Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0085383 (hypocapnia)
 1,697 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This article attempts correlating changes in cellular energy metabolism, acid-base alterations, and ion homeostasis in ischemia and other conditions. It is emphasized that loss of ion homeostasis, with thermodynamically downhill fluxes of K+, Ca2+, Na+, Cl-, and H+, occurs because energy production fails and (or) ion conductances are increased. In ischemia, energy failure is the leading event but, in hypoglycemia, activation of ion conductances is what precipitates energy failure. The initial event is a rise in K+ e, at least in part caused by activation of K+ conductances modulated by Ca2+ or ATP/ADP ratio. Secondarily, this leads to release of excitatory amino acids and massive activation of unspecific cation (and anion) conductances. Production of H+ occurs in states characterized by energy failure (ischemia and hypoxia) or by alkalosis (hypocapnia and ammonia accumulation). H+ equilibrates between intra- and extra-cellular fluid via nonionic diffusion of lactic acid, and transmembrane fluxes of H+ or HCO3- via ion channels. Since the relationship between lactate and either pHi or pHe is linear, there are no abrupt pH shifts explaining why hyperglycemia worsens ischemic damage. The reversible insults seem to induce a sustained stimulation of H+ extrusion from cells giving rise to intracellular alkalosis and extracellular acidosis.
 ...
PMID:Coupling among changes in energy metabolism, acid-base homeostasis, and ion fluxes in ischemia. 128 29

1. Two hours of exposure to heat stress, resulted in hyperthermia in rabbits (Oryctolagus cuniculus). 2. This was accompanied by a severe hypocapnia, partly compensated for by a significant decrease in bicarbonate (HCO3-) concentration. 3. The severest hyperthermia (Tb = 43.5 degrees) was followed by a sharp decreased in both PaCO2 (to 20.2 torr) and HCO3- (to 9.2 mM/l), resulting in extreme metabolic acidosis (pH = 7.290). 4. The significant increase in serum osmolality (27%) is interpreted by the cumulative effect of increased electrolyte and metabolite concentrations. 5. The elevation in blood BUN, creatinine, globulin and GOT levels point to a possible damage to muscle cells by hypothermia. 6. The stable cholesterol and alkaline phosphatase levels, suggest that liver tissue was not damaged. 7. The dramatic increase in glucose from 103.8 to 348.8 mg%, and the significant increase (from 22.0 to 39.9 mg%) in BUN, suggest a possible disability of the cells to metabolize carbohydrates, accompanied by a progressive proteolysis as an alternative process for energy production. 8. The data suggest that the emergence of muscle cell damage, severe hyperglycemia and acidosis under heat stress, precedes and amplifies the deteriorating effects of high Tb in heat stressed rabbits, which often lead to mortality.
 ...
PMID:The effect of heat exposure on blood chemistry of the hyperthermic rabbit. 198 37

Profound hypothermia below 20 degrees C achieved by surface cooling using simple ice water bath equipment and deep ether anaesthesia is used with the aid of autonomic nerve blocking agents to obtain cardiac arrest for periods of over one hour for open-heart surgery. Blood levels of ether were between 40.6 mg/dl and 285.7 mg/dl during anaesthesia. No arrhythmia occurred and vital signs were quite stable. Hypocarbia throughout the procedure, severe base deficit after circulatory arrest, spontaneous recovery of metabolic acidosis, and a nearly normal cH+ (pH) were observed. Catecholamine increased moderately after circulatory arrest, but was far below shock levels. Plasma renin activity was markedly elevated but angiotensin II stayed at non-significant levels throughout the procedure. Excess lactate showed no significant change. Hyperglycaemia was noted. The mortality rate was 7.7 per cent and neurological disorders occurred in less than 5.8 per cent of the recent 52 cases.
 ...
PMID:A study of profound hypothermia by surface cooling. 677 40

Ten splenectomized and ten nonsplenectomized conscious dogs were subjected to hemorrhage of 41% of their blood volume over a 15-minute period. Hemodynamic and metabolic variables were monitored for 4 hours after hemorrhage. Mortality (100%) occurred in the splenectomized group. Significant (P < 0.001) hemodynamic responses after hemorrhage included hypotension, tachycardia, low central venous pressure, and decreased ECG voltage of the R wave. Tachypnea was noted in the absence of hypoxia, hypercapnia, and acidosis inthe nonsplenectomized dogs. Significant (P < 0.001) hypocapnia and mean PCO2 values of 13.9 MM of Hg and 23.5 mm of Hg in splenectomized and nonssplenectomized dogs, respectively, was noted. Mean hemoglobin levels were significantly (P < 0.001) decreased after hemorrhage in the splenectomized dogs. The absence of a change in hemoglobin in thenonsplenectomized dogs was attributed to the translocationof extracellular fluid into the vascular space which diluted the high concentration of RBC from splenic contraction. Other changes noted after hemorrhage were hyperglycemia, increased blood cortisol, and increased pyruvate and lacte levels. Changes were not noted in pyruvate-to-lactate ratios.
 ...
PMID:Experimental hemorrhage in splenectomized and nonsplenectomized dogs. 740 89

A solution containing S-nitroso-N-acetylpenicillamine (SNAP), a nitric oxide (NO.-releasing compound, was microinjected in doses of 0.25-2 mumol into a lateral ventricle of conscious rats. SNAP produced dose-dependent convulsions similar to those associated with limbic stimulation, such as tonic extension of the hindlimbs and tail, and dystonia of the forepaws. At 2 mumol, SNAP evoked hyperventilation (arterial hypocapnia), arterial hyperglycemia and caused necrotic lesions of periventricular gray (e.g. lateral septal nucleus) and white matter structures. In the caudate nucleus and lateral septal nucleus ipsilateral to injection, SNAP elicited a bipolar metabolic pattern of low glucose metabolism proximal to the ventricle with higher values occurring more distally. In control studies, we proved that the residue of SNAP decomposition, N-acetylpenicillamine disulfide injected intraventricularly (2 mumol), was without physiological, behavioral, or histological effects. Ventricular pretreatment with methylene blue (2 nmol), a putative inhibitor of guanylate cyclase and superoxide generator, suppressed several of the behavioral manifestations of 1 mumol SNAP, such as the forepaw dystonia, squinting, and facial clonus, but was ineffective on the physiological and histological variables affected by the 2 mumol SNAP dose. Another NO. donor, sodium nitroprusside (2 mumol), produced fewer behavioral and cytotoxic effects over a 55-min observation period, but caused more intense and widely distributed metabolic stimulation, especially in commissural and projection white matter tracts. The results are the basis for a conscious rat model using intraventricular injection of nitrocompounds to examine the physiological, behavioral, metabolic and cytotoxic properties of NO. in the brain.
 ...
PMID:Neurotoxicity in conscious rats following intraventricular SNAP, a nitric oxide donor. 796 12

The effect of diabetes mellitus on the cerebrovascular response to CO2 is unclear. We examined the effects of diabetes on cerebral blood flow (CBF) and cerebral oxygen uptake (CMRO2) during CO2 alterations. Four groups of dogs were studied: nondiabetic, normoglycemic controls; non-diabetic acute hyperglycemia; diabetic (pancreatectomy) with high-dose insulin treatment to maintain blood glucose between 4.0 and 6.0 mM; and diabetic with low-dose insulin treatment to maintain blood glucose at 13.2 +/- 0.4 mM. Six weeks after either sham surgery or pancreatectomy, dogs were anesthetized with fentanyl (50 micrograms/kg) plus pentobarbital (10 mg/kg), and microsphere determinations of CBF were made during normo-, hypo-, and hypercapnia. On the day of the study, arterial glucose levels in the control, acute hyperglycemia, and high- and low-dose insulin diabetic groups were 4.0 +/- 0.3, 14.9 +/- 2.5, 3.3 +/- 0.8, and 13.3 +/- 0.7 mM, respectively, at control. The corresponding baseline CMRO2 levels were 2.8 +/- 0.2, 3.0 +/- 0.2, 4.1 +/- 0.4, and 4.0 +/- 0.3 ml O2.100 g-1 x min,1, and the values in both diabetic groups were higher than control. Normocapnic CBF in the acute hyperglycemia, high-dose insulin, and low-dose insulin groups was elevated from control (54 +/- 3, 50 +/- 3, 51 +/- 3 vs. 36 +/- 1 ml x 100 g-1 x min-1) and cerebrovascular resistance was lower (2.24 +/- 0.15, 2.51 +/- 0.14, 2.38 +/- 0.21 vs. 3.35 +/- 0.18 mmHg.ml-1 x 100 g.min). CBF responses to both hypercapnia and hypocapnia were similar among groups. Thus both acute hyperglycemia and diabetes decrease cerebrovascular resistance and increase CBF.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Cerebral blood flow responsivity to CO2 in anesthetized chronically diabetic dogs. 847 84

Intracranial pressure depends on cerebral tissue volume, cerebrospinal fluid volume (CSFV) and cerebral blood volume (CBV). Physiologically, their sum is constant (Monro-Kelly equation) and ICP remains stable. When the blood brain barrier (BBB) is intact, the volume of cerebral tissue depends on the osmotic pressure gradient. When it is injured, water movements across the BBB depend on the hydrostatic pressure gradient. CBV depends essentially on cerebral blood flow (CBF), which is strongly regulated by cerebral vascular resistances. In experimental studies, a decrease in oncotic pressure does not increase cerebral oedema and intracranial hypertension (ICHT). On the other hand, plasma hypoosmolarity increases cerebral water content and therefore ICP, if the BBB is intact. If it is injured, neither hypoosmolarity nor hypooncotic pressure modify cerebral oedema. Therefore, all hypotonic solutes may aggravate cerebral oedema and are contra-indicated in case of ICHT. On the other hand, hypooncotic solutes do not modify ICP. The osmotic therapy is one of the most important therapeutic tools for acute ICHT. Mannitol remains the treatment of choice. It acts very quickly. An i.v. perfusion of 0.25 g.kg-1 is administered over 20 minutes when ICP increases. Hypertonic saline solutes act in the same way, however they are not more efficient than mannitol. CO2 is the strongest modulating factor of CBF. Hypocapnia, by inducing cerebral vasoconstriction, decreases CBF and CBV. Hyperventilation is an efficient and rapid means for decreasing ICP. However, it cannot be used systematically without an adapted monitoring, as hypocapnia may aggravate cerebral ischaemia. Hyperthermia is an aggravating factor for ICHT, whereas moderate hypothermia seems to be beneficial both for ICP and cerebral metabolism. Hyperglycaemia has no direct effect on cerebral volume, but it may aggravate ICHT by inducing cerebral lactic acidosis and cytotoxic oedemia. Therefore, infusion of glucose solutes is contra-indicated in the first 24 hours following head trauma and blood glucose concentration must be closely monitored and controlled during ICHT episodes.
 ...
PMID:[The internal environment and intracranial hypertension]. 975 May 95

Brain injury is one of the main causes of death in 20-40-year-old persons. The main causes of fatal outcomes are progressive edema and cerebral ischemia. The strategic task of intensive care in patients with severe brain injury, who are critically ill, is to prevent and treat secondary ischemic brain damages. The major secondary damaging factors include arterial hypotension, hypoxemia, hyper- and hypocapnia, hypoosmolality, and hyperglycemia. This paper presents the advisable treatment protocol for patients with brain injury, which has been developed and used in a neurosurgical intensive care unit of the N. V, Sklifosofsky Research Institute of Emergency Care. The protocol is based on international guidelines and the authors' own studies. It outlines the basic lines of monitoring and intensive care in patients with severe brain injury.
 ...
PMID:[A diagnosis and treatment protocol for brain injury]. 1728 71

The effects of two transportation periods on physio- metabolic hemodynamic changes and gaseous exchange in commercial swine during transportation to the slaughterhouse was studied in 684 pigs, 357 barrows and 327 gilts, transported in 2 groups for 8 and 16 h. Transportation caused an increase of oxygen consumption and body temperature, a decrease in pH, lactic acid accumulation. Both transportation periods caused higher than normal plasma glucose levels, lactic acidosis and evidence of dehydration. The linear regression analysis for pigs transported for 8h indicates that the PO(2,) lactate and Ca(++) variables correlated negatively with the PCO(2.) Whilst the animals that were transported for 16 h had negative correlations between glucose, and calcium, hematocrit, lactate and potassium levels. It was concluded that regardless of transport time acidosis, hypocapnia, hypoxaemia, hypernatraemia, hypercalcaemia, hyperglycemia, lactacidemia and increased hematocrit levels occurred.
 ...
PMID:Changes in blood constituents of swine transported for 8 or 16 h to an Abattoir. 2073 49

Nitric oxide (NO), a short-lived freely diffusible radical gas that acts as an important biological signal, regulates an impressive spectrum of physiological functions in vertebrates including fishes. The action of NO, however, on thyroid hormone status and its role in the integration of acid-base, osmotic and metabolic balances during stress are not yet delineated in fish. Sodium nitroprusside (SNP), a NO donor, was employed in the present study to investigate the role of NO in the stressed air-breathing fish Anabas testudineus. Short-term SNP treatment (1 mM; 30 min) interacted negatively with thyroid axis, as evident in the fall of plasma thyroxine in both stressed and non-stressed fish. In contrast, the cortisol responsiveness to NO was negligible. SNP challenge produced systemic alkalosis, hypocapnia and hyperglycemia in non-stressed fish. Remarkable acid-base compensation was found in fish kept for 60 min net confinement where a rise in blood pH and HCO(3) content occurred with a reduction in PCO(2) content. SNP challenge in these fish, on the contrary, produced a rise in oxygen load together with hypocapnia but without an effect on HCO(3) content, indicating a modulator role of NO in respiratory gas transport during stress response. SNP treatment reduced Na(+), K(+) ATPase activity in the gill, intestine and liver of both stressed and non-stressed fish, and this suggests that stress state has little effect on the NO-driven osmotic competence of these organs. On the other hand, a modulatory effect of NO was found in the kidney which showed a differential response to SNP, emphasizing a key role of NO in kidney ion transport and its sensitivity to stressful condition. H(+)-ATPase activity, an index of H(+) secretion, downregulated in all the organs of both non-stressed and stressed fish except in the gill of non-stressed fish and this supports a role for NO in promoting alkalosis. The data indicate that, (1) NO interacts antagonistically with T(4), (2) modifies respiratory gas transport and (3) integrates acid-base and osmotic actions during stress response in air-breathing fish. Collectively, this first evidence in fish indicate that NO can promote compensatory physiologic modification and that can reduce the magnitude of stress-induced acid-base and osmotic disturbance and that suggests a role for NO in the ease and ease response of this fish.
 ...
PMID:Nitric oxide rectifies acid-base disturbance and modifies thyroid hormone activity during net confinement of air-breathing fish (Anabas testudineus Bloch). 2315 53


1 2 Next >>