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

We superimposed extreme hypercapnia (arterial Pco2 400-450 mmHg) immediately before and during incomplete cerebral ischemia to distinguish the role of intracellular pH (pHi) and bicarbonate [( HCO3-]i) in postischemic metabolic and electrophysiological recovery. Incomplete global ischemia was produced in seven anesthetized dogs by 30 min of intracranial hypertension followed by 4 h of reperfusion. ATP, phosphocreatine (PCr), and pHi were measured with 31P magnetic resonance spectroscopy, and [HCO3-]i was calculated from the Henderson-Hasselbalch equation using the measured pHi and sagittal sinus Pco2. Cerebral blood flow was reduced to 7 +/- 1 ml.min-1.100 g-1 (+/- SE) during ischemia with extreme hypercapnia, and pHi decreased to 5.72 +/- 0.09. During normocapnic reperfusion, pHi rapidly returned to near baseline values by 14 min. [HCO3-]i fell from 12.1 +/- 0.9 to 6.0 +/- 1.2 mM by the midpoint of ischemia and recovered by 30 min of reperfusion. ATP, PCr, and O2 consumption also recovered rapidly and completely. Somatosensory-evoked potentials (SEP) recovered to 43 +/- 10% of control amplitude. These results are in marked contrast to the poor metabolic and SEP recovery previously observed in hyperglycemic dogs in which pHi decreased to the same range as with hypercapnic ischemia, but in which [HCO3-]i was much lower (1.1 +/- 0.5 mM). Therefore, [HCO3-]i depletion during hyperglycemic ischemia may be a more important factor in recovery than end-ischemic pHi per se. We speculate that higher [HCO3-]i may improve glial cell buffering capacity or decrease iron availability for hydroxyl radical production.
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PMID:Bicarbonate conservation during incomplete cerebral ischemia with superimposed hypercapnia. 190 5

We determined whether the rate of metabolic recovery and electrophysiological deficit after incomplete cerebral ischemia is related to intracellular pH (pHi) achieved at the end of ischemia in a dose-dependent manner. End-ischemic pHi was varied by employing two ischemic durations, 12 and 30 min, and by setting preischemic plasma glucose to approximately 80 or 400 mg/dl. Incomplete global ischemia was produced in anesthetized dogs by transient intracranial hypertension followed by 4 h of reperfusion, and pHi, ATP, and phosphocreatine (PCr) were measured with 31P magnetic resonance spectroscopy. Cerebral blood flow was reduced to approximately 6 ml.min-1.100 g-1 during ischemia. End-ischemic pHi was greater than 5.7 in all animals from various treatment groups except for four of seven dogs treated with 30-min hyperglycemic ischemia. When end-ischemic pHi remained greater than 5.7, there was nearly complete recovery of ATP, PCr, pHi, intracellular bicarbonate concentration [( HCO3-]i), and O2 consumption. Partial recovery of somatosensory-evoked potentials (SEP) occurred in most of these animals. In the 30-min hyperglycemic animals in which pHi fell below 5.5, ATP, PCr, and O2 consumption recovered by only one-half over 60 min of reperfusion and then declined to near-zero levels without SEP recovery. In addition, pHi remained less than 6.0, and [HCO3-]i remained less than 2 mM throughout reperfusion. We conclude that there is an apparent in vivo pHi threshold of approximately 5.5-5.7 during incomplete cerebral ischemia that is associated with an inability to significantly restore pHi and [HCO3-]i and with secondary deterioration of high-energy phosphate levels.
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PMID:Dependence of cerebral energy phosphate and evoked potential recovery on end-ischemic pH. 199 96

Secondary mania is increasingly recognized clinically, and consists of acute exhibition of manic symptoms without past or family history of affective disorder. It has been reported with toxic and metabolic disturbances, primary and metastatic brain tumors, epilepsy, and cerebrovascular events. A multifactorial etiology has been suggested. We report two men, 52 and 56 years old, who developed grandiosity, sleeplessness, irritable mood, hyperactivity, and paranoid and religious delusions, with attempted violence in one case. Both had no premorbid psychiatric history and were healthy except for hypertension. One patient had a normal neurologic examination, and the other had mild left hemiparesis and hyperreflexia. EEGs, brainstem auditory-evoked responses, and median nerve somatosensory-evoked potentials were normal. Magnetic resonance studies demonstrated infarction of the ventral pons (on the right in the patient with left-sided signs and on the left in the patient with normal neurologic examination). The two patients responded to lithium carbonate and neuroleptics and have not had further psychiatric symptoms in 18 months of follow-up. These cases emphasize the relationship of late-onset mania with predisposing brain disease, and they suggest that brainstem disturbances can influence mood, sleep, libido, and thought.
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PMID:Secondary mania after ventral pontine infarction. 213 93

This study was designed to determine the cytoplasmic pH (pHi) profile of lymphocytes from a rat model of genetic hypertension that is well suited for study before and after the development of spontaneous hypertension. For this purpose, pHi was measured in thymic lymphocytes obtained from spontaneously hypertensive rats (SHR) and from age-matched Wistar-Kyoto (WKY) control rats using 2',7'-bis carboxyethyl-5,6-carboxyfluorescein (BCECF), a pH-sensitive fluorescence probe. At the age of 16-20 weeks, pHi of lymphocytes suspended in a HCO3-free HEPES-buffered solution, was markedly lower in the SHR than in the WKY rats (7.07 +/- 0.02, n = 16 and 7.22 +/- 0.01, n = 15, respectively, p less than 0.001), whereas systolic blood pressure was higher in SHR than in WKY rats (175 +/- 5.0 and 105 +/- 3.0 mm Hg, respectively, p less than 0.001). In rats less than 5 weeks of age, pHi was also lower in SHR than in WKY rat lymphocytes (7.12 +/- 0.04, n = 11 and 7.23 +/- 0.04, n = 11, respectively, p less than 0.05), although at this age systolic blood pressure was not different between the two groups (87 +/- 4.0 and 85 +/- 3.0 mm Hg, respectively). In lymphocytes suspended in a more physiological HCO3/CO2-buffered solution, pHi was again lower in the adult SHR than in the WKY rat (7.18 +/- 0.02, n = 16 and 7.31 +/- 0.02, n = 16, respectively, p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension 1990 Jan
PMID:Reduced intracellular pH in lymphocytes from the spontaneously hypertensive rat. 215 99

In order to determine the effect of dietary calcium supplementation on blood pressure and calciotropic hormones, we studied two groups (n = 12 each) of mineralocorticoid [deoxycorticosterone (DOC)]-salt hypertensive rats, one receiving a normal-calcium diet (0.6% calcium, as calcium carbonate) and the other a high-calcium diet (2.5% calcium), over an 8-week period. Dietary calcium supplementation significantly attenuated the rise in blood pressure. Serum ionized calcium concentrations were significantly decreased from baseline levels in both groups but tended to be higher among the calcium-supplemented rats. Serum concentrations of parathyroid hormone (PTH) and 1,25-dihydroxyvitamin D3 (1,25-D) were significantly higher in the DOC-salt rats than in normotensive rats fed normal rat chow [PTH: 49 +/- 4 versus 15 +/- 0.9 pg/ml (means +/- s.e.m.); 1,25-D: 108 +/- 7 versus 73 +/- 13 pg/ml, in DOC-salt and normotensive rats, respectively]. In the DOC-salt rats, dietary calcium supplementation did not significantly lower the elevated serum concentration of PTH (from 49 +/- 4 to 40 +/- 4 pg/ml; NS), but did significantly reduce that of 1,25-D (from 108 +/- 7 to 66 +/- 8 pg/ml; P less than 0.01). Since 1,25-D may increase vascular smooth muscle calcium uptake, dietary calcium supplementation may lower blood pressure in DOC-salt hypertension, in part, by suppressing 1,25-D.
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PMID:Effect of dietary calcium supplementation on blood pressure and calciotropic hormones in mineralocorticoid-salt hypertension. 216 85

Some specific features should be taken into consideration when organizing the laboratory of pathology in the cardiosurgical centre: 1) the heart should be opened according to the modified van Pragh method; 2) heart fixation in the Brodie's liquid allowing to retain its almost natural colour, consistency, volume and shape; 3) coronary arteries filling with lead carbonate and gelatin; 4) combination of methods of both pathology and surgical anatomy; 5) investigation of the brain in the vacuum in all clinical cases of the brain coma for the diagnosis of brain artery air embolism; 6) anatomical examination of the heart conductive system; 7) formation of the automatized pathology archives; 8) transmission electron microscopy of the intraoperative heart biopsies; 9) a new method of a quantitative assessment of the lung hypertension by the investigation of lung biopsies in patients with congenital heart malformation to make a conclusion on the feasibility of operation; 10) macroscopical heart analysis at the first stage of morphological investigation.
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PMID:[Experience with the organization of a pathological anatomy laboratory in a heart surgery center]. 228 88

A diet fortified with calcium carbonate has been reported to reduce blood pressure in low-renin and salt-sensitive hypertensive patients. We have therefore examined the effect of increased dietary calcium on the development of reduced renal mass-saline hypertension in rats, a classical, low-renin, volume, and sodium-dependent model of hypertension. Rats with 70-75% reduction in renal mass were divided into experimental and control groups. The experimental rats were fed a sodium-free diet supplemented with calcium carbonate (2.0% calcium) and drank 1% saline for 5 weeks. Control rats consumed the salt-free diet and drank 1% saline for the same period. In control rats, as previously observed, blood pressure progressive increased from a control value of 120.0 +/- 1.2 to 174.2 +/- 1.2 mm Hg by the fifth week. In contrast, in the calcium-supplemented rats the development of hypertension was significantly attenuated; the blood pressure only increased from 117.0 +/- 1.2 to 134.0 +/- 3.8 mm Hg by the fifth week. This was associated with a 30% decrease in saline intake by the fifth week, with proportionate decreases in urine volume and sodium excretion but not potassium excretion. Urinary magnesium excretion increased. No such changes were seen in control rats. At the end of the treatment period, plasma levels of sodium, potassium, calcium, creatinine, BUN, and protein were not different, but plasma chloride and magnesium were lower in experimental rats; vascular smooth muscle cell membrane potentials were also not different. These data show that dietary calcium carbonate can attenuate the development of reduced renal mass-saline hypertension in the rat, possibly in part by altering sodium and water intake.
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PMID:Effect of increased dietary calcium on the development of reduced renal mass saline hypertension in rats. 230 5

To examine the effects of dietary calcium supplementation on systemic and renal hemodynamics and glomerular injury in experimental hypertension, rats with desoxycorticosterone-salt hypertension were fed either standard chow, containing 1% calcium by weight, or chow supplemented with calcium carbonate to achieve a calcium content of 2% by weight. Ingestion of calcium carbonate failed to reduce systemic blood pressure, but was associated with increased proteinuria and morphologic evidence of glomerular injury. Micropuncture studies revealed that afferent arteriolar resistance was reduced and glomerular capillary pressure further increased in the high calcium group. Thus, calcium carbonate, in moderate amounts, not only failed to ameliorate systemic hypertension but, paradoxically, worsened intrarenal hypertension and injury in rats with mineralocorticoid-induced hypertension.
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PMID:Calcium carbonate exacerbates glomerular capillary hypertension and injury in rats with desoxycorticosterone-salt hypertension. 236 95

Chronic infusion of d-aldosterone into uninephrectomized rats on high sodium intake resulted in a significant increase in systolic blood pressure. The steady state efflux of 36Cl in aorta and femoral artery of hypertensive rats was significantly elevated compared to that in arteries of control rats. These elevations in chloride efflux persisted in the presence of the Cl-HCO3 exchange inhibitor, 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (DIDS), and in Cl-HCO3 free solution. The Cl-HCO3-dependent component of the 36Cl efflux was also higher under some conditions. DIDS (100 mumol/l), also significantly reduced the increase in 36Cl efflux caused by norepinephrine (NE) in one of four groups, but had no significant effect on the NE stimulated 42K efflux. Contractile responses to both NE and KCl were unaffected by DIDS treatment. Therefore, it appears that Ca influx and release mechanisms function normally in the presence of DIDS. Similarly, DIDS had either a small or no effect on 42K movements under basal conditions. A slight reduction in the passive efflux of 24Na was observed in aortic smooth muscle exposed to DIDS with no significant effect on active Na transport. These findings indicate that DIDS is reasonably selective for Cl exchange sites in vascular smooth muscle during an exposure of 15 min or less and has little effect on cationic transport processes. The application of this blocker as well as anion substitution indicates that an elevation in the 36Cl leak efflux and related Cl permeability of arterial smooth muscle is associated with aldosterone-salt hypertension.
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PMID:Altered chloride transport in arteries from aldosterone salt-hypertensive rats. 245 89

A 23-year old woman developed headache and papilledema due to benign intracranial hypertension (BIH) while taking lithium carbonate for only seven months because of manic-depressive disease. Having discarded other causes, drug ingestion was the most likely etiology of the syndrome since it was observed that symptoms improved upon lithium withdrawal and worsened when the treatment was restarted. This report shows that BIH may appear as a side-effect of relatively short-term therapy with lithium and, therefore, funduscopic exams should be performed in every patient receiving this drug.
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PMID:Lithium-induced headache. 249 83


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