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Query: UMLS:C0085383 (hypocapnia)
 1,697 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Autoregulation of blood flow denotes the intrinsic ability of an organ or a vascular bed to maintain a constant perfusion in the face of blood pressure changes. Alternatively, autoregulation can be defined in terms of vascular resistance changes or simply arteriolar caliber changes as blood pressure or perfusion pressure varies. While known in almost any vascular bed, autoregulation and its disturbance by disease has attracted particular attention in the cerebrovascular field. The basic mechanism of autoregulation of cerebral blood flow (CBF) is controversial. Most likely, the autoregulatory vessel caliber changes are mediated by an interplay between myogenic and metabolic mechanisms. Influence of perivascular nerves and most recently the vascular endothelium has also been the subject of intense investigation. CBF autoregulation typically operates between mean blood pressures of the order of 60 and 150 mm Hg. These limits are not entirely fixed but can be modulated by sympathetic nervous activity, the vascular renin-angiotensin system, and any factor (notably changes in arterial carbon dioxide tension) that decreases or increases CBF. Disease states of the brain may impair or abolish CBF autoregulation. Thus, autoregulation is lost in severe head injury or acute ischemic stroke, leaving surviving brain tissue unprotected against the potentially harmful effect of blood pressure changes. Likewise, autoregulation may be lost in the surroundings of a space-occupying brain lesion, be it a tumor or a hematoma. In many such disease states, autoregulation may be regained by hyperventilatory hypocapnia. Autoregulation may also be impaired in neonatal brain asphyxia and infections of the central nervous system, but appears to be intact in spreading depression and migraine, despite impairment of chemical and metabolic control of CBF. In chronic hypertension, the limits of autoregulation are shifted toward high blood pressure. Acute hypertensive encephalopathy, on the other hand, is thought to be due to autoregulatory failure at very high pressure. In long-term diabetes mellitus there may be chronic impairment of CBF autoregulation, probably due to diabetic microangiopathy.
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PMID:Cerebral autoregulation. 220 48

The treatment of cerebral edema has changed during recent years. On the one hand, knowledge of the pathophysiology of brain swelling has expanded; on the other, the analysis of biodata such as intracranial pressure, cerebral blood flow, and blood volume has become routine. The methods of measuring intracranial pressure (nowadays without risk due to the use of microtipepidural probes, e.g. Gaeltec) in particular, make it possible to monitor the effects of therapy and enable us to evaluate the different therapeutic measures individually for each patient. Regarding drug treatment, osmotherapy deserves first mention, especially the polyvalent alcohols mannitol and sorbitol, but in spite of possible side effects, glycerin as well. Knowledge of the mechanism of osmotic therapy leads to the proper concept of treatment with bolus administration under control of serum osmolarity and intracranial pressure. Corticosteroids only effectively influence the cerebral edema caused by tumor. The treatment of posttraumatic (and postoperative) cerebral edema is described controversally in the literature. As the side-effects of cortisone therapy are under control, corticosteroids may also be included in the treatment of therapy-resistant cerebral edema. Acting together with sedative drugs, procaine derivatives help to reduce intracranial pressure peaks during intensive care measures. Barbiturates are used as sedatives or in a loading dose until burst suppression is seen in the EEG. The risk of hemodynamic side effects such as reduced cardiac output and cerebral perfusion pressure is decreased by measuring pulmonary arterial pressure and the use of catecholamines. The acidotic impairment of cerebral autoregulation can be regulated using THAM (thrometamine) and the response of the vascular system to hypocapnia can be improved.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Current status of treatment of the cerebral edema]. 311 35

The effect of isoflurane on cerebrospinal fluid pressure (CSFP) was determined in 20 patients undergoing craniotomy for intracranial supratentorial neoplasm or hepatoma. In 15 of these patients, following endotracheal intubation, hyperventilation sufficient to result in PaCO2 25-30 torr was begun simultaneously with the introduction of 1 per cent isoflurane. In the remaining five patients ventilation was equivalent, but normocapnia was maintained by adding CO2 to the inspired gases. In the hypocapnic patients CSFPs did not increase above awake values (range 5-45 torr) following isoflurane administration. In the normocapnic patients (CSFPs consistently increased. In three of these five patients the increases were precipitous, but were corrected rapidly by establishment of hypocapnia. The authors conclude that the known cerebral vasodilator properties of isoflurance can be countered effectively by hypocapnia. Furthermore, unlike the situation with halothane, it is not necessary to establish hypocapnia prior to introducing isoflurane in order to avoid CSFP increases.
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PMID:Isoflurane and cerebrospinal fluid pressure in neurosurgical patients. 678 82

A patient had the rare combination of central neurogenic hyperventilation (PaCO2 of 9 torr) and a normal level of consciousness for eight days. Morphine attenuated but never corrected the hyperventilation. Experimental effects of hypocapnia, which decreases both cerebral blood flow and metabolism in humans, are at odds with the normal mentation initially seen in this patient despite her marked and persistent hypocapnia. Death occurred after progressive brainstem dysfunction. Pathological study showed a well-differentiated astrocytoma involving primarily the medulla and pons, with scattered tumor foci throughout the entire neuraxis. Possible mechanisms for central neurogenic hyperventilation are discussed briefly in relation to the pathological findings and the observed response to morphine.
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PMID:Central neurogenic hyperventilation in an awake patient with brainstem astrocytoma. 681 Jul 46

To study the pathophysiology of idiopathic postoperative brain swelling or hemorrhage after arteriovenous malformation resection, termed normal perfusion pressure breakthrough (NPPB), we performed cerebral blood flow (CBF) studies during 152 operations in 143 patients, using the xenon-133 intravenous injection method. In the first part of the study, CBF was intraoperatively measured (isoflurane/N2O anesthesia) during relative hypocapnia in 95 patients before and after resection. The NPPB group had a greater increase (P < 0.0001) in mean +/- standard deviation global CBF (28 +/- 6 to 47 +/- 16 ml/100 g/min, n = 5) than did the non-NPPB group (25 +/- 7 to 29 +/- 10 ml/100 g/min, n = 90); both arteriovenous malformation groups showed greater increase (P < 0.05) than did controls undergoing craniotomy for tumor (23 +/- 6 to 23 +/- 6 ml/100 g/min, n = 22). Ipsilateral and contralateral CBF changes were similar. In a second cohort of patients with arteriovenous malformations, CBF was measured at relative normocapnia and it increased (P < 0.002) from pre- to postresection (40 +/- 13 to 49 +/- 15 ml/100 g/min, n = 57). There were no NPPB patients in this latter cohort. The feeding mean arterial pressure was measured intraoperatively before resection or at the last embolization before surgery (n = 64). The feeding mean arterial pressure (44 +/- 16 mm Hg) was 56% of the systemic arterial pressure (78 +/- 12 mm Hg, P < 0.0001) and was not related to changes in CBF from pre- to postresection. There was an association between increases in global CBF from pre- to postresection and NPPB-type complications, but there was no relationship of these CBF changes to preoperative regional arterial hypotension. These data do not support a uniquely hemodynamic mechanism that explains cerebral hyperemia as a consequence of repressurization in hypotensive vascular beds.
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PMID:Cerebral hyperemia after arteriovenous malformation resection is related to "breakthrough" complications but not to feeding artery pressure. The Columbia University Arteriovenous Malformation Study Project. 872 37

The aim of this study was to determine what factors beyond age affect post-operative mortality. We included 971 patients (mean age 61 +/- 10 years; 882 men, 89 women). There were 61 patients (6%) 75 years of age and over. Post-operative death rate was 15% in patients 75 and over versus 6% in patients under 75 (p = 0.01). Other variables significantly correlated with post-operative death after univariate analysis were: heart failure, Karnofsky score, VEMS, CV, PaCO2, tumor size, right side resection, pneumonectomy and large exeresis. Multivariate analysis retained 6 independent variables affecting post-operative mortality: age > or = 75 years (p = 0.019), Karnofsky score (p = 0.0001), right side resection (p = 0.0002, pneumonectomy (p = 0.04, large resection (p = 0.029) and hypocapnia (p = 0.01). If these parameters are considered when deciding on surgery, pulmonary exeresis may be proposed in elderly patients.
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PMID:[Pulmonary excisions in patients aged 75 and over. Study of postoperative mortality]. 876 36

Nitrous oxide (N2O) use during anesthesia for intracranial procedures has been a subject of controversy in the past. To date, the isolated influence of N2O on mean cerebral blood flow velocity in the middle cerebral artery (VMCA) has not been investigated during hypocapnia in patients with brain tumors. We compared VMCA during normocapnic (ETCO2: 40 mm Hg) and hypnocapnic (ETCO2: 25 mm Hg) inhalation of air and 50% nitrous oxide in oxygen N2O/O2 in eight patients with unilateral brain tumors on both the tumor side and the healthy side. Six patients completed the study. Mean VMCA increased during normocapnic inhalation of N2O/O2 (tumor side: 86 +/- 16 cm sec-1; healthy side: 74 +/- 17 cm sec-1) when compared with air (tumor side: 72 +/- 18 cm sec-1; healthy side: 62 +/- 14 cm sec-1, p < 0.01), whereas during hyperventilation VMCA decreased on both sides (p < 0.001). Mean VMCA values were quite similar during hypocapnic inhalation of 50% N2O/O2 (tumor side: 50 +/- 12 cm sec-1; healthy side: 45 +/- 13 cm sec-1) and air (tumor side: 51 +/- 14 cm sec-1; healthy side: 45 +/- 12 cm sec-1). The data of our study suggest that in patients with cerebral tumors the N2O-induced increase in mean VMCA can be completely reversed by hyperventilation.
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PMID:Effects of normo- and hypocapnic nitrous-oxide-inhalation on cerebral blood flow velocity in patients with brain tumors. 910 Jan 83

Tumour blood flow is one of the important factors limiting the efficacy of radiation therapy (hypoxic radioresistance), chemotherapy (drug delivery) and thermal therapy (heat dissipation) in treating cancer. The modification of tumour blood flow has been an area of intense investigation. In the current study, the arterial carbon dioxide tension (PaCO2) was changed in order to investigate the tumour vascular response to carbon dioxide. Functional maps of blood flow, blood volume and mean transit time were generated at four PaCO2 levels in VX2 tumour in the rabbit thigh and normal soft tissue. The PaCO2 levels investigated were normocapnia (PaCO2 = 40.9 +/- 1.2 mmHg), hypocapnia (27.2 +/- 2.3 and 33.5 +/- 2.3 mmHg) and hypercapnia (54.9 +/- 4.4 mmHg). The carbon dioxide reactivity of the global tumour blood flow and mean transit time showed significant differences between normocapnia and the two levels of hypocapnia, but not between normocapnia and hypercapnia. The average fractional change of blood flow from normocapnia for the two levels of hypocapnia was -0.41 +/- 0.06 and -0.29 +/- 0.08, respectively (P < 0.05). In the case of mean transit time the fractional change was +0.39 +/- 0.30 and +0.23 +/- 0.24, respectively (P < 0.05). The fractional change of blood volume from normocapnia, however, was not significantly different at any capnic level, as was the case with respect to each of the functional parameters in normal tissue. The ability to reduce blood flow and increase mean transit time through hypocapnia has significant implications in thermal therapy, since heat dissipation is a major factor in limiting the effectiveness of treatment.
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PMID:Carbon dioxide reactivity of computed tomography functional parameters in rabbit VX2 soft tissue tumour. 1270 90

Cerebral pathology may alter the cerebrovascular reactivity to carbon dioxide (CO2). In the present study, in patients with brain tumors, we examined the cerebral vascular reactivity to CO2 in the cerebral hemispheres with and without tumors under intravenous and inhalational anesthesia. Twenty-nine patients undergoing craniotomy for frontotemporal gliomas were randomized to receive intravenous anesthesia with propofol or inhalational anesthesia with isoflurane. Cerebral blood flow velocity in the middle cerebral artery (VMCA) and pulsatality index were measured under normocapnia and hypocapnia in the normal cerebral hemisphere and the hemisphere with tumor. Hypocapnia significantly decreased the VMCA in both the cerebral hemispheres under both the anesthetic techniques (P < 0.006). The percentage change in VMCA was similar between the hemispheres with and without tumor both under isoflurane (3.45 +/- 4.11% on the normal side and 2.91 +/- 2.40% on the tumor side; mean difference 0.54 +/- 1.31%; 95% CI -2.18 to +3.27) and propofol anesthesia (2.32 +/- 2.64% on the normal side and 1.69 +/- 4.04% on the tumor side; mean difference 0.63 +/- 1.2%; 95% CI -1.83 to +3.10). The changes in pulsatality index also were not significantly different between the hemispheres. In conclusion, cerebrovascular response to hypocapnia is similar between the normal and the abnormal cerebral hemispheres both under intravenous and inhalational anesthesia.
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PMID:Cerebrovascular reactivity to carbon dioxide in the normal and abnormal cerebral hemispheres under anesthesia in patients with frontotemporal gliomas. 1679 45

WWOX, the gene that spans the second most common human chromosomal fragile site, FRA16D, is inactivated in multiple human cancers and behaves as a suppressor of tumor growth. Since we are interested in understanding WWOX function in both normal and cancer tissues we generated mice harboring a conditional Wwox allele by flanking Exon 1 of the Wwox gene with LoxP sites. Wwox knockout (KO) mice were developed by breeding with transgenic mice carrying the Cre-recombinase gene under the control of the adenovirus EIIA promoter. We found that Wwox KO mice suffered from severe metabolic defect(s) resulting in growth retardation and all mice died by 3 wk of age. All Wwox KO mice displayed significant hypocapnia suggesting a state of metabolic acidosis. This finding and the known high expression of Wwox in kidney tubules suggest a role for Wwox in acid/base balance. Importantly, Wwox KO mice displayed histopathological and hematological signs of impaired hematopoiesis, leukopenia, and splenic atrophy. Impaired hematopoiesis can also be a contributing factor to metabolic acidosis and death. Hypoglycemia and hypocalcemia was also observed affecting the KO mice. In addition, bone metabolic defects were evident in Wwox KO mice. Bones were smaller and thinner having reduced bone volume as a consequence of a defect in mineralization. No evidence of spontaneous neoplasia was observed in Wwox KO mice. We have generated a new mouse model to inactivate the Wwox tumor suppressor gene conditionally. This will greatly facilitate the functional analysis of Wwox in adult mice and will allow investigating neoplastic transformation in specific target tissues.
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PMID:Generation and characterization of mice carrying a conditional allele of the Wwox tumor suppressor gene. 1993 20


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