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Biomedical subjects

D Howland

Publications and source records attributed to D Howland.

12 recordsLinked to original sources
PubMed1979

Halothane anesthesia in calves.

Because of the calf's popularity as an experimental animal and its often noted sensitivity to anesthetics and anesthesia, the potency of halothane was studied in eight, young (x = 5.85 weeks), healthy, male Holstein-Friesian calves. The minimal alveolar halothane-O2 concentration (MAC) which just prevented calf movement in response to a tail clamp was 0.76 +/- SEM 0.03 vol% and is less than predictions based on studies in man. The addition of 50% N2O to inspired gases decreased the halothane MAC to 0.59 +/- 0.03%. In the absence of common modifying factors of anesthesia, halothane-O2 caused cardiopulmonary depression in these calves in proportion to anesthetic dose. Only two (total protein and albumin) of 17 selected blood clinical biochemical values were significantly (P less than 0.05) altered from base line within seven days of anesthesia, indicating insults to major organ systems did not occur.

Anesthesia, Inhalation↗
PubMed1978

Potency of enflurane in dogs: comparison with halothane and isoflurane.

Circulatory and respiratory responses to graded increases in alveolar concentrations of enflurane were investigated in unpremedicated healthy dogs during conditions of spontaneous and controlled ventilation. The minimal alveolar concentration (MAC) of enflurane that prevented movement in response to a standard painful stimulus was determined for each dog and averaged 2.06 vol%. In these studies, enflurane produced cardiopulmonary depression in proportion to the alveolar dose. The average end-tidal enflurane concentration that produced at least 60 s of apnea was 5.29 vol% (ie, MAC 2.57). A comparison of these data with previous studies in dogs indicates that equipotent concentrations of enflurane are at least as depressant to the cardiopulmonary system as halothane and isoflurane.

Anesthesia, Inhalation↗
PubMed1978

Cardiovascular effects of halothane in the horse.

Cardiovascular effects of venous alveolar concentrations of halothane in oxygen were studied in 8 young, healthy horses under conditions of constant arterial carbon dioxide tension. The alveolar concentration of halothane was expressed as a multiple of the minimal alveolar concentration (MAC) which was known for each animal. Increasing alveolar halothane concentrations to MAC 2.0 resulted in a progressive and significant (P less than 0.05) decline in systemic arterial pressure and left ventricular work. Cardiac output decreased between MAC 1.0 and MAC 2.0 as a result of a significant (P less than 0.05) decrease in stroke volume. Heart rate, total peripheral resistance, pulmonary artery pressure, hematocrit, plasma protein concentration, arterial oxygen tension, and arterial pH remained constant over the same range of anesthetic dosages. Continuation of anesthesia, spontaneous ventilation, and the accompanying rise in arterial carbon dioxide tension and electrical stimulation of the horse's oral mucous membranes produced varying degrees of stimulation of cardiovascular function at MAC 1.5.

Anesthesia, Inhalation↗
PubMed1978

Potency of halothane-N20 in the horse.

The minimal alveolar concentration (MAC) of halothane which just prevented purposeful movement in response to electrical stimulation was determined in 11 young, healthy, unpremedicated horses breathing oxygen (O2) or nitrous oxide (N2O) and O2. Ventilation was controlled during these MAC studies. The arterial PO2 was always greater than 90 mm of Hg and the average PaCO2. range was 36 to 40 mm of Hg. The MAC for halothane in O2 was 0.93 vol %. Alveolar N2O concentrations of 25% and 50% reduced the halothane MAC about 12% and 25%, respectively. In 8 of these horses, the cardiovascular effects of halothane-50% N2O-balance O2 (H50N2O) were determined during spontaneous and controlled ventilation and were compared with previously reported results of halothane-O2 studies. Similar to halothane-O2 anesthesia, increasing dosages of H50N2O caused a decrease in cardiovascular function. With the exception of N2O-associated increase in cardiac output and left ventricular work at MAC 1.0 and 1.5, little difference was seen between the 2 forms of general anesthesia during controlled ventilation. However, when H50N20 was administered to spontaneously breathing horses, most indices of cardiovascular function were depressed less than with a similarly administered equipotent level (MAC 1.5) of halothane-O2 anesthesia.

Anesthesia, Inhalation↗
PubMed1977

Meperidine-halothane interaction in dogs.

We studied the interaction of meperidine and halothane in 24 unmedicated, spontaneously breathing dogs. Intramuscular (i.m.) injections of meperidine, 2.75 mg/kg, 5.5 mg/kg and 11.0 mg/kg reduced the minimal alveolar concentration (MAC) of halothane required for anaesthesia. The magnitude and duration of MAC depression were dose related. Plasma meperidine concentrations following an i.m. injection of 2.75 mg/kg were lower in the awake, unsedated dogs than in the dogs anaesthetized with halothane.

Anesthesia↗
PubMed1977

Rate of change of halothane concentration in a large animal circle anesthetic system.

The slow rate of change of inspired halothane concentration which results in a conventional large animal circle anesthetic delivery system when low carrier gas flow rates are used was confirmed, using a model system. To obtain a 63% change in inspired halothane concentration in the 32-L large animal circle anesthetic machine at fresh gas inflow rates of 3, 6, and 12 L/minute required 10.7, 5.3, and 2.7 minutes, respectively. At a given inflow rate, increasing the rebreathing bag size from 20 to 40 L prolonged the time for equilibration between the gas flowing into the anesthetic circuit and the inspired gas. The extent to which an adult horse further slowed the rate of rise of inspired anesthetic concentration was also demonstrated.

Anesthesia, Inhalation↗
PubMed1977

Enflurane, halothane, and isoflurane potency in horses.

The minimal alveolar concentration of anesthetic required to prevent gross purposeful movement in response to electrical stimulation of oral mucous membranes was determined in horses for 3 agents. Equipotent concentrations of enflurane were 2.12 volumes %; of halothane, 0.88 volumes %; and of isoflurane, 1.31 volumes +. The alveolar concentration required to produce at least 60 seconds of apnea was also determined for these agents. From these data and the minimal alveolar concentration information, anesthetic indices were determined for each agent. The indices for enflurane, halothane, and isoflurane were 2.26, 2.60, and 2.33, respectively.

Anesthesia, Inhalation↗
PubMed1977

Isoflurane potency in the dog and cat.

Cardiopulmonary effects of isoflurane, a new inhalation anesthetic, were investigated in healthy unpremedicated dogs and cats under conditions of spontaneous and controlled (dogs only) ventilation. Measurements were made at minimal alveolar concentration (MAC) multiples of 1.0, 1.5, 2.0, and 3.0 in dogs and 1.0, 1.5, 2.0, and 2.4 in cats. The isoflurane MAC was previously determined in these animals and was 1.28 +/- 0.06% for dogs and 1.63 +/- 0.02% for cats. We found that as anesthetic dose increased, mean arterial pressure consistently and significantly (P less than 0.05) decreased. Cardiac output, measured only in dogs, was sustained only during light-moderate levels (1.0 to 2.0 MAC) of anesthesia because the heart rate significantly increased. Stroke volume, total peripheral resistance, and left ventricular work tended to decrease as anesthesia deepened. We found no significant difference in cardiovascular measurements in dogs between spontaneous and controlled ventilation at equal MAC multiples. That isoflurane is a profound respiratory depressant in dogs and cats is supported by our findings of a dose-dependent increase in PaCO2. In addition, the alveolar isoflurane concentration required to produce at least 60 seconds of apnea divided by MAC (i.e., the anesthetic index) averaged 2.5 for dogs and 2.4 for cats. The anesthetic index which we determined for isoflurane in dogs equals or is less than the index reported for other inhaled anesthetics in this species.

Anesthesia, Inhalation↗
PubMedDate not supplied

Nitrous oxide: effect on accumulation rate and uptake of bowel gases.

Breathing 79% nitrous oxide (N2O) in oxygen increased the rate of accumulation of bowel gas during intraluminal bowel segment infusions of hydrogen, methane (CH4), air, or carbon dioxide (CO2) in four pentobarbital-anesthetized dogs more than did breathing 100% oxygen. A N2O-associated increase in the volume of naturally produced intestinal gas in five halothane-anesthetized ponies corroborated the findings in the dog studies. In a second group of four dogs a bolus of CH4 or CO2 was injected into the bowel lumen. When the dogs breathed O2 the bowel gas volume decreased. Gas was virtually absent in the CO2-containing segment within 20 minutes. Breathing N2O increased the volume of the segments containing CH4 while the CO2 segments decreased less rapidly than during O2 breathing. Breathing O2 after 30 minutes of N2O breathing caused little change in the rate of decrease in CO2 segment volumes. However, the CH4 segment volume ceased to increase and eventually returned toward control volumes.

Air↗