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Biomedical subjects

R F Albrecht

Publications and source records attributed to R F Albrecht.

At least 127 records · Page 7Linked to original sources

Dual action of pancuronium on succinylcholine block.

The effects of pretreatment with both sub-paralyzing and paralyzing doses of pancuronium and d-tubocurarine, on the onset and duration of succinylcholine-induced neuromuscular blockade were evaluated and compared in 225 patients. D-tubocurarine antagonized both onset and duration of succinylcholine block, while pancuronium produced a dual effect, antagonizing the onset and potentiating the duration of succinylcholine block. Pretreatment with d-tubocurarine (0.07 mg/kg, 0.3 mg/kg and 0.6 mg/kg) increased the time to onset of succinylcholine paralysis from 28 to 118%, and decreased the duration from 16 to 37%. Pancuronium (0.02 mg/kg, 0.04 mg/kg and 0.08 mg/kg) also antagonized the onset of succinylcholine paralysis with increases of 32 to 114%, but potentiated its duration from 30 to 103% compared with succinylcholine alone in the same patients. Although pancuronium markedly inhibited serum cholinesterase in vitro (I50=5 X 10(-7) mol) there was only a 10% inhibition of cholinesterase in vivo after pancuronium 0.08 mg/kg.

Adult↗

Sodium nitroprusside and cerebral blood flow in the anesthetized and unanesthetized goat.

The effects of dodium nitroprusside (SNP) on total, ipsilateral cerebral blood flow (CBF) in the unanesthetized and anesthetized goat was evaluated under four conditions: 1) bolus injection of SNP into the cerebral circulation via the temporal artery; 2) continuous infusion of SNP into the temporal artery in amounts too small to affect the peripheral circulation (0.57-1.14 mug/kg/min); 3) intravenous infusion of SNP; 4) continuous intravenous infusion of SNP with a bolus injection af angiotensin. Small doses (20, 40, and 80 mug) of SNP injected directly in the cerebral circulation of the awake goat produced immediate increases of 21 +/- 8, 36 +/- 8, and 48+/- 10 per cent, respectively, in CBF lasting 1 to 3 min without causing peripheral cardiovascular changes. The effects of SNP were attenuated by 1.5 per cent halothane anesthesia. Continuous infusion of SNP into the temporal artery in amounts too small to cause peripheral cardiovascular effects produced sustained increases in CBF averaging 31+/- 8 percent; CBF returned to preinfusion values upon cessation of infusion. Intravenous infusion of SNP in both anesthetized and unanesthetized animals in recommended clinical dosages (3-8 mug/kg/min) produced hypotension but did not significantly alter CBF. However, upon injection of angiotensin (1.43 mug/kg), both peripheral blood pressure and CBF increased sharply, suggesting that SNP may impair autoregulation of CBF. The results of this study indicate that SNP dilates the cerebral vascular system in a way that is probably similar to its effects on other vascular beds.

Anesthesia, Inhalation↗

Cardiovascular effects of intraperitoneal insufflation with carbon dioxide and nitrous oxide in the dog.

Cardiovascular changes caused by intraperitoneal insufflation with CO2 or N2O were measured in 15 mongrel dogs. Moderate progressive increases in intra-abdominal pressure (to 40 mm Hg) with either gas produced increases in mean arterial, right atrial, pleural, and femoral-vein pressures. Cardiac output and inferior vena caval flow were momentarily increased following the commencement of insufflation. However, both flows decreased precipitously as insufflation pressure was increased. At an intra-abdominal pressure of 40 mm Hg cardiac output and inferior vena caval flow were reduced more than 60 per cent in most cases. Peripheral resistance increased by approximately 200 per cent. Upon sudden release of abdominal pressure cardiac output and inferior vana caval flow increased but then returned to pre-insufflation values within seconds. Directly measured right atrial pressure increased with increasing insufflation pressure, but calculated transmural right atrial pressure decreased with the increase in intra-abdominal pressure. Insufflation with CO2 produced significant increases in PaCO2. However, cardiostimulatory effects due to elevated blood CO2 levels were not seen. The data from this study indicate that intraperitoneal insufflation produces serious hemodynamic alterations which are manifested by low cardiac output and elevated total peripheral resistance. In addition, directly measured right atrial pressure cannot be used clinically as an indicator of venous return to the heart since it reflects a composite of pleural and intra-abdominal insufflation pressure. (Key words: Anesthetics, gases, nitrous oxide; Carbon dioxide, intraperitoneal; Surgery, intraperitoneal insufflation; Heart, function, intraperitoneal insufflation.).

Acid-Base Equilibrium↗

The effect of pancuronium on myocardial contraction and catecholamine metabolism.

The effects of pancuronium bromide infusion on the uptake and release of [14C] noradrenaline (14C-NA) by the isolated, perfused rat heart and on the chronotropic and inotropic activity of the isolated heart were evaluated. Hearts were removed from animals under light ether anaesthesia, transferred to a modified Langendorff perfusing apparatus and perfused with Krebs-Ringer bicarbonate solution at a rate of 5 ml min-1. The effect of pancuronium on the uptake of noradrenaline was determined by perfusing hearts for 5 min with perfusate containing various concentrations of pancuronium and 200 ng ml-1 of 14C-NA. After 5 min pancuronium-treated hearts contained less 14C-NA. The degree of reduced uptake increased with increasing concentrations of pancuronium. In addition, the combination of pancuronium perfusion and electrical stimulation (15 mA for 10 ms at 4 Hz) blocked the 50 min uptake of 14C-NA by the heart to a greater degree than either factor separately. The release of noradrenaline was determined after perfusing hearts with 14C-NA followed by perfusion with solution containing pancuronium but no 14C-NA for 1 h. Pancuronium infusion did not significantly alter the release of 14C-NA from the heart after 1 h of perfusion. The infusion of pancuronium caused a reduction in both the rate and strength of myocardial contraction of the isolated heart which was reversed by perfusion with perfusate free of pancuronium. Following perfusion with pancurnium the rate and strength of contraction of the heart was seen to "rebound" above pre-pancuronium values for a short period. The rebound of myocardial rate and contraction may have been due to the presence of myocardial noradrenaline previously blocked from reuptake by pancuronium since hearts removed from reserpinized animals did not demonstrate "rebound."

Animals↗

Cerebral hemodynamics following internal maxillary artery ligation in the goat.

Changes in cerebral and extracerebral blood flow in the goat after ligation of the internal maxillary artery and deliberate thrombosis of the extracerebral arteries (buccinator, ethmoidal, and ophthalmic) with thrombin were compared to changes seen in animals after internal maxillary artery ligation only and in normal animals where no surgical manipulations were performed. Blood flow was measured by injecting 51-Cr-labeled microspheres into the internal maxillary artery via a catheter placed into the temporal artery. Analysis of the radioactivity in extracerebral and intracerebral tissues indicated that when the internal maxillary artery is ligated and the extracerebral arteries are thrombosed, virtually all of the blood flow from the carotid artery is destined from the brain. However, if only the internal maxillary artery is ligated nearly one-fourth of the blood flow from the maxillary travels to extra-cerebral tissues. In normal animals, it was determined that only one-fourth of the blood flow in the internal maxillary is destined for the cerebral circulation. Results from this study indicate that if the former method is employed an accurate measure of cerebral blood flow is possible without the complications of extra-cerebral flow. If the latter technique is used care must be taken in evaluating cerebral blood flow since a large component of extra-cerebral blood flow is present.

Animals↗

Dose and time dependent cerebrovascular and metabolic effects of ethanol.

The purpose of these experiments was to determine the effect of ethanol dose and time of administration on cerebral blood flow (CBF) and cerebral oxygen consumption (CMRO2). CBF and CMRO2 were measured in Sprague-Dawley rats 30 and 90 minutes after intraperitoneal injections of ethanol. Blood alcohol concentrations ranged from 1 to 3 mg/ml and were equivalent at both time periods. Ethanol produced small but significant increases in CBF and CMRO2 with blood alcohol concentrations. The above changes were not time dependent and were similar between 30 and 90 minute testing periods. The dose dependent effects of ethanol on cerebral metabolism are consistent with in vitro studies suggesting a dose related effect of ethanol on neuronal metabolism. The time of application appears to have little effect on the cerebral metabolic effects of alcohol.

Animals↗

Regional vascular changes during hypotensive anesthesia.

The regional vascular effects of three different hypotensive drug treatments were compared in enflurane anesthetized rats. Controlled hypotension was induced with sodium nitroprusside (SNP), nitroglycerin (NTG),and deep enflurane anesthesia. Regional blood flow was measured during each hypotensive treatment using radioactive microspheres. All hypotensive treatments were compared with control rats, anesthetized with 2% inspired enflurane anesthesia. Results indicate that when the mean blood pressure was decreased from 124 to 70 torr with all three hypotensive treatments regionally specific blood flow changes occurred. These ranged from approximately 50% decreases seen in skin blood flow with all hypotensive drugs to 50-90% increases in flow in muscle and spleen tissues. When regional vascular resistance changes were compared between hypotensive drug treatments, SNP produced significantly less cerebrovasodilation than either NTG or deep enflurane. Deep enflurane induced hypotension resulted in significantly greater decreases in intestinal vascular resistance than either SNP or NTG. These results indicate that hypotensive anesthesia with SNP, NTG, or deep enflurane shift blood flow away from skin and toward skeletal muscle and spleen tissues. Blood flow in other tissues is relatively well maintained.

Anesthesia↗

Comparative metabolic effects of halothane and enflurane in rat heart cell culture.

The effects of halothane and enflurane on the oxygen consumption rates and substrate utilization by beating and nonbeating rat heart myocytes in cell culture were compared. Halothane, on an equal dose and equal MAC (minimum alveolar concentration producing immobilization of 50% of subjects) basis, was significantly more effective than enflurane in reducing total myocyte oxygen consumption and contractile rate. The greater effect of halothane on oxygen consumption was not due entirely to its effect on myocyte contractile rate, since quiescent (nonbeating) cells and cells rendered nonbeating by large doses of halothane also showed greater reductions in oxygen consumption than with large doses of enflurane. Both halothane and enflurane reduced glucose and palmitic acid metabolism by myocytes when compared with controls. However, there were no significant differences between halothane or enflurane with regard to glucose metabolism. Halothane was significantly more effective than enflurane in reducing cellular palmitic acid metabolism. Although palmitic acid uptake by myocytes was reduced to the same extent by both anesthetics when compared with control uptake values, halothane reduced myocyte uptake of glucose to a greater degree than enflurane. The results of this study indicate that halothane is a more potent myocardial metabolic depressant than enflurane.

Animals↗

Cerebrovascular and metabolic effects of bradykinin, ATP and hypercapnia in the goat.

Cerebral blood flow (CBF) and cerebral O2 metabolism (CMRO2) changes were measured in these studies during treatment with three reputed cerebral vasodilators: bradykinin, adenosine triphosphate (ATP) and increased arterial PCO2. Intracerebrovascular bradykinin infusions increased CMRO2 and CBF to a similar degree. Intramaxillary ATP infusions increased CBF to an extent greater than that required for increases seen in CMRO2. Hypercapnia increased CBF without a significant change in CMRO2. Results suggest that increases in cerebral metabolism may mediate most, some and none of the cerebrovascular changes produced by bradykinin, ATP or hypercapnia, respectively.

Adenosine Triphosphate↗