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Query: UMLS:C0020440 (hypercapnia)
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We studied the response of cerebral blood flow to acute step decreases in arterial blood pressure noninvasively and nonpharmacologically in 10 normal volunteers during normocapnia, hypocapnia, and hypercapnia. The step (approximately 20 mm Hg) was induced by rapidly deflating thigh blood pressure cuffs following a 2-minute inflation above systolic blood pressure. Instantaneous arterial blood pressure was measured by a new servo-cuff method, and cerebral blood flow changes were assessed by transcranial Doppler recording of middle cerebral artery blood flow velocity. In hypocapnia, full restoration of blood flow to the pretest level was seen as early as 4.1 seconds after the step decrease in blood pressure, while the response was slower in normocapnia and hypercapnia. The time course of cerebrovascular resistance was calculated from blood pressure and blood flow recordings, and rate of regulation was determined as the normalized change in cerebrovascular resistance per second during 2.5 seconds just after the step decrease in blood pressure. The reference for normalization was the calculated change in cerebrovascular resistance that would have nullified the effects of the step decrease in arterial blood pressure on cerebral blood flow. The rate of regulation was 0.38, 0.20, and 0.11/sec in hypocapnia, normocapnia, and hypercapnia, respectively. There was a highly significant inverse relation between rate of regulation and PaCO2 (p less than 0.001), indicating that the response rate of cerebral autoregulation in awake normal humans is profoundly dependent on vascular tone.
Stroke 1989 Jan
PMID:Cerebral autoregulation dynamics in humans. 249 26

We studied the hemodynamic effects of acute alterations in PaCO2 in ten ventilator-dependent children after open heart surgery. Despite end-tidal CO2 monitoring, five children inadvertently developed PaCO2 greater than 50 torr during the study. Increasing and decreasing PaCO2 in these children resulted in significant parallel changes in cardiac index (CI), oxygen delivery, physiologic shunt, mean pulmonary pressure, and right ventricular stroke work index, and inverse changes in systemic vascular resistance index (p less than .01). No significant hemodynamic changes were observed with alterations in PaCO2 in children whose PaCO2 remained less than 50 torr. These findings are partly related to significantly larger reductions in PaCO2 which occurred in the hypercarbic children compared to the others (25 vs. 12 torr; p less than .001). Heart rate, mean arterial BP, and venous filling pressures did not change significantly in either group. We conclude that mean alterations in PaCO2 less than or equal to 12 torr (range 28 to 50) have no significant effect on CI in children after open heart surgery. However, moderate hypercarbia and its correction to a mean PaCO2 of 30 torr are associated with significant effects on central hemodynamics. Moreover, no significant changes in the commonly monitored physiologic variables were observed despite large variations in PaCO2.
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PMID:Hemodynamic responses to PaCO2 in children after open heart surgery. 250 38

The cardiopulmonary effects of 2 planes of halothane anesthesia (halothane end-tidal concentrations of 1.78% [light anesthesia] and 2.75% [deep anesthesia]) and 2 ventilatory modes (spontaneous ventilation [SV] or mechanically controlled ventilation [CV]) were studied in 8 cats. Anesthesia was induced and maintained with halothane in O2 only, and each cat was administered each treatment according to a Latin square design. Cardiac output, arterial blood pressure, pulmonary arterial pressure, heart rate, respiratory frequency, and PaO2, PaCO2, and pH were measured during each treatment. Stroke volume, cardiac index, and total peripheral resistance were calculated. A probability value of less than 5% was accepted as significant. In the cats, cardiac output, cardiac index, and stroke volume were reduced by deep anesthesia and CV, although only the reduction attributable to CV was significant. Systemic arterial pressure was significantly reduced by use of deep anesthesia and CV. Respiratory frequency was significantly lower during CV than during SV. Arterial PO2 was significantly decreased at the deeper plan of anesthesia, compared with the lighter plane. At the deeper plane of anesthesia, arterial PCO2 and pulmonary arterial pressure were significantly lower during CV than during SV. The deeper plane of halothane anesthesia depressed cardiopulmonary function in these cats, resulting in hypotension and considerable hypercapnia. Compared with SV, CV significantly reduced circulatory variables and should be used with care in cats. Arterial blood pressure was judged to be more useful for assessing anesthetic depth than was heart rate or respiratory frequency.
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PMID:Cardiopulmonary effects of halothane anesthesia in cats. 250 15

1. Pithed rats were respired at a fixed rate of 54 cycles min-1 and with a ventilation volume of either 20 (control) or 10 ml kg-1. In these two preparations, the dose-response relationships for the systemic blood pressure responses to endothelin-1, administered i.v., were examined. Also, cardiac output, its distribution, tissue blood flows and vascular resistances were determined at both respiratory volumes in pithed rats given saline or during pressor responses to endothelin-1 (750 ng, i.v.). Finally, a comparison was made of the pressor responses to endothelin-1 in the blood perfused superior mesenteric arterial bed of pithed rats respired at 10 or 20 ml kg-1. 2. In control rats the systemic blood pressure responses to i.v. endothelin-1 were biphasic with an initial, transient (30 s) decrease in blood pressure followed by a well sustained pressor response. These responses were dose-dependent (the ED50 for the pressor response being 0.27 +/- 0.04 micrograms). The pressor effect of endothelin-1 was due to an increase in total peripheral resistance with no change in heart rate or cardiac output. This increased total peripheral resistance was due to vasoconstriction of the spleen, stomach, large intestine, small intestine and the pancreas/mesentery (in which it was most severe). Endothelin-1 also increased blood flow through the heart, lungs, liver, epididimides, fat and skin through redistribution of cardiac output to these vascular beds. 3. At the lower ventilation volume there was moderate acidosis, hypoxia and hypercapnia relative to those rats respired at 20 ml kg-1. With respiration at 10 ml kg-1, the pressor response to endothelin-1 was not sustained and, after oscillations in both blood pressure and heart rate, death occurred 15-20 min after administration. The pressor effect resulted from increases in cardiac output (due to increased stroke volume) and total peripheral resistance: the latter was caused by vasoconstriction in the stomach, small intestine, large intestine and pancreas/mesentery. Endothelin-1 increased blood flow through the heart, lungs, liver, kidneys, testes, fat and skin due to either an increase in cardiac output, redistribution of cardiac output or both. 4. Endothelin-1 induced dose-dependent pressor responses in the mesenteric bed in situ. At the lower ventilation volume the potency of endothelin-1 in this vascular bed was increased approximately two fold with the ED50 being 68 +/- 7 pmol compared to 113 +/- 15 pmol in the rats respired at 20 ml kg-1. 5. This study indicates that, in normoxic control pithed rats, the pressor response to endothelin-1 was due largely to vasoconstriction of the splanchnic vascular bed. In rats with moderate hypoxia, hypercapnia and acidosis, the pressor response was due to vasoconstriction of the gastrointestinal tract as well as an increase in cardiac output. Endothelin-1 induced profound vasoconstriction in the mesenteric bed of the pithed rat both in vivo and in situ. The potency of endothelin-1 on this bed in situ was doubled by lowering the ventilation volume. An increase in cardiac contractility and severe gastrointestinal vasoconstriction may be the initial events leading to the eventual toxic effect of endothelin-1 in the hypoxic pithed rat.
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PMID:Effects of moderate hypoxia, hypercapnia and acidosis on haemodynamic changes induced by endothelin-1 in the pithed rat. 251 90

Regional cerebral blood flow was simultaneously determined using the stable xenon computed tomographic and the radioactive microsphere techniques over a wide range of blood flow rates (less than 10-greater than 300 ml/100 g/min) in 12 baboons under conditions of normocapnia, hypocapnia, and hypercapnia. A total of 31 pairs of determinations were made. After anesthetic and surgical preparation of the baboons, cerebral blood flow was repeatedly determined using the stable xenon technique during saturation with 50% xenon in oxygen. Concurrently, cerebral blood flow was determined before and during xenon administration using 15-microns microspheres. In Group 1 (n = 7), xenon and microsphere determinations were made repeatedly during normocapnia. In Group 2 (n = 5), cerebral blood flow was determined using both techniques in each baboon during hypocapnia (PaCO2 = 20 mm Hg), normocapnia (PaCO2 = 40 mm Hg), and hypercapnia (PaCO2 = 60 mm Hg). Xenon and microsphere values in Group 1 were significantly correlated (r = 0.69, p less than 0.01). In Group 2, values from both techniques also correlated closely across all levels of PaCO2 (r = 0.92, p less than 0.001). No significant differences existed between the slopes or y intercepts of the regression lines for either group and the line of identity. Our data indicate that the stable xenon technique yields cerebral blood flow values that correlate well with values determined using radioactive microspheres across a wide range of cerebral blood flow rates.
Stroke 1989 Dec
PMID:Stable xenon versus radiolabeled microsphere cerebral blood flow measurements in baboons. 251 92

We developed techniques to assess the utility of a nuclear magnetic resonance (NMR) indicator for cerebral blood flow studies in cats, using Freon-22 for the first candidate. A PIN-diode-switched NMR experiment allowed the acquisition of an arterial as well as a cerebral fluorine-19 signal proportional to concentration vs. time in a 1.89 T magnet. Mean +/- SD blood:brain partition coefficients for Freon-22 were estimated at 0.93 +/- 0.08 for gray matter and 0.77 +/- 0.12 for white matter. Using maximum-likelihood curve fitting, estimates of mean +/- SD resting cerebral blood flow were 50 +/- 19 ml/100 g-min for gray matter and 5.0 +/- 2.0 ml/100 g-min for white matter. Hypercapnia produced the expected increases in gray and white matter blood flow. The physiologic effects of Freon-22, including an increase in cerebral blood flow itself with administration of 40% by volume, may limit its use as an indicator. Nevertheless, the NMR techniques described demonstrate the feasibility of fluorine-19-labeled compounds as cerebral blood flow indicators and the promise for their use in humans.
Stroke 1989 Feb
PMID:Cerebral blood flow measured by NMR indicator dilution in cats. 264 93

Many of the drugs used in anesthesia and intensive care may cause blockade of the central cholinergic neurotransmission. Acetylcholine is of significance in modulation of the interaction among most other central transmitters. The clinical picture of the central cholinergic blockade, known as the central anticholinergic syndrome (CAS), is identical with the central symptoms of atropine intoxication. This behaviour consists of agitation including seizures, restlessness, hallucinations, disorientation or signs of depression such as stupor, coma and respiratory depression. Such disturbances may be induced by opiates, benzodiazepines, phenothiazines, butyrophenones, ketamine, etomidate, propofol, nitrous oxide, and halogenated inhalation anesthetics as well as by H2-blocking agents such as cimetidine. There is an individual predisposition for CAS--but unpredictable from laboratory findings or other signs. Reports of postanesthetic occurrence of the CAS requiring treatment are not unanimous, varying between 1 and 40%. Differential diagnosis of the CAS includes disorders of glucose and electrolyte metabolism, severe hormonal imbalance, respiratory disorders (hypoxia, hypercarbia), hypothermia, hyperthermia and neuropsychiatric diseases (cerebral hypoxia, stroke, catatony, acute psychosis). The CAS may considerably impair the postanesthetic period especially when agitation is prevalent, which may endanger the patient or the surgical results. The diagnosis is confirmed ex iuvantibus by the sudden increase in the acetylcholine level in the brain. This is achieved with physostigmine, a cholinesterase inhibitor able to easily cross the blood-brain barrier. Its peripheral muscarinic effects are minimal. Postanesthetic CAS can be prevented by administration of physostigmine during the anesthesia procedure. During intensive care (IC), agitated forms of CAS may occur in patients undergoing mechanical ventilation, particularly during prolonged high-dose sedation. Artificial ventilation of such patients becomes very difficult and muscle relaxation may be necessary. In these cases of IC-CAS, physostigmine is of value and has proven beneficial during weaning from mechanical ventilation. Dealing with the CAS for more than a decade has improved knowledge of the central cholinergic transmission. For example, it can be said that CAS occurs alongside general anesthesia, being no more than a frequent side-effect. Furthermore, acetylcholine is involved in nociception through the endorphinergic and the serotoninergic systems. There is a close relation between the central cholinergic transmission and actions of nitrous oxide. Moreover, cholinergic transmission is involved in withdrawal from (among others) alcohol, opiates, hallucinogens and nitrous oxide. In some intoxications with psychoactive agents, physostigmine is useful for reversal of the central nervous symptoms of the acute intoxication itself. In addition it can be used for prevention of some withdrawal states. In
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PMID:Central anticholinergic syndrome (CAS) in anesthesia and intensive care. 268 49

Adenosine has been proposed as a metabolic factor involved in the regulation of cerebral blood flow. The evidence in support of this hypothesis, presented in this review, includes information on the adenosine receptors associated with cerebral blood vessels, the synthesis and metabolism of adenosine, and the release of adenosine from the brain. Adenosine dilates cerebral blood vessels, acting at an A2 receptor. The critical evidence implicating an involvement of adenosine in cerebrovascular regulation is derived from experiments with adenosine antagonists and potentiators. The antagonists include methylxanthine adenosine receptor antagonists and the enzyme adenosine deaminase. Potentiators include transport inhibitors, enzyme inhibitors, and adenosine precursors. Adenosine has been implicated in vascular regulation during hypoxia/ischemia, hypercapnia, seizures, severe hypotension, and hypoglycemia. Adenosine possesses a number of properties that can be used to minimize neuronal degeneration during cerebral insults, such as ischemia, including vasodilatation, reduction of excitatory transmitter release, reduction of membrane calcium permeability, inhibition of platelets, and neutrophil aggregation. Several recent studies have demonstrated that manipulation of central adenosine tone can alter the extent of cerebral ischemic damage, indicating a potential new therapeutic approach for the treatment of stroke.
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PMID:Adenosine in the control of the cerebral circulation. 270 69

We examined mitochondrial oxidative function 5 minutes and 2 hours after a gradual asphyxial insult in newborn lambs. We subjected 16 ventilated newborn lambs to 75-90 minutes of hypoxia and hypercarbia that resulted in bradycardia and systemic hypotension over the final 15 minutes of the insult. At the end of asphyxia, the lambs were resuscitated and returned to control ventilator settings. Samples of brain were removed 5 minutes (n = 8) and 2 hours (n = 8) after asphyxia. Each group of eight lambs was subdivided into those less than 3 or greater than 3 days old to evaluate the effect of age on postasphyxia mitochondrial function. After classification into nonsynaptic and synaptic mitochondria, mitochondrial respiration (oxygen consumption) was measured using five different substrates. Data from asphyxiated lambs were compared with that from a control group of ventilated nonasphyxiated lambs (n = 8). In the lambs less than 3 days old, there was significant depression of mean +/- SEM nonsynaptic mitochondrial state 3 (adenosine diphosphate-dependent) respiration to 29.5 +/- 5.2% of control with four of the five substrates and of state 4 respiration to 33.7 +/- 0.9% of control with three of the five substrates 5 minutes after asphyxia. By 2 hours after asphyxia, mean +/- SEM nonsynaptic mitochondria state 3 respiration increased to 70.4 +/- 6.4% of control while state 4 respiration increased to 58.2 +/- 4.5% of control. In contrast, lambs greater than 3 days old exhibited no inhibition of nonsynaptic mitochondrial function after asphyxia.(ABSTRACT TRUNCATED AT 250 WORDS)
Stroke 1989 May
PMID:Mitochondrial function after asphyxia in newborn lambs. 271 9

1. The effect of varying artificial respiratory volume (at a fixed rate of 54 min-1) on cardiac output, its distribution and tissue blood flows were determined with tracer microspheres in control pithed rats or during pressor responses to either the alpha 1-adrenoceptor agonist phenylephrine or the alpha 2-agonist xylazine. Phenylephrine was investigated in the presence of propranolol (3 mg kg-1). The rats were pithed under halothane anaesthesia. 2. A respiratory volume of 15 ml kg-1 produced modest hypercapnia (PaCO2 = 47 mmHg), hypoxia (PaO2 = 60 mmHg) and acidosis (pH = 7.35) relative to control animals respired at 20 ml kg-1 (PaCO2 = 32 mmHg; PaO2 = 77 mmHg; pH = 7.47). In rats respired at 15 ml kg-1, total peripheral resistance was lower, and cardiac output greater (due to increased stroke volume), than in the controls. Lowering respiratory volume reduced distribution of cardiac output to the kidneys, increased it to the large intestine and also increased blood flow through the gastrointestinal tract, skin and spleen. A respiratory volume of 30 ml kg-1 gave mild hypocapnia (PaCO2 = 19 mmHg), hyperoxia (PaO2 = 101 mmHg) and alkalosis (pH = 7.59) compared to 20 ml kg-1 but had no effect on cardiac output distribution or organ blood flow although heart rate was 29% greater at 30 ml kg-1. 3. Xylazine (500 micrograms bolus followed by 100 micrograms min-1 infusion) at all three respiratory volumes gave well-sustained mean pressor responses of 62-64 mmHg by increasing both total peripheral resistance and cardiac output (resulting from increased stroke volume). It increased the proportion of cardiac output passing to the liver, reduced that going to the spleen and gastrointestinal tract and increased cardiac, renal and hepatosplanchnic blood flows. 4. The secondary, relatively sustained, pressor effect of phenylephrine (5 micrograms bolus followed by 0.4 micrograms min-1 infusion, i.v.) varied at the 3 respiratory volumes with mean values from 32 to 53 mmHg. This response was due to both increased total peripheral resistance and cardiac output (resulting from greater stroke volumes and/or heart rates). Phenylephrine increased the proportion of cardiac output passing to the gastrointestinal tract, heart, kidneys and hepatosplanchnic bed and increased cardiac, hepatosplanchnic, renal and gastrointestinal blood flows. 5. Respiratory volume had no effect on the cardiovascular effects of xylazine. However, respiratory volume modified the effects of phenylephrine on heart rate and changed the relative contributions of stroke volume and heart rate to the increased cardiac output. It also influenced the effects of phenylephrine on cardiac output distribution to the liver, epididimides and hepatosplanchnic bed and on blood flow through skeletal muscle and the large intestine. 6. Changes in respiratory volume of air ventilated pithed rats thus influence cardiac output, its distribution and regional blood flows. Such changes can also differently influence the responses of various vascular beds to phenylephrine whilst having no effect on their responses to xylazine.
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PMID:Effect of artificial respiratory volume on the cardiovascular responses to an alpha 1- and an alpha 2-adrenoceptor agonist in the air-ventilated pithed rat. 289 57


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