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

The authors report the values of mean hemispheric blood-flow and cerebral arterial consumption they found in 34 neurosurgical comatous cases in acute state. In basal conditions, mean values of mean hemispheric bloodflow and oxygen consumption are lowered. There seems to be a relation between the values found and the comatous stage on one hand, the prognosis on the other hand. The cerebral response to hypercapnia (16 assays) allows to separate 2 groups, one with a noticeable improvement of cerebral bloodflow, the other with only a minimal response. There was no significant variation of cerebral oxygen consumption in both group. Cerebral response to CO2 seems to be clearly related to the stage of coma (low in the most severe cases) but pronostic incidence remained uncertain. A hypertensive test by means of Aramine (18 assays) allows to separate 3 groups : 1 group (8 cases) where the mean hemispheric bloodflow remained stable during hypertension as did the cerebral oxygen consumption -(autoregulation remained unchanged), 1 group (4 cases) where mean hemispheric bloodflow and cerebral oxygen consumption were lowered (excessive autoregulation), 1 group (6 cases) where mean hemispheric bloodflow increases clearly while under Aramine perfusion (loss of autoregulation). Those dynamic tests, either hypercapnic or hypertensive, allow, in comparing oxygen consumption variations with cerebral bloodflow variations, the distinction between : patients where metabolic autoregulation seems maintained (good prognosis) - (10 cases), patients where metabolic regulation is lost with either "luxury perfusion" (14 cases) - poor prognosis, or "insufficient perfusion" (10 cases). The authors are discussing the treatment concerning those last mentioned patients.
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PMID:[Value of cerebral metabolic exploration in post-traumatic coma states in the acute phase]. 1 86

The present studies were performed in order to determine whether "filtration edema" will develop as a consequence of cerebral vasoparalysis, vasoparalysis in combination with arterial hypertension or arterial hypertension alone. A series of dogs, anaesthetised with i.v. Chloralose-Urethane were exposed 1) to cerebral vasoparalysis, produced by hypercapnia (PaCO2 about 150 mm Hg) and hypoxaemia (PaO2 40-60 mm Hg); 2) to arterial hypertension and 3) to a combination of cerebral vasoparalysis and arterial hypertension. Following cerebral vasoparalysis and arterial hypertension, a significant decrease of total cerebrovascular resistance and moderate increase of venous resistance was observed. Regional cerebral blood flow (133Xe), intracranial pressure, as well as the pressure in postcapillary venous outflow (sinus sagittalis wedge pressure and confluence sinuum pressure) were increased. Neither normotonic vasoparalysis nor vasoparalysis in combination with slight arterial hypertension (MABP more than 90 min above 180 mm Hg) resulted in cerebral edema. In contrast, cerebral vasoparalysis in combination with severe arterial hypertension (MABP more than 90 min above 220 mm Hg) resulted in a statistically significant increase in the water content in the white matter without evidence of protein extravasation. Multiple small foci of Evans blue extravasates, however, were found in the cortex following arterial hypertension in combination with vasodilation, indicating a damage of the blood brain barrier. In these blue stained cortical areas the water content was significantly in creased. The following conclusions were drawn from the results. Vasoparalysis during normotension does not produce brain edema despite the slightly elevated hydrostatic pressure gradient between intravasal and extracellular space. Only considerable increase of this hydrostatic pressure gradient caused by a combination of vasoparalysis with severe arterial hypertension is able to produce brain edema in the white matter. In addition, acute hypertension may cause minor multifocal damage of the blood brain barrier in the cerebral cortex. It is concluded that so-called brain swelling, which has been described by several authors in states of cerebral vasoparalysis, is not predominantly caused by brain edema but by vascular congestion. The clinical aspects of the result are discussed.
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PMID:[Cerebral vasoparalysis, arterial hypertension and brain edema (author's transl)]. 5 29

In a group of 21 cats, the middle cerebral artery pressure (MCAP) was recorded by means of a catheter introduced into the artery at its origin, just distal to the occlusion. The effects of hypertension, hypercapnia, and hypocapnia were studied. In a group of five cats, both middle cerebral arteries (MCA) were catherized and the pressure was recorded simultaneously on both sides. In another group of five cats, O2 tension measurements were made with the aid of oxygen electrodes in the brain tissue, the occluded MCA, and the common carotid artery. Some of the results obtained in this study are compared with the results of a previous study where monkeys were used as experimental animals.
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PMID:Haemodynamic changes in the cerebral circulation of the cat during occlusion of the middle cerebral artery. 10 Oct 24

Hypercarbia was induced in 12 patients anesthetized with either halothane or fluroxene in an inspired concentration of approximately 1.3 MAC (1% halothane and 4-5% fluroxene). The six patients receiving halothane anesthesia responded to hypercarbia with a pronounced tachycardia, an increased arterial pressure and an electrocardiographically monitored threshold level for ventricular arrhythmias at a Paco2 level averaging 98 mmHg. The six patients receiving fluroxene anesthesia responded to hypercarbia with both tachycardia and hypertension, but in spite of an average Paco2 level of 109 mmHg, no ventricular arrhythmias could be provoked. It is therefore suggested that within the non-narcotic level of hypercarbia a threshold level for cardiac arrhythmias does not exist under fluroxene anesthesia.
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PMID:Effects of respiratory acidosis on the arrhythmia threshold during fluroxene and halothane anesthesia. 23 95

Sixty patients out of 1,844 recovery room admissions had significant postoperative arterial hypertension. Nearly 60% of them had a history of hypertension. The postoperative hypertension usually began within 30 min from the end of operation and lasted about 2 hours. In 20% of the patients it lasted 3 hours or longer. Complications attributable to hypertension were confined to this latter group. The principal factors possibly contributing to the pressure elevations were pain (35%), hypercarbia (15%) and emergence excitement (16%). Ten of the patients (17%) had no demonstrable cause for hypertension. The hypertension in this group appeared to have a shorter and more benign course.
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PMID:Hypertension in the immediate postoperative period. 23 47

The effects of an acute cryogenic injury on cerebral flow (CBF) and cerebral vascular reactivity were studied in 12 anaesthetised, ventilated baboons. Autoregulation, defined in this study as intact with a greater than 20% change in cerebrovascular resistance in response to a change in cerebral perfusion pressure, was tested before the lesion by arterial hypotension. Intact autoregulation was found in half the animals, but all animals showed an increase in CBF with hypercarbia. The cryogenic lesion was followed by a marked rise in intracranial pressure, and a fall in CBF which was only partly related to the status of autoregulation beforehand. After injury, arterial hypertension caused an increase in cerebrovascular resistance of more than 20% in half the animals. This response was not related to the presence of autoregulation before the lesion, and was accompanied by a greater impairment of the cerebrovascular response to carbon dioxide, more severe brain oedema, and lower cerebral oxygen consumption, than in the remaining baboons which had a pressure passive response to arterial hypertension. This study confirms that the failure of CBF to increase with arterial hypertension may indicate severe brain damage rather than intact physiological autoregulation.
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PMID:Vascular reactivity in the primate brain after acute cryogenic injury. 41 85

Cerebral blood flow autoregulation (CBFA) to changes in perfusion pressure has not been previously reported in the rat. A modification of the Kety and Schmidt technique employing 133Xenon was used to measure cerebral blood flow (CBF) in paralyzed adult Sprague Dawley rats passively ventilated with 70% nitrous oxide and 30% oxygen. At a mean arterial blood pressure (MABP) of 121 +/- 19 mm Hg, and a mean arterial PCO2 of 36.2 +/- 2.9 mm Hg, mean CBF was 103 +/- 22 ml/min/100 gm of brain. CBF responses to hypercarbia were 4.9 ml/min/100 gm per mm Hg change in arterial PCO2. CBF was measured during steady state levels of hypo- and hypertension induced by phlebotomy, or by intravenous metaraminol, over the MABP range of 48-205 mm Hg. From a MABP of 80 to 160 mm Hg. CBF remained nearly constant, indicating the presence of CBFA. However, when MABP exceeded 160 mm Hg, CBF became pressure dependent, indicating a "breakthrough" of autoregulation in acute severe hypertension.
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PMID:Cerebral blood flow autoregulation in the rat. 64 8

Paroxysmal hypertension occurred during the first 8 hours after cardiac valve replacement in 15 of 186 consecutive patients. The clinical characteristics of this hypertension were similar to those of hypertension after myocardial revascularization, except that this complication occurred much less frequently after valve replacement (8.1%) than after myocardial revascularisation (33%) (P less than 0.001). Hypertension resulting from hypoxia, hypercapnia, shivering, or arousal from anaesthesia was excluded from consideration. The rise in systemic arterial pressure (average 34/35 mmHg +/- 4.9/4.3 SE) was usually associated with a reduction in central venous pressure (12/15 patients) and a mild increase (2 to 4 cm saline) in left atrial pressure. The incidence of hypertension was not related to the valve replaced (aortic or mitral), type of lesion (stenosis or regurgitation), preoperative level of blood pressure, or use of hypothermia during operation. However, none of the 18 patients who had double valve replacement showed significant rise in blood pressure after operation. It is suggested that these hypertensive episodes may be related to pressor reflexes from the heart and/or great vessels.
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PMID:Arterial hypertension in immediate postoperative period after valve replacement. 68 68

In 7 baboons and 5 macaques the effects of hypercapnia, hypocapnia, hypertension, and combinations of hypertension plus hypocapnia and of hypertension plus hypercapnia on the regional perfusion pressure (rPP) in the brain area rendered ischaemic by occlusion of the middle cerebral artery (MCA) were studied. A new technique for recording the pressure in the occluded MCA was used. The regional tissure pressure (rTP) was recorded with the so called wick type pressure transducers. Hypercapnia produced a marked decrease in rPP in the ischaemic brain area. Hypertension, especially in combination with hypocapnia, produced a very pronounced increase in rPP in the ischaemic brain area. The clinical implications of these findings are discussed. Occlusion of the homolateral common carotid artery (CCA) was followed by a very slight and transient drop in the occluded MCA pressure. Occlusion of the occluded MCA pressure.
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PMID:The influence of changes in arterial CO2 and blood pressure on the collateral circulation and the regional perfusion pressure in monkeys with occlusion of the middle cerebral artery. 81 1

In 7 baboons and 5 macaques the effects of hypercapnia, hypocapnia, hypertension, and combinations of hypertension plus hypocapnia and of hypertension plus hypercapnia on the regional perfusion pressure (rPP) in the brain area rendered ischaemic by occlusion of the middle cerebral artery (MCA) were studied. A new technique for recording the pressure in the occluded MCA was used. The regional tissue pressure (rTP) was recorded with the so called wick type pressure transducers. Hypercapnia produced a marked decrease in rPP in the ischaemic brain area. Hypertension, especially in combination with hypocapnia, produced a very pronounced increase in rPP in the ischaemic brain area. The clinical implications of these findings are discussed. Occlusion of the homolateral common carotid artery (CCA) was followed by a very slight and transient drop in the occluded MCA pressure. Occlusion of the contralateral CCA was followed by a marked and persistent drop in the occluded MCA pressure.
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PMID:The influence of changes in arterial CO2 and blood pressure on the collateral circulation and the regional perfusion pressure in monkeys with occlusion of the middle cerebral artery. 81 73


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