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

Previous experiments have demonstrated that hypoxia stimulates the release of arginine vasopressin in conscious animals including the rat. The present study was designed to test whether AVP may exert a vasoconstrictor influence during hypoxia at varying levels of CO2. Systemic hemodynamics were assessed in conscious rats for 30 min under hypocapnic hypoxic, isocapnic hypoxic, hypercapnic hypoxic, and room air conditions. Progressive effects on heart rate (HR), cardiac output (CO), and total peripheral resistance (TPR) were observed with varying CO2 under hypoxic conditions. Hypocapnic hypoxia [arterial PO2 (PaO2) = 32 Torr; arterial PCO2 (PaCO2) = 22 Torr] caused HR and CO to rise and TPR to fall. Isocapnic hypoxia (PaO2 = 36 Torr; PaCO2 = 35 Torr) was associated with no significant changes in HR and CO or TPR, whereas hypercapnic hypoxia (PaO2 = 35 Torr; PaCO2 = 51 Torr) caused HR and CO to fall and TPR to rise. Room air time control experiments were associated with no change in measured hemodynamic variables. To determine the possible role of circulating AVP on these cardiovascular responses, additional experiments were performed where the specific V1-vasopressinergic antagonist d(CH2)5Tyr(Me)AVP (10 micrograms/kg iv) was administered at the midpoint of hypoxic exposure. Antagonist administration had no effect on hypocapnic hypoxic animals or animals breathing room air; however, blood pressure and TPR were significantly reduced by d(CH2)5Tyr(Me)AVP in both isocapnic and hypercapnic hypoxic animals. The heart rate response to hypoxia at the various CO2 levels was unaffected; however, cardiac output and stroke volume were increased after V1-antagonism in the isocapnic and hypercapnic hypoxic animals.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Role of vasopressin in the cardiovascular response to hypoxia in the conscious rat. 309 15

Gaseous metabolism and carboanhydrase activity of erythrocytes of the capillary and venous blood were studied in 115 persons, including 19 apparently normal subjects, 66 patients with ischemic stroke, and 30 with discirculatory encephalopathy. Patients with cerebral stroke presented gross disorders in the function of carboanhydrase and gaseous metabolism from the first day of the disease which was expressed in an increased oxygenation of the venous blood and hypocapnia, whose severity was correlated with the gravity of the disease course. The authors have established an important pathogenetic role in gaseous metabolism impairment of erythrocyte carboanhydrase, whose activity in the capillary bed in hypocapnia was drastically inhibited, compromising, therefore, the entry of carbon dioxide into erythrocytes, which deteriorated oxyhemoglobin dissociation. The authors consider the possibility of normalizing gaseous metabolism in stroke patients via eliminating CO2 deficit in tissues.
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PMID:[Erythrocyte carboanhydrase and gas metabolism in patients with ischemic stroke]. 312 92

The reactivity of cerebral blood vessels to changes in PaCO2 in areas of the cerebral cortex with or without diaschisis was investigated in 13 patients in a subacute or chronic stage after a small capsular infarct. A focal area of hypoperfusion (area of diaschisis) was detected in the ipsilateral sensorimotor cortex in each patient. Hyperventilation caused a significant reduction of regional cerebral blood flow in the area without diaschisis and only a tendency for regional cerebral blood flow to decrease in the area with diaschisis; CO2 inhalation induced a slight increase in regional cerebral blood flow in the area without diaschisis and a significant increase in regional cerebral blood flow in the area with diaschisis. Regional cerebral blood flow reactivity to hypocapnia was significantly less in the area with diaschisis than in the area without, whereas the hypercapnic response was more marked in the area with diaschisis than in the area without. Our results suggest that in the area with diaschisis, the arterioles may be abnormally vasoconstricted at rest such that they cannot constrict further in response to hypocapnia but can dilate more during hypercapnia than in the area without diaschisis. This excessive resting vasoconstriction may result from decreased tissue elaboration of CO2 due to local decrease of metabolic function.
Stroke 1988 Jul
PMID:Vascular response to carbon dioxide in areas with and without diaschisis in patients with small, deep hemispheric infarction. 313 40

To evaluate the CO2-induced vasomotor reactivity of the cerebral vasculature, relative changes of blood flow velocity within the middle cerebral artery were measured by transcranial Doppler ultrasonography during normocapnia and various degrees of hypercapnia and hypocapnia. We studied 40 normal individuals and 40 patients with unilateral and 15 patients with bilateral internal carotid artery occlusions. When blood flow velocity changes as percent of normocapnic values were plotted against end-tidal CO2 volume percent, a biasymptotic curve (a tangent-hyperbolic function) gave the best fit of the scattergram. The distance between the upper and lower asymptotes was defined as cerebral vasomotor reactivity. In the normal individuals, mean +/- SD vasomotor reactivity was 85.63 +/- 15.96%. In patients with internal carotid artery occlusions, vasomotor reactivity was significantly lower than normal on both the occluded (mean 45.2%, median 50.4%; p less than 0.0001) and the nonoccluded (mean +/- SD 67.7 + 13.3%, p less than 0.01) sides in the unilateral group and on both sides (mean +/- SD 36.6 +/- 15.9% and 44.9 +/- 24.6%, p less than 0.0001) in the bilateral group. The difference between vasomotor reactivity for symptomatic and asymptomatic unilateral occlusions was also highly significant (mean 37.6% and 62.9%, p less than 0.006). Vasomotor reactivity was also significantly lower in patients with low-flow infarctions on computed tomography than in patients with normal scans (mean +/- SD 36.7 +/- 25% and 60.2 +/- 16.9%, p less than 0.008). A striking association of low-flow infarctions, ischemic ophthalmopathy, and hypostatic transient ischemic attacks was found with vasomotor reactivities of less than 34% or even paradoxical reactions.(ABSTRACT TRUNCATED AT 250 WORDS)
Stroke 1988 Aug
PMID:Noninvasive assessment of CO2-induced cerebral vasomotor response in normal individuals and patients with internal carotid artery occlusions. 313 41

We determined regional cerebral blood flow (rCBF) using [125I]HIPDm [N,N,N'-trimethyl-N'-(2-hydroxy-3-methyl-5-iodobenzyl)-1,3-propanediamin e] and [125I]iodoantipyrine autoradiography under control and pathologic conditions (hypercapnia [acidosis], hypocapnia [alkalosis], and disrupted blood-brain barrier) conditions in 35 rats. In control rats, HIPDm rCBF (indicator fractionation method, n = 5) was lower than the corresponding IAP rCBF (diffusible indicator method, n = 4), most notably in the infratentorial regions and subcortical nuclei. In hypercapnia, rCBF increased by 100% and 37% in the HIPDm (n = 5) and IAP (n = 5) groups, respectively. In hypocapnia, IAP rCBF (n = 4) decreased 34% but HIPDm rCBF (n = 4) did not change. Following disruption of the blood-brain barrier by intracarotid infusion of mannitol in eight rats, both radiotracers (HIPDm n = 4, IAP n = 4) showed decreased rCBF to regions of disruption as defined by trypan blue extravasation. Our work indicates that modeling HIPDm uptake to quantify rCBF using the indicator fractionation method will underestimate blood flow and that HIPDm kinetics are influenced by compartmental pH dynamics that will limit the accuracy of this method in quantifying rCBF in pathologic conditions.
Stroke 1988 Nov
PMID:Comparison of [125I]HIPDm and [125I]iodoantipyrine in quantifying regional cerebral blood flow in rats. 318 25

Cerebral blood flow and oxygen metabolism have been measured with the steady-state oxygen-15 technique and positron emission tomography in anesthetized dogs. Regional microembolization was induced by infusing Sephadex particles (diameter, 40 micron) into one of the common carotid arteries. In the first series of experiments, 2.5 mg Sephadex was infused, and the dogs were examined within 3-4 hours after embolization. In a second series 0.55 mg Sephadex was infused, and the dogs were examined either in the first 3-4 hours or 24-48 hours after embolization. Cerebral blood flow, oxygen extraction ratio, and cerebral oxygen utilization were measured at 3 PCO2 levels. In the acute experiments, cerebral oxygen utilization in the embolized hemisphere was 6 (0.55 mg Sephadex) and 25% (2.5 mg Sephadex) lower than on the contralateral side. While cerebral blood flow was symmetrically distributed in normocapnia and hypocapnia, it was 9 (0.55 mg Sephadex) and 35% (2.5 mg Sephadex) lower in the embolized hemisphere during hypercapnia. In normocapnia and hypocapnia the lower oxygen utilization in the embolized hemisphere was characterized by a lower oxygen extraction ratio, and in hypercapnia by an unchanged (0.55 mg Sephadex) or by a higher (2.5 mg Sephadex) extraction ratio. The different effect on oxygen extraction ratio in the control and embolized hemispheres resulted in images of uncoupling between perfusion and oxygen demand that varied according to the PCO2. The experiments also showed a fall in cerebral blood flow in the embolized hemisphere after 3-4 hours, indicating delayed hypoperfusion. After 24-48 hours, blood flow was about 10% higher in the embolized hemisphere, and this was observed at the 3 PCO2 levels, while the oxygen extraction ratio was systematically lower. Oxygen utilization in the embolized hemisphere was depressed to practically the same extent as in acute experiments. It can be concluded that between 4 and 24 hours after microembolization the cerebral microcirculation shows important changes, with installation of luxury perfusion in the face of an unchanging decreased oxygen metabolism.
Stroke
PMID:PET studies of changes in cerebral blood flow and oxygen metabolism after unilateral microembolization of the brain in anesthetized dogs. 349 88

In this study hemodynamic and morphometric consequences of atherosclerosis were examined in cynomolgus monkeys. We tested the hypothesis that atherosclerosis augments cerebral vasoconstrictor responses to serotonin. We studied 8 normal and 8 atherosclerotic monkeys, which were fed an atherogenic diet for 17 months. Morphometric studies indicated marked intimal proliferation of extracranial carotid arteries, with only modest reduction in the vascular lumen, as atherosclerotic lesions were displaced outward. Cerebral blood flow was measured with microspheres and microvascular pressure was measured with a micropipette in pial arteries approximately 350 microns diameter. Intracarotid infusion of serotonin reduced microvascular pressure, which indicates constriction of large arteries upstream, but cerebral blood flow did not decrease. Serotonin produced a 2-fold greater reduction in cerebral microvascular pressure in atherosclerotic monkeys than in normal monkeys. Intracarotid histamine increased flow and hypocapnia reduced flow in both normal and atherosclerotic monkeys, without altering cerebral microvascular pressure. We conclude: First, atherosclerosis potentiates constrictor responses to serotonin in large cerebral arteries. Because platelets release serotonin when they aggregate, augmentation of responses by atherosclerosis may have implications for cerebral vascular responses during aggregation of platelets at carotid lesions. Second, despite marked proliferation of intima, atherosclerotic lesions are displaced outward during a prestenotic phase of the disease, so that the lumen is relatively well preserved.
Stroke
PMID:Effects of atherosclerosis on cerebral vessels: hemodynamic and morphometric studies. 381 Jul 23

Cerebral vascular responses to hypocapnia during hypotension to a mean arterial blood pressure (MAP) = 50 mm Hg induced with sodium nitroprusside (SNP, n = 12) or trimethaphan (TMP, n = 12) were examined in dogs. Cerebral vascular resistance (CVR) and cerebral blood flow (CBF) at PaCO2 = 40 mm Hg, and PaCO2 = 20 mm Hg were examined first at normal MAP then at hypotension in six dogs in the SNP group and six dogs in the TMP group. In both the SNP group and the TMP group, CO2 responsiveness, as indicated by increased CVR and decreased CBF, was intact at normal MAP, but absent during hypotension. In the remaining 6 of 12 dogs in the SNP group and 6 of 12 dogs in the TMP group, CO2 responsiveness at MAP = 50 mm Hg was examined without prior determination of CO2 responsiveness at normal MAP. These additional studies were performed to rule out the possibility that absent CO2 responsiveness during hypotension in the initial groups resulted from (1) physiologic deterioration of the preparation with time, or (2) adaptation of brain extracellular fluid pH to a preceding period of hypocapnia. Again, during both SNP- or TMP-induced hypotension CO2 responsiveness was absent.
Stroke
PMID:Cerebral blood flow responses to hypocapnia during hypotension. 643 18

We compared vasoactive effects of intravenous nicotine (36 micrograms/kg/min) in regional cerebral circulations under pentobarbital and chloralose anesthesia. Experiments were conducted in three groups of dogs: Group I, pentobarbital anesthesia with fixed ventilation; Group II, chloralose anesthesia with fixed ventilation; Group III, chloralose anesthesia with free breathing. Values for regional cerebral blood flow measured with 15 mu radioactive microspheres were used to compute regional cerebral vascular resistance (rCBR). In Group I, nicotine had no effect on rCVR in cerebral cortex, and it increased significantly rCVR in cerebellum (+17%), pons (+13%), medulla (+23%), and spinal cord (+19%). Using chloralose instead of pentobarbital in dogs with fixed ventilation (Group II), caused a significant reduction in rCVR in the cerebral cortex during nicotine, although it did not alter significantly nicotine-induced changes in rCVR in other regions of the brain. Hypocapnic alkalosis during nicotine-induced hyperventilation (Group III) resulted in significant increases in rCVR in all regions of the brain; however, the increases in rCVR in non-cortical regions more than doubled those in the cerebral cortex. The present results indicate: Nicotine-induced vasodilation in cerebral cortex was blunted by pentobarbital anesthesia. Nicotine-induced vasodilation in cerebral cortex under chloralose anesthesia was sufficient to nullify in part the potent vasoconstrictor effect of hypocapnic alkalosis.
Stroke
PMID:Regional blood flow in canine brain during nicotine infusion: pentobarbital vs. chloralose anesthesia. 646 62

To study the relationship between the degree of hypertension and experimentally-induced cerebral ischemia, brain metabolites, including lactate, pyruvate and adenosine triphosphate (ATP) were determined one hour after bilateral carotid occlusion in 119 spontaneously hypertensive rats (SHR) with a variety of mean arterial pressures (MAP). Of these, 36 SHR were given antihypertensive agents for 10 weeks to reduce blood pressure prior to the experiment. There was a significant linear correlation between MAP before and either supratentorial lactate (r = 0.482, p less than 0.001) or the lactate/pyruvate ratio (r = 0.388, p less than 0.001) in the brain after carotid occlusion. An inverse correlation was observed between supratentorial lactate and either ATP (r = -0.627, p less than 0.001) or arterial PCO2 (r = -0.477, p less than 0.001) after carotid occlusion. The changes suggest that the animals with a higher MAP had a greater increase in ischemic metabolites with a decrease in ATP and a more pronounced hypocapnia after carotid occlusion. This hypocapnia is believed to be due to hyperventilation induced by cerebral ischemia. It is concluded that hypertensive rats are more susceptible to cerebral ischemia and the susceptibility is related to the degree of hypertension. By long-term lowering of the blood pressure prior to carotid occlusion, the ischemic changes are lessened in this experimental model.
Stroke
PMID:Experimental cerebral ischemia in spontaneously hypertensive rats (SHR): Importance of degree of hypertension. 678 15


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