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Biomedical subjects

J E Cottrell

Publications and source records attributed to J E Cottrell.

At least 73 records · Page 4Linked to original sources
PubMed1986

Effect of vecuronium on intracranial pressure, mean arterial pressure and heart rate in cats.

The effect of vecuronium on intracranial pressure (ICP) was investigated in six cats with normal and increased ICP. Cats were anaesthetized with pentobarbitone 33 mg kg-1 i.p. and acepromazine 0.6 mg kg-1 i.p., the trachea was intubated, and the lungs ventilated with nitrous oxide in oxygen. Mean arterial pressure (MAP), heart rate (HR), twitch response and ICP were recorded continuously. After the effect of vecuronium had been ascertained under the condition of normal ICP, and after full recovery of twitch response, pH-adjusted Ringer's lactate solution was infused to the cisterna magna until an ICP baseline of 26 +/- 2 mm Hg was established, and had stabilized. Vecuronium was administered again to determine its effect under the condition of increased ICP. Complete ablation of twitch response was obtained in 68 +/- 15 s with vecuronium 80 micrograms kg-1, and there was no significant change in ICP, MAP, HR or cerebral perfusion pressure (CPP) under either ICP condition.

Animals↗
PubMed1985

Comparison of metaproterenol, isoetharine and salbutamol in the relief of methacholine-induced bronchospasm in dogs.

We evaluated cardiovascular effects and effectiveness of isoetharine, metaproterenol and salbutamol, when administered intratracheally to relieve methacholine-induced bronchospasm in dogs anaesthetized with 50 per cent nitrous oxide, oxygen, halothane and mechanically ventilated. Methacholine 2 micrograms X kg-1 X hour-1 was administrated first followed by halothane (1 MAC) for 30 minutes (control), then metaproterenol, isoetharine or salbutamol. Metaproterenol (15 mg) significantly decreased transpulmonary pressure to 20.1 +/- 0.5 (SE) from 22.5 +/- 1.15 cmH2O (p less than 0.025) after three min and to 15 +/- 0.5 cmH2O (p less than 0.005) after 90 min. Isoetharine (2.5 mg) decreased transpulmonary pressure after five min to 22.1 +/- 1 from 24.5 +/- 1.5 cmH2O (p less than 0.05), and to 21.75 +/- 0.55 mmH2O after 90 min. Salbutamol 25 micrograms X kg-1 decreased transpulmonary pressure to 20.7 +/- 0.75 from 24.25 +/- 1.28 after three min and to 16 +/- .5 after 90 min. The peak effects on airway pressure occurred at 15 min for metaproterenol, 25 min for salbutamol and 20 min for isoetharine. Pulmonary vascular resistance was not significantly changed during halothane anaesthesia alone but decreased significantly after metaproterenol and isoetharine infusion. Heart rate increased ten per cent after metaproterenol, three per cent after isoetharine, and five per cent after salbutamol. No arrhythmias occurred in any group. Cardiac output increased significantly to 3.25 +/- 0.2 from 1.5 +/- 0.17 L X min-1 (p less than 0.025) after metaproterenol to 3.2 +/- .025 from 1.45 +/- .009 after salbutamol and was unchanged after isoetharine. Metaproterenol and salbutamol in the presence of 1 MAC halothane anaesthesia relieved methacholine-induced bronchospasm more rapidly than did isoetharine. The onset of effect was 3 +/- 0.05 min for metaproterenol and salbutamol and 5 +/- 0.01 min for isoetharine. The effect lasted 210 +/- 10.5 min for metaproterenol, 170 +/- 12.5 min for salbutamol and 90 +/- 4.75 min for isoetharine.

Airway Resistance↗
PubMed1985

Intracranial pressure mean arterial pressure and heart rate after rapid paralysis with atracurium in cats.

The effect of atracurium on intracranial pressure (ICP) was investigated in six cats with normal and increased ICP. The cats were anaesthetized with intraperitoneal pentobarbitone (33 mg . kg-1), acepromazine (0.6 mg . kg-1) and incremental fentanyl (p.r.n. approximately equal to 20 micrograms . kg-1), intubated, and ventilated with nitrous oxide in oxygen. Mean arterial pressure (MAP), heart rate (HR), twitch response and ICP were continuously recorded. After the effect of atracurium had been ascertained under the condition of normal ICP, and after full recovery of twitch response, pH-adjusted Ringer's lactate solution was infused into the cisterna magna until an ICP baseline of 26 +/- 2 mmHg was established and stabilized. Atracurium was then administered again to determine its effect under the condition of elevated ICP. Complete ablation of twitch response was obtained in 68 +/- 15 sec with 0.4 mg . kg-1 atracurium, and there was no significant change in ICP, MAP, HR or cerebral perfusion pressure (CPP) whether initial ICP was normal or elevated.

Anesthesia, General↗
PubMed1985

Intracranial pressure during diltiazem-induced hypotension in anesthetized dogs.

The effect of diltiazem-induced hypotension on intracranial pressure (ICP) was studied in dogs with normal and elevated ICP. Eight dogs were anesthetized with intravenous pentobarbital, intubated, and ventilated with N2O:O2. Mean arterial pressure (MAP), heart rate (HR), pulmonary artery pressure (PAP), pulmonary capillary wedge pressure (PCWP), central venous pressure (CVP), and cardiac out-put (CO) were recorded. A ventriculostomy was performed for measurement of ICP. Baselines were established, and diltiazem was infused to reduce MAP 40 +/- 1% for 10 min. After recording the effects of diltiazem-induced hypotension during normal ICP, ICP was elevated by infusion through a ventriculostomy cannula of pH-adjusted Ringer's lactate, baselines were reestablished, and MAP was again reduced by 40 +/- 1% with diltiazem. When baseline ICP was normal, diltiazem-induced hypotension produced a statistically significant increase in ICP (4.8 +/- 0.6 mm Hg) and a decrease in cerebral perfusion pressure (CPP). When baseline ICP was elevated, a smaller increase in ICP occurred (1.3 +/- 0.5 mm Hg). Although these increases in ICP were not clinically significant, the dose of diltiazem required to lower MAP 40% caused significant alterations in HR, systemic vascular resistance, CO, and PCWP. Serious cardiac rhythm disturbances occurred in five of eight dogs when baseline ICP was normal and in six of eight dogs when baseline ICP was elevated. The relatively long duration of diltiazem's hemodynamic effect and the high incidence of cardiac rhythm disturbances make it an unsuitable drug for inducing deliberate hypotension.

Anesthesia↗
PubMed1984

Effect of volatile anaesthetics and nitrous oxide-fentanyl anaesthesia on bleeding time.

Fifty-one patients were divided randomly into four groups: halothane in oxygen; fentanyl plus nitrous oxide in oxygen; enflurane in oxygen; or isoflurane in oxygen. Standardized bleeding time was measured using a Simplate II bleeding device before and at least 40 min after the induction of anaesthesia. Arterial pressure was maintained at +/- 20% of control values and temperature was kept at 35-37 degrees C. The bleeding time was prolonged by 33% in the halothane group (P less than 0.01) and by 20% in the nitrous oxide-fentanyl group (n.s.). There was essentially no change in bleeding time in the groups receiving enflurane or isoflurane, although there was considerable variability within each group, which did not seem to be related to differences in sex, age, type of surgery, concentration of agent used or surgical procedure.

Adult↗
PubMed1984

Intracranial pressure during tetrodotoxin-induced hypotension.

The effect of tetrodotoxin-induced hypotension on intracranial pressure (ICP) was investigated in cats with normal and artificially increased ICP. Cats were anesthetized with intraperitoneal pentobarbital (25-30 mg/kg), intubated, and ventilated with nitrous oxide in oxygen. Mean arterial pressure (MAP), heart rate (HR), and pulmonary arterial pressure (PAP) were continuously recorded. A double 18-gauge needle was inserted into the cisterna magna; ICP was continuously monitored from one needle and the other was used to increase and maintain ICP at 27 +/- 4 mm Hg by infusion of pH-adjusted Ringer's lactate solution. After control measurements were taken, tetrodotoxin (TTX) was given intravenously in each cat when ICP was normal and increased. Injection of 8-16 micrograms TTX (approximately equal to 2-4 micrograms/kg) decreased MAP 40-50% for 8-12 min under both initial ICP conditions. Whether initial ICP was normal or elevated, no significant increase occurred in ICP (0.6 to 1 mm Hg), and cerebral perfusion pressure (CPP) was not jeopardized. When initial ICP was normal, TTX caused a decrease in HR that was statistically but not clinically significant. The change in HR when initial ICP was increased was not statistically or clinically significant. No significant change in PAP was apparent during TTX-hypotension under either initial ICP condition.

Anesthesia, General↗
PubMed1984

Cell membrane fusion by chloroprocaine.

The cytotoxicity of the local anesthetics chloroprocaine, procaine, and lidocaine was studied in murine and human cells. Murine glial and hepatic cells, and human fibroblasts were individually exposed to chloroprocaine, procaine, and lidocaine in concentrations ranging from 1.6 X 10(-3) M to 0.2 X 10(-3) M. The cells of all three cell lines underwent membrane fusion after exposure to chloroprocaine as indicated by the presence of the high number of multinucleated cells in the cultures. The 0.8 X 10(-3) M concentration was the most fusogenic, and caused multinucleation in 30% of glial and hepatic cells, and in 23% of fibroblasts. Membrane fusion and multinucleation also occurred in mixed human and murine cell cultures that were exposed to 0.8 X 10(-3) M concentration of both commercial and crystalline solutions of chloroprocaine, with a portion of multinucleated cells that was 27 and 17%, respectively. Cell membrane fusion was not caused by procaine, lidocaine, sodium bisulfite (the antioxidant present in the commercial solutions of chloroprocaine), or chloro-aminobenzoic acid and diethylamino-ethanol (the two chloroprocaine metabolites). The fusogenic effect of chloroprocaine on cell membrane has not been previously described for any local anesthetic.

Anesthetics, Local↗
PubMed1983

Intracranial and hemodynamic changes after succinylcholine administration in cats.

Bolus injections of succinylcholine (1.5 mg/kg) significantly increased intracranial pressure (ICP) in cats under normal conditions from control levels of 8 +/- 1 mm Hg to 16 +/- 3 mm Hg (+/- SEM, P less than 0.01), and in the presence of artificially increased ICP from control levels of 27 +/- 1 mm Hg to 47 +/- 4 mm Hg (P less than 0.01). These approximately 100% increases in ICP were accompanied by a transitory decrease in mean arterial pressure (approximately 10 sec), followed by a 15-20% increase (P less than 0.05). Pulmonary arterial pressure increased 20-30% (P less than 0.05). These results, when considered in conjunction with results previously obtained in humans, suggest that succinylcholine may be contraindicated in neurosurgical patients.

Animals↗
PubMed1983

Intracranial pressure during nifedipine-induced hypotension.

The effect of nifedipine-induced hypotension on intracranial pressure (ICP) was investigated in cats with normal and artificially increased ICP. Eleven cats were anesthetized with intraperitoneal pentobarbital (25 mg/kg), intubated, and ventilated with nitrous oxide in oxygen. Mean arterial pressure (MAP), heart rate (HR), and mean pulmonary artery pressure (PAP) were continuously recorded. A double 19-gauge needle was inserted into the cisterna magna; ICP was continuously monitored from one needle and the other was used to increase and maintain ICP at 27 +/- 4 mm Hg by infusion of pH-adjusted Ringer's lactate solution. After control measurements were taken, nifedipine was given intravenously in each cat when ICP was normal and increased. Infusion of 96 +/- 12 micrograms (SEM) nifedipine (approximately equal to 33 micrograms/kg) reduced MAP 35-45% for 2.5 +/- 0.8 min when ICP was normal, and for 2.0 +/- 0.6 min when ICP had been increased. When initial ICP was normal, nifedipine-induced hypotension produced a small (2.2 mm Hg) but statistically significant increase in ICP and decrease in cerebral perfusion pressure (P less than 0.01). When ICP was initially elevated, nifedipine-induced hypotension produced a larger increase in ICP (5 +/- 1 mm Hg) and a proportionately larger decrease in cerebral perfusion pressure (P less than 0.01).

Animals↗
PubMed1982

Intrapulmonary shunting during induced hypotension.

The effect of sodium nitroprusside (SNP) and nitroglycerin (TNG) on pulmonary shunting (Qs/Qt) in 14 consenting adults [nine with normal lung function and five with chronic obstructive pulmonary disease (COPD)] was studied under general anesthesia. Qs/Qt significantly increased (p less than 0.005) from 5.19% to 8.81%, whereas pulmonary arterial pressure (PAP) decreased from 18.5 to 8 torr (p less than 0.005) and pulmonary vascular resistance (PVR) decreased from 235 to 147.75 dynes . sec/cm5 (p less than 0.025) when SNP was administered to patients with normal lung function. Nitroglycerin increased Qs/Qt from 5.13% to 6.19% (p less than 0.005), whereas PAP decreased from 18 to 10 torr (p less than 0.005) and PVR decreased from 237 to 162.6 dynes . sec/cm5 (p less than 0.025) in these patients. In patients with COPD, SNP and TNG produced no significant changes in Qs/Qt, PAP, or PVR. Cardiac output remained unchanged in both groups of patients. Various mechanisms to explain these results can be postulated. When hypotension is induced in patients with normal pulmonary function. PAP decreases and the effect of gravity puts more blood through dependent areas where most of the shunt units are. In patients with COPD, destructive vascular changes increase PAP, preventing vasodilators from decreasing PVR. In addition, dilation of hypoxic pulmonary vasoconstriction (if present) by SNP and TNG will occur independent of the two previously mentioned mechanisms. These results provide evidence that SNP- and TNG-induced hypotension may cause significant impairment in pulmonary gas exchange in patient with normal lung function. In patients with COPD pulmonary gas exchange is not affected after deliberate hypotension with SNP or TNG.

Adult↗
PubMed1982

Hemodynamic and catecholamine changes after administration of naloxone.

The hemodynamic and catecholamine response to intravenously administered naloxone, 0.2 mg and 0.4 mg, were determined in one group of surgical patients and one group of volunteers. Naloxone, 0.2 mg, was administered 30 minutes before the 0.4-mg dose. Group I consisted of six normotensive (IA) (aged 18 to 64, mean 35.7 years) and six hypertensive surgical patients (IB) (aged 35 to 67, mean 49.1 years) who were receiving a nitrous oxide, oxygen, and halothane anesthetic. Group II consisted of six normotensive (IIA) (aged 27 to 38, mean 36.1 years) and five hypertensive (IIB) unanesthetized volunteers (aged 41 to 60, mean 51.4 years). Mean arterial pressure, heart rate, plasma norepinephrine, epinephrine, and dopamine levels were compared before and after intravenous naloxone. Changes in mean arterial pressure, heart rate, plasma norepinephrine, epinephrine, and dopamine levels were not statistically significant in any group. This study suggests that intravenous naloxone, per se, alters neither mean arterial pressure, heart rate, or plasma catecholamine levels in normotensive or hypertensive humans.

Adolescent↗
PubMed1981

Cerebrospinal fluid cyanide after nitroprusside infusion in man.

Sodium nitroprusside (SNP) is frequently used as an hypotensive agent for clipping of intracranial aneurysms, repair of arteriovenous malformations and resection of vascular tumours. Cyanide (CN), which is its main metabolic product, has been recovered from the cerebrospinal fluid (CSF) of the rat after intravenous administration of CN, but recovery of CN from CSF after SNP has not been reported in man. Seven consenting adults were studied. Adequate premedication was provided with pentobarbitone 2 mg x kg-1 and atropine 0.4 mg one hour before operation. Anaesthesia was induced with thiopentone 8 mg x kg-1 and maintained with nitrous oxide 60 per cent with oxygen and supplemental fentanyl 0.05 mg and pancuronium 0.5-1 mg as needed. Lumbar subarachnoid, radial artery, central venous, and Foley urinary catheters were inserted. Arterial carbon dioxide tension (PaCO2) was maintained between 4.6-5.32 kPa (35-40 torr) with an Air Shields ventilator. Red cell, plasma and CSF cyanide were measured using a digital ionanalyzer before and at 30 minutes interval after infusing SNP at a rate sufficient to maintain the blood pressure at two thirds of the pre-operative level. Average total dose of SNP was 0.51 mg x kg-1. CN concentration in the red blood cells increased from 9.5 +/- 2.05 to 75.12 +/- 17.12. Plasma CN increased from 0.54 +/- 0.05 to 1.09 +/- 0.14 micrograms per cent. CSF CN increased from 0.11 +/- 0.04 to 0.72 +/- 0.07 micrograms per cent. Significant increase in red cell, plasma and CSF CN occurred five minutes after the start of SNP and returned to the preoperative level 19 hours later. Conclusion CN crosses the blood-brain barrier. Large doses of SNP in patients with neurovascular brain disorders warrants caution because cytotoxic cerebral oedema and CN encephalopathy have been described in rats after intravenous injection of sodium cyanide or exposure to hydrogen cyanide.

Adult↗