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Biomedical subjects

G A Rooke

Publications and source records attributed to G A Rooke.

29 records · Page 2Linked to original sources
PubMed1993

The effect of halothane on the sarcoplasmic reticulum in normal and right ventricular hypertrophy in rabbits.

Calcium accumulation and storage by the sarcoplasmic reticulum is affected adversely by both inhaled anesthetics and hypertrophy. The interaction of these two conditions in right ventricular muscle was examined in a skinned fiber preparation whereby the sarcolemma was disrupted mechanically to permit external control of the chemical composition of the cytoplasm. Skinned fibers were obtained from the right ventricles of rabbits 4 mo after surgical banding of the pulmonary artery (n = 5) or sham banding (n = 4). Right ventricles after pulmonary artery banding weighed an average of twice that of normal right ventricles. The sarcoplasmic reticulum of the skinned fibers was permitted to accumulate Ca2+ and then maximal or submaximal Ca2+ release was induced with 25 mM or 2 mM caffeine, respectively. The magnitude of the Ca2+ release was estimated by the area of the ensuing tension over time. When 1%, 2%, or 3% halothane accompanied the 2 mM caffeine, both normal and hypertrophied muscle exhibited an area of the tension transient twice that of the tension transients without halothane (control). When present during Ca2+ accumulation, 1%, 2%, and 3% halothane reduced the 25 mM caffeine-induced tension transient in normal and hypertrophied muscle to 36%, 17%, and 11%, respectively, of the controls. The equal depression in normal and hypertrophied right ventricles was in contrast to a previous study in which hypertrophy provided some protection against the decrease in sarcoplasmic reticulum Ca2+ storage by halothane.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia, Inhalation↗
PubMed1992

Left ventricular hypertrophy in rabbits does not exaggerate the effects of halothane on the intracellular components of cardiac contraction.

Inhalational anesthetics and ventricular hypertrophy have adverse effects on cardiac muscle contraction. The effects of 1, 2, and 3% halothane on the contractile protein and sarcoplasmic reticulum, but not the sarcolemma, were examined in normal left ventricular tissue from rabbits that underwent a sham surgical procedure (n = 5) and in left ventricular hypertrophied tissue from surgically induced aortic coarctation (n = 7). Muscle samples were mechanically "skinned" to disrupt the sarcolemma. Fiber bundles were mounted in photodiode transducers and bathed in a series of solutions designed to examine the contractile protein [Ca2+]-tension responses or to examine Ca2+ storage by and release from the sarcoplasmic reticulum. Hill equation analysis of the [Ca2+]-tension relationship of the contractile protein was performed. Compared to normal muscle, hypertrophied muscle was associated with an 8.2% decrease in the [Ca2+] necessary for 50% maximum tension (more sensitive to Ca2+) (P less than 0.001) and an increase in the slope constant of 23% (P less than 0.001). In normal and hypertrophied tissue, each 1% of halothane incrementally decreased the contractile protein response to maximal [Ca2+] by 5% (P less than 0.01), increased the [Ca2+] at 50% maximum tension by 5% (P less than 0.01), and had no effect on the slope of the Hill equation. Halothane also inhibited Ca2+ storage by the sarcoplasmic reticulum. In normal muscle, 1, 2, and 3% halothane decreased the stored Ca2+ to 42, 22, and 9%, respectively, of Ca2+ storage without halothane (P less than 0.001). However, hypertrophied muscle demonstrated slightly less depression (P less than 0.05 by analysis of variance).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

Low-dose halothane anesthesia does not affect the hemodynamic estimation of myocardial oxygen consumption in dogs.

The accuracy of the product of systolic blood pressure and heart rate as a correlate of myocardial oxygen consumption has been questioned in anesthetized patients, suggesting that anesthesia alters the relationship between myocardial oxygen consumption and the hemodynamics. This relationship was reexamined in the awake state and during 0.95% end-tidal halothane anesthesia in seven chronically instrumented dogs. Measurements of myocardial oxygen consumption were compared with two indices, the systolic pressure rate product and the pressure work index. The latter is a weighted combination of the systolic pressure rate product and external cardiac work. A wide range in myocardial oxygen consumption (3.0-38.2 ml O2.min-1.100g-1) and hemodynamic states (range in pressure rate 4,100-40,700 mmHg/min and range in pressure work 3.7-37.0 ml O2.min-1.100g-1) was achieved with infusions of norepinephrine, nitroglycerin, neosynephrine, nitroprusside, and isoproterenol. Both the pressure rate product and the pressure work index correlated closely with myocardial oxygen consumption not only when the animals were awake but also during anesthesia. For each animal best-fit regression analysis for the awake and the anesthetized data did not reveal any significant change in the slope or y-intercept. Pooled data analysis that only permitted a change in slope with the addition of anesthesia (intercept unchanged) revealed a 17% decrease (P less than 0.05 on t test) in the slope constant when the pressure rate product was applied and no change in slope when the pressure work index was used to estimate myocardial oxygen consumption. It was concluded that myocardial oxygen consumption can be estimated during 0.95% halothane anesthesia by either index but that the pressure work index performs better than the systolic pressure rate product.

Anesthesia↗
PubMed1982

Work as a correlate of canine left ventricular oxygen consumption, and the problem of catecholamine oxygen wasting.

Neither stroke volume nor external cardiac work (the integral of pressure times flow during ejection) has been considered an important correlate of myocardial oxygen consumption. An initial set of experiments re-examined this question of independently varying heart rate, systolic blood pressure, and stroke volume in seven closed-chest, anesthetized dogs. This was achieved by cardiac pacing, a pressure control reservoir, phenylephrine infusion, and adjustment of arteriovenous shunts. Propranolol was used to minimize changes in contractility which might affect myocardial oxygen consumption. Stroke volume in the form of external work had a significant effect on oxygen consumption. From these results, a new pressure-work index of myocardial oxygen consumption was devised, and fitting parameters for the following indexes were determined: systolic pressure-rate product, estimated wall tension, external left ventricular work, triple product, mean pressure-rate product, Et (Bretschneider), and tension-time index. These indexes were prospectively applied to a second set of experiments in 11 closed-chest, anesthetized dogs given norepinephrine, isoproterenol, dobutamine, Nembutal, and propranolol to alter myocardial contractility. Inotropic oxygen wasting was observed with the tension-time, mean pressure-rate, triple product, and estimated wall tension indexes, but not with the pressure-work or systolic pressure-rate indexes. It is concluded that stroke work is an important correlate of myocardial oxygen consumption, and that the pressure-work of systolic pressure-rate indexes can account for catecholamine-induced, changes in myocardial oxygen consumption without postulating an oxygen-wasting effect.

Adrenergic beta-Antagonists↗
PubMedDate not supplied

Calcium channel blockers do not enhance increases in plasma potassium after succinylcholine in humans.

STUDY OBJECTIVE: To determine whether chronic calcium channel blocker therapy exaggerates the rise in plasma potassium concentration ([K+]) after succinylcholine administration. DESIGN: Prospective clinical study. SETTING: University and Veterans Affairs hospitals. PATIENTS: 36 ASA physical status III and IV male patients: 21 patients taking chronic calcium channel blockers and 15 patients not receiving calcium channel blockers, all of whom were scheduled for inpatient surgical procedures with general anesthesia. INTERVENTIONS: In all patients, anesthesia was induced with high-dose opioids plus a sedative-hypnotic, and intubation was facilitated with 1 to 1.5 mg/kg succinylcholine without nondepolarizing neuromuscular blocker pretreatment. MEASUREMENTS AND MAIN RESULTS: Plasma [K+] was measured prior to induction and 1, 3, 5, 8, 11, and 15 minutes after succinylcholine was administered. A modest average peak rise of 0.5 mEq/L in plasma [K+] was observed, but there were no differences between patients who were or were not receiving calcium channel blockers. CONCLUSIONS: Patients receiving chronic calcium channel blocker therapy are at no greater risk of hyperkalemia after succinylcholine than those not taking such medications.

Anesthesia, Intravenous↗
PubMedDate not supplied

Failure of an epinephrine test dose to elicit tachycardia after intravascular epidural catheter placement.

A 58-year-old woman who was not taking beta-adrenergic block medication had a lumbar epidural catheter placed intravascular unintentionally. Epinephrine 15 micrograms in 3 ml saline or 2% lidocaine caused an increase in blood pressure and a decrease in heart rate. Observation of the patient for other signs of intravascular injection besides an increase in heart rate is discussed.

Blood Vessels↗