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

The role of a sudden increase in brain perfusion on ventral medullary surface pH (Vm pH) and minute ventilation (VI) was assessed in anesthetized peripherally chemo denervated cats. Acute hypertension (AH), produced by rapid inflation of an aortic balloon, and hypoxemia, produced with either inhalation of 1% CO (COHx) or inhalation of a hypoxic gas (HHx), were used to increase brain blood flow. In the AH group, increasing arterial blood pressure (from 122 +/- 3 to 180 +/- 5 mmHg) caused a rapid (less than 5 s) increase in Vm pH in every trial (n = 18). Associated with the mean peak increases in Vm pH (0.003 +/- 0.0004 pH units) were significant decrease in tidal volume (7-9%). In the COHx group, 17% HbCO caused a significant increase in Vm pH (0.003 +/- 0.0005 pH unit) and diminution of VI (9%). Further increases in HbCO caused a progressive ventral medullary acidosis and greater reductions in VI. The results from the HHX group were qualitatively similar to the COHx group; there was a biphasic response of Vm pH, i.e., an initial increase in Vm pH (0.008 +/- 0.001) followed by a steady decrease in Vm pH, with reductions in VI associated with both phases. We conclude that hyperperfusion, per se, produces an increase in Vm pH and a reduction in VI equivalent in magnitude to that predicted from the CO2 stimulus-response curve; the alkalotic shift in Vm pH and concomitant diminution in VI associated with mild hypoxia is probably related to an increase in ventral medullary perfusion; and the ventilatory depression associated with the medullary acidosis of moderate brain hypoxia must be attributed to another mechanism.
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PMID:Ventral medullary pH and ventilatory responses to hyperperfusion and hypoxia. 399 29

The importance of cerebral blood volume (CBV) as a physiological parameter has been well recognized, especially in its relation to the intracranial pressure (ICP). Although various methods have been applied to measure CBV, several problems and difficulties still remain to be settled. In the present study, noninvasive monitoring of CBV on the cortical surface was done with organ reflectance spectrophotometry. Through the cranial window, the cat brain was illuminated by the white light via optical fibers and reflected light was analized by spectrophotometer equipped with microcomputer and image-sensor (Sumitomo Elec. Co., Spectrum analyzer TS-200), which enables to estimate CBV on real time as the absorbance value at the isobestic point of the spectral curve of hemoglobin (Hb). In order to ascertain the reliability and reproducibility, the change of CBV was examined by 5% & 10% CO2 inhalation, 5% O2 inhalation and bilateral jugular vein occlusion. A linear correlation was found between PaCO2 and Hb absorbance value on CO2 inhalation. By the bilateral jugular vein occlusion, Hb increased concomitantly with ICP, while cerebral blood flow (CBF) decreased. On 5% O2 inhalation, absorbance spectral pattern of tissue Hb changed from that of oxy-Hb to deoxy-Hb without change of absorbance value at the isobestic point. Thus, the Hb absorbance value obtained by this spectrophotometer was considered to be reliable for the estimation of CBV on the cortical surface. Using this, the change of CBV was examined on the drug-induced seizure and post-decompression state after sustained intracranial hypertension.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Continuous monitoring of cerebral blood volume in cats using a reflectance spectrophotometer]. 400 77

We tested the hypothesis that in renal hypertension the increased peripheral vascular resistance of neurogenic origin might be due to a reflex through resetting of the carotid body chemoreceptors. The reflex respiratory and cardiovascular functions of the carotid bodies were studied in a one-kidney wrapped hypertension model in conscious rabbits, and compared with a control group of animals, by breathing 100% oxygen, three hypoxic gas mixtures to which were added sufficient CO2 to maintain the PaCO2 constant, and 2 and 4% CO2 in 21% O2 and N2. In the control state (breathing room air) the renal hypertensive animals had a slightly higher respiratory minute volume, a higher level of arterial blood pressure and increased calculated systemic vascular resistance, compared with the normal group, but there was no difference in cardiac output. Hyperoxia had no consistent effect on respiration, heart rate or arterial blood pressure. Increasing degrees of isocapnic hypoxia caused the same degree of hyperventilation and bradycardia in both groups of animals. The arterial blood pressure did not change in either group but there was a transient increase in systemic vascular resistance in the renal hypertensives breathing 9 and 7.5% O2. The respiratory responses to 2 and 4% CO2 were similar in the two groups of animals. In the renal hypertensive animals, serial sections of the carotid bodies showed pathological changes, including subendothelial proliferation in vessels supplying the carotid bodies with narrowing of their lumens, fragmentation of the elastic laminae of the media, hypertrophy of the smooth muscle and extensive fibrosis with occasional haemorrhages. The capillaries, however, were normal. The rostral-caudal lengths of the carotid bodies were similar in the two groups. In view of our findings we conclude that the relatively normal carotid chemoreceptor responses in renal hypertensive rabbits may, in part at least, be the result of the carotid body blood flow through the partially occluded vessels being maintained at near normal levels by the elevated blood pressure.
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PMID:Respiratory and cardiovascular responses to hyperoxia, hypoxia and hypercapnia in the renal hypertensive rabbit: role of carotid body chemoreceptors. 402 Jan 28

Blood pressure, heart rate and evoked cardiovascular reflexes were examined in cats following chronic treatment with haloperidol, at a dose of 1 mg kg-1 per day, orally for 23 days. Five days after the final dose the animals were anaesthetized and tested for their reaction to various cardiovascular stimuli and to a number of agonist and antagonist drugs, given both intravenously and into the vertebral artery. It was found that treatment with haloperidol caused hypertension in the cats, as well as a potentiation of the pressor response to bilateral carotid occlusion. The response to 30 degrees head-up tilting was also altered so that in treated cats, the blood pressure returned to normal more rapidly during the tilt. There was no difference in the heart rate of the two groups of cats, nor in the pressor response to intravenous noradrenaline or angiotensin II or to afferent brachial nerve stimulation, nor was the depressor action of bradykinin altered. Hexamethonium reduced the blood pressure in both control and treated cats to approximately the same level. Blood O2, CO2, pH and bicarbonate levels were also unaltered by the treatment, as was plasma renin activity. Of the drugs given into the vertebral artery, only noradrenaline, prazosin, ketanserin and haloperidol caused a significantly greater fall in blood pressure in treated than in control cats, while clonidine and St91 were equally effective in both groups. These results suggest that haloperidol treatment has caused a greater modulation of central alpha 1- than of alpha 2-adrenoceptors.
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PMID:The effect of chronic haloperidol treatment on some cardiovascular parameters in cats. 406 87

The mechanisms of metabolic acidosis and hyperkalemia were investigated in a patient with chronic mineralocorticoid-resistant renal hyperkalemia (5.3 to 6.8 mM), metabolic acidosis (arterial blood pH 7.27, total CO2 17 mM), arterial hypertension, undetectable plasma renin activity (less than 0.10 ng/ml/hr), high plasma aldosterone (32 to 100 ng/dl), normal GFR (131 +/- 2.5 ml/min/1.73 m2). During hyperkalemic period, urine was highly acidic (pH 4.6 to 5.0), urinary NH4 excretion (13 mumoles/min) and urinary net acid excretion (24 mumoles/min) were not supernormal as expected from a chronic acid load. During NaHCO3 infusion, maximal tubular HCO3 reabsorption (Tm HCO3) was markedly diminished (19 mmoles/liter GF), fractional excretion of HCO3 (FE HCO3) when plasma HCO3 was normalized, was 20%. Urine-minus-blood PCO2 increased normally (31 mmHg) during NaHCO3 infusion, and urinary pH remained maximally low (less than 5.3) when buffer urinary excretion sharply increased after NH4Cl load. When serum K was returned toward normal limits, metabolic acidosis disappeared, urinary NH4 excretion rose normally after short NH4Cl loading while urinary pH remained maximally low (4.9 to 5.2), Tm HCO3 returned to normal value (24.8 mmoles/liter GF), and FE HCO3 became nil. The renal handling of K was improved with acute NaHCO3 loading and normalized after DDAVP nasal insufflation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Type II pseudohypoaldosteronism: proximal tubular acidosis and distal tubular hyperkalemia corrected by DDAVP]. 408 72

Early systemic hemodynamic adjustments to antihypertensive therapy with the cardioselective beta inhibitor, atenolol, were investigated in 12 hospitalized men, mean age 52 years, with uncomplicated mild-to-moderate essential hypertension. Twice daily measurements of cardiac output (CO) by CO2 rebreathing, blood pressure by cuff, and heart rate were performed in all subjects for 3 days before and 5 days after initiation of oral atenolol therapy (50 or 100 mg daily). Cardiac output by CO2 rebreathing was checked with dye dilution just before, and 4 hours and 4 days after the start of therapy. Plasma volume (radioiodinated albumin) was measured before therapy and on Day 5 of therapy. The CO results obtained with the two methods were not significantly different (r = 0.88, p less than 0.01, n = 12). A reduction in heart rate, 18 +/- 2 beats/min (mean +/- SE), occurred in all patients while taking atenolol. By 4 hours after the first dose of atenolol, CO fell from 5.49 +/- 0./30 to 4.24 +/- 0.21 liters/min (p less than 0.01), while the control mean arterial pressure (MAP) of 108 +/- 4 mm Hg was not significantly changed, 110 +/- 4 mm Hg. At 24 hours, CO returned near baseline (5.10 +/- 0.21 liters/min) but MAP was reduced (95 +/- 3 mm Hg, p less than 0.001) and remained so thereafter. CO remained at baseline at 48 hours (5.50 +/- 0.29 liters/min) but fell again (p less than 0.01) to 4.81 +/- 0.11 on Day 4 and to 4.68 +/- 0.25 liters/min on Day 5 of atenolol therapy. Plasma volume, 3110 +/- 100 ml before therapy, was reduced to 2850 +/- 100 by Day 5 of atenolol therapy (p less than 0.01). The findings indicate a delayed onset of the antihypertensive action of atenolol. The transient return to baseline of CO on Day 2 and 3 of atenolol therapy suggests a reverse autoregulatory adjustment to the initial fall in CO.
Hypertension
PMID:Short-term systemic hemodynamic adaptation to beta-adrenergic inhibition with atenolol in hypertensive patients. 611 32

The vessel wall tension is the product of pressure and internal radius divided by the vessel wall thickness. Hence, dilated vessels will be exposed to higher tension at a given intraluminal pressure. Provided the rise in cerebrovascular intraluminal pressure is sufficiently prominent, transient opening of the morphologic blood-brain barrier will occur. In the present study pressure increase, not sufficient in itself to cause barrier opening, was induced. However, at concomitant dilatation of the vessels--as induced by CO2 or papaverine--under otherwise identical pressure conditions a barrier opening was obtained. Hence, vasodilatation of cerebral vessels will increase their vulnerability to hypertension.
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PMID:Vasodilatation augments the blood-brain barrier lesions induced by an acute rise in intracarotid pressure. 616 93

Although it is known that hypercarbia increases and benzodiazepines decrease cerebral blood flow (CBF), the effects of benzodiazepines on CBF responsiveness to CO2 are not well documented. The influence on CBF and CBF-CO2 sensitivity of placebo or midazolam, which is a new water-soluble benzodiazepine, was measured in eight healthy volunteers using the noninvasive 133Xe inhalation method for CBF determination. Under normocarbia, midazolam decreased CBF from 40.6 +/- 3.2 to 27.0 +/- 5.0 ml 100 g-1 min-1 (means +/- SD). At a later session under hypercarbia, CBF was 58.8 +/- 4.4 ml 100 g-1 min-1 after administration of placebo, and 49.1 +/- 10.2 ml 100 g-1 min-1 after midazolam. The mean of the slopes correlating PaCO2 and CBF was significantly steeper with midazolam (2.5 +/- 1.2 ml 100 g-1 min-1 mm Hg-1) than with placebo (1.5 +/- 0.4 ml 100 g-1 min-1 mm Hg-1). Our results suggest that midazolam may be a safe agent to use in patients with intracranial hypertension, since it decreases CBF and thus cerebral blood volume; however, it should be administered with caution in nonventilated patients with increased intracranial pressure, since its beneficial effects on cerebrovascular tone can be readily counteracted by the increase in arterial CO2 tension induced by this drug.
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PMID:Effects of midazolam on cerebral hemodynamics and cerebral vasomotor responsiveness to carbon dioxide. 640 14

The question of the significance of the cerebrovascular effects of stressful situations in animals is still controversial. In the present article, an experimental model of immobilization stress in the rabbit is described, and its specificity in relation to arterial blood pressure and PaCO2 is investigated. CBF was measured with the multiregional tissue sampling technique using [14C]-ethanol as tracer. After dissipation of althesin anesthesia, the stress reaction was elicited by tactile abdominal stimuli. The response was evidenced by an instantaneous acute hypertension (+33.8% during the CBF measurement period). Within the first minute of the reaction, the CBF was significantly increased in all nine structures studied by 39% (caudate nucleus) to 82% (parieto-temporal cortex). The study of the influence of arterial blood pressure and the PaCO2 on CBF showed that cerebrovascular autoregulation and CO2 sensitivity were differently affected in the various structures during the stress reaction. However, the stress response of the brain circulation could not be entirely ascribed to one or both of these two systemic factors, thus suggesting the contribution of a local intrinsic activation. The model presented here could be useful for long-term studies of cerebrovascular repercussions of repeated acute hypertensions of a stressful nature.
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PMID:Significance of the cerebrovascular effects of immobilization stress in the rabbit. 643 9

In pentobarbital-anesthesized cats, bolus i.v. injections of sodium azide produced dose-dependent transient hypotension accompanied by a modest tachycardia and a brief hyperpnea. Intracerebroventricular injections of azide elicited graded effects similar to the i.v. doses, but the responses were slower in onset and could be delayed by occluding the cranial blood supply. This is interpreted to mean that intracerebroventricular azide acts systematically after escaping from the cerebrospinal fluid into the bloodstream. The hypotensive response to i.v. azide was not affected by cholinergic or adrenergic blockade or buffer nerve section. The tachycardia was blocked by sympathetic neural blockade or buffer nerve section indicating that it is a baroreflex response to the vasodepressor effect. Respiratory effects of bolus i.v. azide occurred independently of the hypotensive response and were abolished by peripheral chemodenervation. Infusion of azide facilitated CO2-tidal volume responsiveness in the steady state, an effect that was essentially eliminated by carotid sinus neurotomy. The azide did not affect the tidal volume-respiratory frequency relationship mediated by the pulmonary stretch receptors. Thus, the respiratory stimulant effect of azide in subtoxic doses is attributable to an excitatory action on the arterial chemoreceptors. Toxic doses of azide resulted in centrally mediated hypertension, tachycardia, cardiac arrhythmia, respiratory depression, seizures and death.
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PMID:Peripheral and central actions of sodium azide on circulatory and respiratory homeostasis in anesthesized cats. 643 70


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