence of the inflammatory response to necrosis. The mechanical behavior of the isolated papillary muscle was normal, except for an early increased myocardial passive stiffness.
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PMID:Myocyte necrosis is the basis for fibrosis in renovascular hypertensive rats. 945 75

Fawn-hooded hypertensive (FHH) rats constitute a spontaneous model of chronic renal failure with early systemic and glomerular hypertension, proteinuria, and development of focal and segmental glomerulosclerosis. The goal of the present study was to elucidate a step-by-step sequence of histopathologic events leading from an initial glomerular injury to segmental sclerosis. Segmental sclerosis in the FHH rat is consistently associated with the glomerular vascular pole. The initial injury involves the expansion of primary branches of the afferent arteriole. Apposition of those capillaries to Bowman's capsule, together with the degeneration and detachment of corresponding podocytes, allows parietal cells to attach to the naked glomerular basement membrane of this capillary, i.e., allows the formation of a tuft adhesion to Bowman's capsule. The adhesion enlarges to a broad synechia by encroaching to neighboring capillaries, apparently based on progressive podocyte degeneration at the flanks of the adhesion. Capillaries inside the adhesion--before undergoing collapse or hyalinization--appear to stay perfused for some time and to maintain some kind of filtration misdirected toward the cortical interstitium. Thereby, a prominent paraglomerular space comes into existence, enlarging in parallel with the adhesion. Toward the cortical interstitium this space is delimited by a layer of sheetlike fibroblast processes, which has obviously been assembled in response to the formation of this space. Toward the urinary space, the paraglomerular space is demarcated by the parietal epithelium and by the interface between the adhesion and the "intact" tuft remnant. Thus, the sclerotic tuft portions all become enclosed within the paraglomerular space.
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PMID:Development of vascular pole-associated glomerulosclerosis in the Fawn-hooded rat. 951

This study investigated the relationship between brain tissue oxygen tension (PbtO2) and cerebral microdialysate concentrations of several compounds in five patients with refractory intracranial hypertension after severe head injury. The following substances were assayed: lactate and glucose; the excitatory amino acids glutamate and aspartate; and the cations potassium, calcium, and magnesium. Glucose concentrations did not correlate with PbtO2, but lactate increased as PbtO2 decreased. The lactate/glucose ratio exhibited a close relationship to PbtO2, increasing sharply only when oxygen tension reached zero. Although glucose and oxygen eventually reached very low levels and zero, respectively, in these fatally head-injured patients, the terminal decrease in PbtO2 slightly preceded that of glucose in four of the five patients. This time lag is the cause of the poor correlation between glucose and PbtO2. Glutamate and aspartate concentrations both demonstrated a close relationship to PbtO2, with sharp increases not occurring until PbtO2 was zero. Concentrations of these amino acids exhibited a similar pattern in response to decreasing glucose concentrations. Potassium concentrations began increasing at a PbtO2 of 35 mm Hg, which is not generally considered indicative of hypoxia. Sharper increases began occurring once PbtO2 dropped below 15 mm Hg, with a slight rise in the minimum potassium concentrations recorded at these low PbtO2 values. Calcium and magnesium concentrations did not vary in response to PbtO2. In summary, the most robust biochemical indicators of cerebral anoxia were elevations in the lactate/glucose ratio and in the concentrations of lactate and of the excitatory amino acids glutamate and aspartate. Furthermore, the fact that glucose concentrations continue to decrease for a short period after oxygen levels reach zero suggests that cells continue to utilize glucose anaerobically for such functions as maintenance of cellular integrity, with collapse of the cell membrane as evidenced by increases of extracellular glutamate and aspartate not occurring until both oxygen and glucose concentrations reach zero.
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PMID:Comparison of brain tissue oxygen tension to microdialysis-based measures of cerebral ischemia in fatally head-injured humans. 967 54


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