Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020538 (hypertension)
170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This study was conducted to investigate the degree of insult from asphyxia leading to total body circulatory arrest, as a model for brain resuscitation studies in rats. Of 78 male rats, 68 were anesthetized with halothane in O2/N2O, controlled ventilated, paralyzed with pancuronium and asphyxiated, 5, 7.5, 10, 12.5 and 15 min, respectively. Asphyxiation led to circulatory arrest in 244 +/- 22 s (mean +/- S.E.M.). Resuscitation was successful in 65% within 60 s using controlled ventilation with 100% O2, extrathoracic compressions and epinephrine intravenously. Subsequent intensive care to 6, 12 or 24 h was successful in 50% of resuscitated rats. At 6, 12 and 24 h of recovery, neurologic deficit scores and light microscopic neuropathology scores of the brain after in vivo fixation of the total body with intraventricular paraformaldehyde 3%, revealed a large scatter variability without a clear pattern. Lesions were located mostly in the frontal cortex and hippocampus (footplate) with ischemic neuronal change as the most frequent structural change. Brain cell necrosis was not seen after successful resuscitation. It seems that both scores were influenced by post-insult stress, as indicated by paroxysmal hypertension and motor activity, by complications, such as obstruction of the tracheotomy cannula by abundant sputum production, and by partial sedation with N2O and paralysis with pancuronium. This study indicates the feasibility of an asphyxial insult in rats for use in resuscitation studies of short duration. Although 24 h post-insult recovery is possible, up to 6 h seems most practical, with asphyxia of 7.5-10 min most successful and controllable. Questions are raised about the effects of irritation during the post-insult intensive care on both neurological deficit and neuropathology scores.
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PMID:Asphyxia, cardiac arrest and resuscitation in rats. I. Short term recovery. 609 Dec 5

The haemodynamic effects of isoflurane, halothane and enflurane when used to control intraoperative hypertension were evaluated in 30 patients undergoing coronary artery bypass grafting. The patients were anaesthetized with flunitrazepam, fentanyl, pancuronium and N2O-O2. Control measurements were made after skin incision. When mean arterial pressure increased to 110 mmHg due to sternal spread or surgical manipulation of the aorta, halothane, enflurane or isoflurane were administered to return arterial pressure to control levels. Using a non-rebreathing system, inspired halothane concentrations of 1.0-1.5 vol.%, enflurane concentrations of 2.0-2.5 vol.% and isoflurane concentrations of 1.5-2.0 vol.% were necessary. Measurements were repeated during the hypertensive episodes and after treatment with halothane, enflurane or isoflurane while surgical stimulation continued. During the hypertensive episodes marked elevations in systemic vascular resistance were observed, four patients developed ischaemic ST-segment changes. Each of the three inhalational anaesthetics decreased mean arterial pressure to baseline values within 5 to 10 minutes. The fall in blood pressure caused by halothane was mainly due to a reduction in cardiac index, since the elevated systemic vascular resistance almost remained unaffected. Enflurane produced a similar fall in cardiac index, although left ventricular afterload was significantly reduced, suggesting that enflurane caused more impairment of cardiac performance than halothane. In contrast, the administration of isoflurane was associated with an increase of the cardiac index in the presence of marked systemic vasodilation and a slight decrease in left ventricular filling pressure. Halothane, enflurane and isoflurane reduced the rate-pressure product by a comparable degree and, when present, abnormalities in the ST-segments disappeared.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Blood pressure control with an inhalation anesthetic in acute intraoperative hypertension. Hemodynamic profile of halothane, enflurane and isoflurane in coronary surgery patients]. 633 55

The hemodynamic effects of isoflurane and halothane when used to control intraoperative hypertension were evaluated in 20 patients undergoing coronary artery bypass grafting. The patients were anesthetized with flunitrazepam, fentanyl, pancuronium, and N2O-O2. Control measurements were made after skin incision. When mean arterial pressure increased to 110 mm Hg due to sternal spread or surgical manipulation of the aorta, isoflurane or halothane were used to return arterial pressure to control levels. Using a non-rebreathing system, inspired isoflurane concentrations of 1.5-2.0 vol% or halothane concentrations of 1.0-1.5 vol% were necessary. Measurements were repeated during the hypertensive episode and after treatment with isoflurane or halothane while surgical stimulation continued. Both inhalation anesthetics decreased arterial pressure to baseline values within 5-10 min. The lowering of arterial pressure with halothane was not accompanied by significant decreases in the elevated systemic vascular resistance and pulmonary capillary wedge pressure. Cardiac index and stroke volume index decreased markedly when halothane was used (18% and 25%, respectively). In contrast, isoflurane significantly decreased systemic vascular resistance (42%). This reduction of left ventricular afterload was associated with an increase in cardiac index (22%) and a decrease in left ventricular filling pressure. Heart rate did not change significantly. These findings indicate that isoflurane is superior to halothane for controlling intraoperative hypertension during coronary artery bypass surgery.
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PMID:Comparison of isoflurane and halothane when used to control intraoperative hypertension in patients undergoing coronary artery bypass surgery. 660 Mar 81

Intraoperative hypertensive episodes are a common problem in patients undergoing coronary artery bypass grafting. Twenty patients who developed acute hypertension (mean arterial pressure increase to 110 mmHg) were studied. Ten patients received nifedipine (about 3 micrograms kg-1 min-1) and ten patients nitroprusside (about 0.75 micrograms/kg-1 min-1) to return arterial blood pressure to control levels. All patients were anaesthetized with flunitrazepam, fentanyl, pancuronium and N2O/O2. The study compares the effects of nifedipine and nitroprusside on systemic and pulmonary haemodynamics. Both nifedipine and nitroprusside decreased arterial pressure to baseline values within about 3 min by reducing the elevated systemic vascular resistance. Cardiac filling pressures and pulmonary artery pressure decreased significantly only with nitroprusside. Following nitroprusside cardiac output remained unchanged whereas nifedipine increased cardiac output and stroke volume when blood pressure was lowered by a comparable degree. The data suggest that nifedipine primarily affects resistance vessels in the systemic circulation without significantly changing venous tone as opposed to the effect of nitroprusside. Thus, nifedipine appears to be an appropriate vasodilator for controlling arterial hypertensive episodes in patients with coronary artery disease and normal left ventricular function.
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PMID:Nifedipine versus nitroprusside for controlling hypertensive episodes during coronary artery bypass surgery. 660 18

To study the physiological tolerance to asphyxia and hypokalemia during anesthesia, the cardiovascular responses to clamping of the endotracheal tube during mechanical ventilation were evaluated in ten anesthetized mongrel dogs before and after they had been made hypokalemic by administration of furosemide, 10 mg X kg-1 X day-1 for 3-4 weeks. Furosemide reduced the serum potassium to 2.93 +/- 0.03 from 4.16 +/- 0.07 mEq/L. The animals were anesthetized with halothane in N2O-O2 (60/40) and mechanically ventilated to a PaCO2 of approximately 30 torr during continuous monitoring of heart rate, mean arterial pressure, ECG, and periodic determinations of serum electrolyte levels and arterial blood-gas tensions. The endpoint for unclamping of the endotracheal tube and reestablishing ventilation of the lungs was when mean arterial pressure decreased to levels present before clamping the trachea, approximately 100 torr, after an initial response of hypertension and tachycardia. The duration of clamping was not significantly different in normokalemic (8.41 +/- 1.47 min) and hypokalemic (9.01 +/- 0.47 min) dogs, but the time required to regain circulatory stability and normal ECG rhythm was longer for the hypokalemic group (2.95 +/- 0.44 min vs 2.17 +/- 0.47). In addition, while all normokalemic dogs survived, three of the hypokalemic dogs could not be resuscitated. The results suggest that chronic hypokalemia reduces the tolerance of the cardiovascular system to severe physiologic trespass.
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PMID:Cardiovascular responses to asphyxial challenge in chronically hypokalemic dogs. 662 18

Cerebral blood flow (CBF) and cerebral oxygen consumption (CMRO2) were measured in young (4 months) and aged (24-26 month) spontaneously hypertensive (SHR) rats and Wistar Kyoto (WKY) controls under control anesthetized conditions (70 per cent N2O, 30 per cent O2) and during hypotension induced with intravenous sodium nitroprusside (SNP) infusions. CBF was measured with radioactive microspheres and cerebral arterial-venous blood O2 measurements were determined from arterial and sagittal sinus blood samples. Arterial blood PCO2 was maintained at approximately 35 mmHg and body temperature at 37 degrees C. Under control conditions blood pressure was increased in SHR but there was no significant difference in CBF or CMRO2 between SHR and WKY or young and aged rats. CBF and CMRO2 were maintained in WKY when mean blood pressure was decreased to 65 mmHG with SNP infusion. CBF was significantly decreased in young and aged hypertensive rats during SNP-induced hypotension. CMRO2 was also decreased in both young and aged hypertensive animals. These results support previous reports that SNP-induced hypotension will maintain CBF and CMRO2 in normotensive subjects, but suggest that the direct cerebrovasodilating effects of SNP are moderate and will not reverse the cerebrovascular changes induced by chronic hypertension.
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PMID:Cerebrovascular and metabolic effects of SNP-induced hypotension in young and aged hypertensive rats. 708 26

The autoregulation of myocardial blood flow was studied under: (a) haemorrhagic hypotension (mean pressure decrease 40% from baseline); (b) drug-induced hypotension with sodium nitroprusside or trimetaphan (40% pressure decrease); (c) drug-induced hypotension (40% pressure decrease) after moderate blood loss of 20%. Dogs were used in experiments under general anaesthesia with sodium thiopentone and artificially ventilated with N2O/O2 (70%, 30%) and pancuronium. Under haemorrhagic hypotension, the flow was pressure-dependent from the beginning. During nitroprusside hypotension, there was autoregulation of coronary flow to the level of mean pressure decrease 30% from control. Under trimetaphan, a constant flow persisted to the level of mean pressure decrease 20% from the baseline. Identical changes were seen during drug-induced hypotension after moderate blood loss (20%). Central venous pressure, cardiac output, left ventricular stroke work and minute work changes are demonstrated. Blood gas data pH, PO2, PCO2 in the aortic and coronary sinus under drug-induced hypotension are compared with control groups. There is a level of autoregulation of myocardial blood flow under hypotension. This level can be unfavourably changed in cases with hypertension and coronary obstructive diseases.
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PMID:Autoregulation of myocardial blood flow under controlled hypotension in the dog. 711 27

An anaesthetic technique using high-dose fentanyl for coronary artery surgery is described. Fentanyl 60 or 70 micrograms kg-1 was used as the sole anaesthetic agent, and patients were ventilated with air/O2 (fentanyl 70 micrograms kg-1) or N2O/O2 (fentanyl 60 micrograms kg-1). Cardiovascular data from 30 patients are presented. Fentanyl caused no significant cardiovascular depression. The only statistically significant changes in cardiovascular parameters were seen in the patients who received fentanyl 60 micrograms kg-1. Five minutes after skin incision there was an increase in peripheral resistance. Diastolic pressure was increased following sternotomy. Problems associated with this technique of anaesthesia are a 50% incidence of hypertension following sternotomy (requiring treatment with sodium nitroprusside) and prolonged respiratory depression. The lack of cardiovascular depression produced by fentanyl and the ability of fentanyl to reduce hormonal and metabolic responses to surgery make it a satisfactory technique for cardiac anaesthesia.
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PMID:Cardiovascular effects of high-dose fentanyl anaesthesia. 712 5

The effectiveness of intravenously administered lidocaine for rapid control of acute intracranial hypertension was compared to the effectiveness of thiopental in 20 patients with brain tumors undergoing craniotomy. Despite normal radial arterial and intracranial pressures (ICP) after induction of N2O-O2-morphine anesthesia, mean ICP increased from 13.8 torr +/- 1.5 SE to 31 torr +/- 2.3 SE (p less than 0.001) in response to application of a pin-holder or scalp incision. To treat the elevated ICP a bolus injection of lidocaine, 1.5 mg/kg IV, was given to 10 patients, whereas the other 10 received thiopental, 3 mg/kg IV. Lidocaine reduced ICP 15.7 torr +/- 5.6 SE (p less than 0.025) did not significantly affect mean arterial pressure. In contrast, thiopental lowered ICP 18.4 torr +/- 9.6 SE (p less than 0.02) and also lowered mean arterial pressure by 26.1 torr +/- 9.6 SE (p less than 0.025). Mean time for injection of medication to ICP nadir was 66 seconds +/- 10 SE after lidocaine versus 48 seconds +/- 9 SE after thiopental (p greater than 0.20). It is concluded that lidocaine is as effective as thiopental for rapid reduction of intraoperative intracranial hypertension but that it causes less cardiovascular depression. Lidocaine may be of particular benefit to patients with both intracranial hypertension and marginal circulatory function.
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PMID:Lidocaine or thiopental for rapid control of intracranial hypertension? 718 82

In order to assess the influence of severe hypoglycemia on local cerebral blood flow (1-CBF) artificially ventilated rats, maintained on 70% N2O, were injected with insulin to provide either an EEG pattern of slow-wave polyspikes, or cessation of spontaneous EEG activity for 5, 15 or 30 min ("coma"). In other animals, glucose was injected at the end of a 30 min period of "coma" and 1-CBF was measured after recovery periods of 5, 30, 90, or 180 min. Local CBF was measured autoradiographically with 14C-iodoantipyrine as the diffusible tracer. In the slow-wave polyspike period 1-CBF was increased in most of the structures studied, and reached values that were 1.4 to 3.2 times greater than control. In many structures, cessation of EEG activity was accompanied by a further increase in 1-CBF, with some structures (thalamus, hypothalamus, pontine gray, and cerebellar cortex) showing flow rates of 400--500% of control. The increase in 1-CBF was unrelated to arterial hypertension, hypercapnia, or hypoxia. 5 min after glucose injection the hyperemia persisted in only some of the structures studied; in others, the 1-CBF were close to, or below, control values. During the subsequent recovery period 1-CBF was markedly reduced with some structures (cerebral cortical areas, hippocampus, and caudate-putamen) showing flow rates of only 20--35% of control. In others, notably pontine gray and cerebellar cortex, secondary hypoperfusion was never observed. The hypoperfusion was unrelated to arterial hypertension, hypocapnia, or increase in intracranial pressure. It is concluded that, like hypoxia and ischemia, substrate deficiency due to hypoglycemia is accompanied by vasodilatation in the brain. Furthermore, like long-lasting ischemia, severe hypoglycemia is followed by a delayed hypoperfusion syndrome that, by restricting oxygen supply, may well contribute to the final cell damage incurred.
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PMID:Local cerebral blood flow in the rat during severe hypoglycemia, and in the recovery period following glucose injection. 744 74


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