alpha-Adrenoreceptor stimulation of the systemic circulation in dogs.

The influence of phenylephrine (an alpha-adrenoreceptor agonist) on the arterial and venous systems of the systemic circulation was studied in 10 anesthetized dogs during a right ventricular bypass procedure. Phenylephrine (1 microgram X kg-1 of body weight X min-1) produced a significant (P less than 0.001) increase in arterial resistance, no change in venous resistance, and a mild decrease in venous compliance. Seemingly in the clinically normal dog, a dose of phenylephrine sufficient to double total peripheral resistance will redistribute a small amount of blood volume from the venous to arterial systems with a slight decrease in venous return and concomitant attenuation of cardiac output.

Ventilatory changes associated with changes in pulmonary blood flow in dogs.

To examine the influence of pulmonary blood flow (Qp) on spontaneous ventilation (VE), we isolated the systemic and pulmonary circulations and controlled the arterial blood gases and blood flow (Q) in each circuit as we measured VE. Each dog was anesthetized with ketamine and maintained with halothane. Systemic Q was drained from the right atrium and pumped through an oxygenator and heat exchanger and returned to the aorta. An identical bypass was established for the pulmonary circulation, draining blood from the left atrium and pumping it to the pulmonary artery. The heart was fibrillated, all cannulas were brought through the chest wall, and the median sternotomy was closed. The dog was then allowed to breathe spontaneously. The arterial O2 partial pressure (PO2) of both circuits was maintained greater than 300 Torr. Systemic Q was maintained at 0.080 l X min-1 X kg-1. Initially the arterial CO2 partial pressure (PCO2) of both circuits was set at 40 Torr as Qp was varied randomly between approximately 0.025 and 0.175 l X min-1 X kg-1. The average VE-Qp relationship was linear with a slope of 1.45 (P less than 0.0005). Increasing the arterial PCO2 of both circuits to 60 Torr elevated VE an average of 0.37 l X min-1 X kg-1 at each level of Qp (P less than 0.0005). Vagotomy abolished the effect of Qp on VE. Increasing Qp affected the systemic arterial PCO2-VE response curve by shifting it upward without altering its slope. These results demonstrate that increases in Qp are associated with increases in VE. This phenomenon may contribute to exercise hyperpnea.

Evidence for pulmonary CO2 chemosensitivity: effects on ventilation.

To determine whether there is a pulmonary chemoreceptor for CO2 that influences spontaneous ventilation (VE), we separated the systemic and pulmonary circulations and controlled partial pressure of CO2 (PCO2) independently in each circuit under hyperoxic conditions and measured VE. Dogs were anesthetized with ketamine and maintained with 1% halothane. Systemic venous return was drained from the right atrium and passed through an oxygenator and heat exchanger; blood was returned to the ascending aorta. An identical bypass was established for the pulmonary circulation, draining blood from the left atrium and returning it to the pulmonary artery. The heart was fibrillated; all cannulas were brought through the chest wall; and the median sternotomy was closed. Blood flow through both circuits was maintained at 0.080 l . kg-1 . min-1. Systemic PCO2 (PSCO2) was held constant at three different nonoscillatory levels. At each level, pulmonary PCO2 (PpCO2) was randomly varied between approximately 7 and 85 Torr. With PSCO2 at 43.5 +/- 0.4 Torr, VE increased 2.67 +/- 0.61 l . min-1 as PpCO2 was varied between these limits. With PSCO2 at 63.8 +/- 2.5 Torr, VE increased 3.95 +/- 0.73 l . min-1 over these same limits of PpCO2. With PSCO2 below 25--30 Torr, the dogs were apneic and no longer responded to changes in PpCO2. The effect of PpCO2 on VE was abolished by vagotomy. These results suggest the presence of a CO2 chemoreceptor in the lung that interacts with the nonpulmonary chemoreceptors in the control of VE.

Diagnosis of acute cholecystitis using hepatobiliary scan with technetium-99m PIPIDA.

Sixty patients were evaluated for acute abdominal pain using technetium-99m PIPIDA hepatobiliary imaging. The sensitivity of the test was 90.6 percent in all patients and the accuracy was 93.3 percent. In the evaluation of acutely ill patients with right upper quadrant pain, fever, nausea and vomiting, hepatobiliary imaging with PIPIDA is the preferred test for diagnosing acute cholecystitis. If the test is positive, disease of the gallbladder and probably acute cholecystitis are present. Early operation can proceed if desirable. If the test is negative and the bilirubin level is less than 5.0 mg/dl, acute cholecystitis is not present. In such cases conservative treatment is appropriate, and follow-up tests should be performed to evaluate the possibility of chronic cholecystitis. When the bilirubin level exceeds 5.0 mg/dl, the test is often indeterminate.

Maximal nerve excitability testing versus neuromyography: prognostic value in patients with facial paralysis.

Neuromyography (NMG) is compared with maximal nerve excitability testing (NET) as a prognostic tool in facial paralysis. Normal latencies, summation muscle action potentials, and test/retest reliability were determined in three groups of subjects. NMG was performed in 33 control subjects of Group 1 to determine test/retest reliability. To determine the range of normal facial nerve conduction latency and amplitude and configuration of the summation muscle action potentials, NMG was performed in 172 otolaryngologic control patients without facial paralysis. NMG and NET were then compared in Group 3, which consisted of 43 patients with Bell's palsy. Fluctuations in NMG were then analyzed in a fourth test series of three subjects from Group 1, in whom summatin muscle action potentials at various positions of the electrodes were compared. The high rate of fluctuations observed indicates the need for further assessment of test/retest reliability and standardization of normal values in NMG. Our results indicate that maximal NET is more reliable than NMG for prognosis of facial paralysis.

The true nature of Bell's palsy: analysis of 1,000 consecutive patients.

In a series of 1502 patients seen in our Facial Paralysis Research Clinic 1048 were diagnosed as having Bell's palsy. Review of clinical, epidemiologic, and laboratory data, plus review of the literature, has led to the conclusion that Bell's palsy is an acute benign cranial polyneuritis probably caused by reactivation of the herpes-simplex virus, and the dysfunction of the motor cranial nerves (V, VII, X) may represent inflammation and demyelinization rather than ischemic compression. Spinal fluid analysis suggests that the disease is a phenomenon of the central nervous system with secondary peripheral neural manifestations. With our presently available information, treatment of a viral disease with an anti-inflammatory agent is rational. Prednisone treatment started within the first week of the disease can restore better function to the paralyzed face than is achieved without such therapy, and facial nerve decompression has been unnecessary.

A comparison of the effects of morphine and forced running upon the incorporation of 14-C-tyrosine into 14-C-catecholamines in mouse brain, heart and spleen.

Morphine increases both the locomotor activity of mice and the incorporation of 14-C-tyrosine into 14-C-catecholamines in the mouse brain. To determine whether a relationship exists between increases in locomotor activity and increases in catecholamine synthesis, mice were treated with either morphine (100 mg/kg i.p.) or saline and were forced to run on a treadmill (5.4 m/min). When mice were given saline and forced to run, incorporation of 14-C-tyrosine into 14-C-catecholamines was increased over control values in the heart and spleen but unchanged in the brain. When mice were given morphine, but not forced to run, the incorporation of 14-C-tyrosine into 14-C-catecholamines was increased over control values in the brain but unchanged in the heart and spleen. Morphine decreased the catecholamine content of the mouse brain but not of the heart or spleen. Forced running did not change the catecholamine content of any tissue. The differences between the effects of morphine and forced increases in locomotor activity upon the incorporation of 14-C-tyrosine into 14-C-catecholamines and upon the catecholamine content in various tissues of the mouse indicate that the effects of morphine on catecholamine synthesis are not the result of changes in locomotor activity.

Tolerance to morphine-induced increases in [14C]catecholamine synthesis in mouse brain.

Morphine sulfate increased the incorporation of carbon-14-labeled tyrosine into labeled catecholamines in the mouse brain. Tolerance was manifested by a shift to the right in the dose-response curve for morphine after mice were treated repeatedly with morphine. Naloxone, a specific morphine antagonist, also shifted the dose-response curve for morphine to the right.