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Query: UMLS:C0020440 (hypercapnia)
 7,939 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Acute severe hypertension induced by intravenous norepinephrine or angiotensin in anesthetized cats equipped with a cranial window caused prolonged arteriolar vasodilation associated with reduced responsiveness to arterial hypercapnia or hypocapnia and passive response to changes in arterial blood pressure. Scanning and transmission electron microscopy of such pial arterioles showed discrete destructive endothelial lesions the density of which correlated with the degree of vasodilation. Abnormalities of the vascular smooth muscle were seen in all dilated arterioles but affected only a small number of smooth muscle cells. The oxygen consumption of pial arterioles from cats subjected to hypertension was significantly reduced in comparison to that of vessels from normal animals. The arteriolar abnormalities induced by hypertension were inhibited by pretreatment with inhibitors of cyclooxygenase (indomethacin or AHR-5850) or by topical application on the brain surface of scavengers of free oxygen radicals (mannitol or superoxide dismutase). The results suggest that the mechanism of the arteriolar abnormalities from acute hypertension involves a sudden increase in prostaglandin synthesis that leads to generation of free oxygen radicals.
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PMID:Mechanism of cerebral arteriolar abnormalities after acute hypertension. 722 3

We have developed a method for virtually continuous measurement of changes in cerebral blood flow (CBF) in cats and dogs. CBF was computed by multiplying cross-sectional area (CSA) and mean blood velocity in a pial artery. CSA was determined by measuring pial artery diameter with an electronic micrometer every 2-4 s through a cranial window. Velocity was measured continuously with a pulsed Doppler crystal positioned under a pial artery. CBF was determined in 12 anesthetized cats during 1) control, 2) hypocapnia, 3) hypercapnia, and 4) hypercapnia plus hypertension. Microspheres were injected under steady-state conditions to compare the two methods. During control, the diameter of the cerebral arteries observed was 388 +/- 28 (SE) micrometers, and CBF measured with microspheres was 40 +/- 4 ml.min-1.100 g-1. CBF decreased 18 +/- 2% during hypocapnia and increased 152 +/- 36% during hypercapnia. During steady-state conditions, the correlation coefficient between changes in CBF (CSA X velocity and microspheres) was 0.94, and the slope of the regression line was 1.02. In similar studies on seven anesthetized dogs, the correlation coefficient between CSA X velocity and microspheres was 0.98, and the slope of the regression line was 0.94. We conclude that the product of CSA and blood velocity of a pial artery provides accurate on-line measurement of changes in CBF.
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PMID:Continuous measurement of cerebral blood flow in anesthetized cats and dogs. 727 Jul 11

High incidence of postoperative arterial hypertension, confined to the first 24-48 hours and independent of the preoperative pressure situation, has been noted in patients following vascular surgery. The phenomenon is more frequent in patients whose angiosclerotic symptomatology goes back more than 2 years, and in those in whom preoperative investigation showed high daily variability in measured values, always however within non-pathological limits. Analysis of possible intraoperative pathogenetic factors in postoperative hypertension reveals a significant relationship between this phenomenon and inhalatory anesthesia, particularly with fluothane and curarization with D-tubocurarine. Co-responsibility of respiratory factors, particularly hypercapnia, has never been documented by haemogasanalysis. As for the pathogenetic mechanisms responsible for this type of hypertension, measurement of urinary catecholamines has revealed a close relationship between the two phenomena. The same investigation, extended to a wider group of patients, showed that by comparison with patients submitted to balanced anaesthesia, those who had received inhalatory anaesthesia with fluothane show, with much greater frequency, increased urinary elimination of catecholamines during the operation and for 24-48 hours afterwards. Catecholaminic hyperincretion, more frequent in fluothane anaesthesia, thus seems to be an important pathogenetic factor in these hypertensive manifestations in which the angiosclerotic medium presumably acts as an amplifier.
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PMID:[Postoperative hypertension in the surgery of the large arteries]. 733 78

Superior sagittal sinus pressure, intracranial pressure and arterial pressure were recorded in an experimental series on 10 cats. During drug-induced, severe, acute arterial hypertension and parallel hypercapnia, venous pressure could exceed intracranial pressure in both the supra- and infratentorial compartment. From these data it is concluded that cerebral venous pressure during acute arterial hypertension may contribute to protein extravasation at the postcapillary-venular level.
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PMID:Cerebral venous pressure during actively induced hypertension and hypercapnia in cats. 736 47

In twelve anaesthetised, ventilated dogs the effects of hypercapnia and pharmacologically induced arterial hypotension and hypertension on the interrelation between volume-pressure response (VPR) and cerebro-spinal fluid (CSF) pulse pressure were studied during continuous inflation of a supratentorial extradural balloon. Hypercapnia did not significantly affect the intracranial volume-pressure relationships, but did cause a significant increase in gradient of the relationship between CSF pulse pressure and intracranial pressure (ICP). Alteration of the arterial blood pressure showed opposite effects on VPR and CSF pulse pressure. A decrease in VPR and an increase in pulse pressure were observed during arterial hypotension; the reverse was found during arterial hypertension. The discrepancy between the effects on VPR and CSF pulse pressure of the variables under study was explained by changes in the transient increase in cerebral blood volume per cardiac cycle. On the basis of the results of this study it will be possible, during clinical ICP monitoring, to interpret changes in the CSF pulse pressure to ICP ratio in terms of changes in intracranial volume-pressure relationships.
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PMID:Effects of hypercapnia and arterial hypotension and hypertension on cerebrospinal fluid pulse pressure and intracranial volume-pressure relationships. 737 19

To test the hypothesis that concussive brain injury autoregulation of cerebral blood flow (CBF), 24 cats were subjected to hemorrhagic hypotension in 10-mm Hg increments while measurements were made of arterial and intracranial pressure, CBF, and arterial blood gases. Eight cats served as controls, while eight were subjected to mild fluid percussion injury of the brain (1.5 to 2.2 atmospheres) and eight to severe injury (2.8 to 4.8 atmospheres). Injury produced only transient changes in arterial and intracranial pressure, and no change in resting CBF. Impairment of autoregulation was found in injured animals, more pronounced in the severe-injury group. This could not be explained on the basis of intracranial hypertension, hypoxemia, hypercarbia, or brain damage localized to the area of the blood flow electrodes. It is, therefore, concluded that concussive brain injury produces a generalized loss of autoregulation for at least several hours following injury.
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PMID:Autoregulation of cerebral blood flow after experimental fluid percussion injury of the brain. 742 Jan 72

Pial arterial vessels were inspected in hypercapnia (PaCO2 97 +/- 9 (S.E.) mmHg) and in acute hypertension induced by 5 microgram kg-1 noradrenaline i.v. (mean arterial pressure 210 +/- 5 mmHg) by means of a cranial window. The diameter of arterial vessels with a resting diameter of 10 to 150 micrometer was measured either from photographs or by aid of an image splitting eyepiece. Arterioles with a resting diameter less than or equal to 30 micrometer exhibited the highest degree of dilatation both in hypercapnia and acute hypertension. The mean dilatation was higher in hypertension than in hypercapnia in vessels of all sizes, the difference being statistically significant in arterioles up to 50 micrometer resting diameter.
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PMID:Dilatation of pial arterial vessels in hypercapnia and in acute hypertension. 744 69

In order to assess the influence of severe hypoglycemia on local cerebral blood flow (1-CBF) artificially ventilated rats, maintained on 70% N2O, were injected with insulin to provide either an EEG pattern of slow-wave polyspikes, or cessation of spontaneous EEG activity for 5, 15 or 30 min ("coma"). In other animals, glucose was injected at the end of a 30 min period of "coma" and 1-CBF was measured after recovery periods of 5, 30, 90, or 180 min. Local CBF was measured autoradiographically with 14C-iodoantipyrine as the diffusible tracer. In the slow-wave polyspike period 1-CBF was increased in most of the structures studied, and reached values that were 1.4 to 3.2 times greater than control. In many structures, cessation of EEG activity was accompanied by a further increase in 1-CBF, with some structures (thalamus, hypothalamus, pontine gray, and cerebellar cortex) showing flow rates of 400--500% of control. The increase in 1-CBF was unrelated to arterial hypertension, hypercapnia, or hypoxia. 5 min after glucose injection the hyperemia persisted in only some of the structures studied; in others, the 1-CBF were close to, or below, control values. During the subsequent recovery period 1-CBF was markedly reduced with some structures (cerebral cortical areas, hippocampus, and caudate-putamen) showing flow rates of only 20--35% of control. In others, notably pontine gray and cerebellar cortex, secondary hypoperfusion was never observed. The hypoperfusion was unrelated to arterial hypertension, hypocapnia, or increase in intracranial pressure. It is concluded that, like hypoxia and ischemia, substrate deficiency due to hypoglycemia is accompanied by vasodilatation in the brain. Furthermore, like long-lasting ischemia, severe hypoglycemia is followed by a delayed hypoperfusion syndrome that, by restricting oxygen supply, may well contribute to the final cell damage incurred.
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PMID:Local cerebral blood flow in the rat during severe hypoglycemia, and in the recovery period following glucose injection. 744 74

Spontaneous hypertensive rats (SHR) are less prone to develop a dysfunction of the blood-brain barrier (BBB) when exposed to an abrupt increase in blood pressure than normotensive rats (NR), probably as a result of vessel wall hypertrophy and increased vessel wall to lumen ratio. Hemodynamic studies have indicated that structural adaptation develops early as a response to the increased pressure load in renal hypertensive rats (RHR). In the present study RHR (one renal artery constricted and the contralateral kidney intact) were subjected to acute hypertension induced by bicuculline, a drug that induces an abrupt increase in blood pressure concomitant with pronounced cerebral vasodilatation. Protein leakage in the brain, as indicated by Evans blue-albumin and 125IHSA (human serum albumin) extravasation, was not reduced in RHR compared to NR. The cerebrovascular permeability was slightly but significantly (p < 0.01) increased in RHR even in the absence of further blood pressure manipulation. No neurological symptoms were observed in conscious RHR when the BBB dysfunction was aggravated by hypercapnia. The increased cerebrovascular permeability in RHR cold be due to a lower degree of structural adaptation in RHR compared to SHR and/or to some permeability-increasing humoral factor in renal hypertension.
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PMID:The blood brain barrier in renal hypertensive rats. 744 83

Tissue oxygen tension of the cervical cord was measured by the polarographic technique described in the preceding paper on dogs whose cervical cords had sustained combined compression and ischemia. Both hypercarbia and systemic hypertension elevated the tissue oxygen of the cord effectively even at the compressed and ischemic segments, and their effects were additive. Clinical applicability of combined hypercarbia and hypertension to the treatment of ischemia of the human cord was suggested.
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PMID:Effect of hypercarbia and hypertension on spinal cord tissue oxygen in experimental cervical myelopathy. 745 64


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