The distribution of postganglionic autonomic nerve fibers in the lacrimal gland and gland of the third eyelid of dogs was studied by use of histochemical techniques. Adrenergic nerve distribution was identified by use of the sucrose-potassium phosphate-glyoxylic acid technique. A loose network of adrenergic nerves was found throughout the interstitium around acini and blood vessels and in vessel walls. Acetylcholinesterase staining was used to identify cholinergic nerve fibers. A cholinergic distribution pattern around acini and blood vessels similar to the adrenergic pattern was found, although the cholinergic innervation appeared more dense than the adrenergic. In the gland of the third eyelid, mucus-secreting lobules and lipid-secreting lobules appeared to be equally innervated by parasympathetic fibers. These lobules could not be differentiated when the sucrose-potassium phosphate-glyoxylic acid technique was used. The techniques used in this study could not demonstrate whether direct contact was made by either cholinergic or adrenergic nerve fiber with secretory or myoepithelial cells. The presence of both nerve fiber types around acini suggests an interrelationship between the sympathetic and parasympathetic nervous system in lacrimal gland secretion in dogs.

Exogenously administered vasopressors (sympathomimetics) were evaluated in halothane-anesthetized dogs to determine the effects of these drugs on cardiovascular function before and after hemorrhage. Six dogs were anesthetized with thiamylal sodium (20 mg/kg of body weight) and halothane (1.25 minimal alveolar concentration) in 100% oxygen. After instrumentation, cardiac output, systemic arterial blood pressure (SAP), heart rate (HR), left ventricular pressure, pulmonary arterial pressure, and an index of cardiac contractility (dP/dT) were measured. Stroke volume, cardiac index (CI), stroke index (SI), rate-pressure product, and systemic vascular resistance (SVR) were calculated. Epinephrine (0.1, 0.3, and 0.5 micrograms/kg/min [low, medium, and high doses, respectively]) and dobutamine (1, 5, and 10 micrograms/kg/min [low, medium, and high doses, respectively]) were infused. Methoxamine was given in a bolus of 0.22 mg/kg, IV. All measurements were taken at 2.5 minutes after infusion, and were repeated after removal of 40% of the estimated blood volume. Dobutamine administered at the low dose before hemorrhage increased SAP and dP/dT. At the high and medium dose, dobutamine significantly increased CI, dP/dT, and SAP with no significant change in HR or SVR. The medium dose of epinephrine was the most effective dose of epinephrine at increasing key variables (CI, SI, dP/dT). The response of CI and SI to this dose was not significantly different from the changes seen with high-dose administration of dobutamine. The dP/dT was significantly lower with epinephrine than with dobutamine, and SVR and HR were unchanged with epinephrine, except at the low dose, which decreased SVR. Methoxamine significantly decreased CI, SVR, and HR, whereas SVR and SAP were increased significantly. After hemorrhage, the only variables that had a significant change in the absolute magnitude of the response to a drug, relative to the response before hemorrhage, were a significantly reduced ability of dobutamine and methoxamine to increase SAP, and a significantly decreased ability of methoxamine to decrease CI. We concluded that dobutamine and epinephrine provide beneficial short-term support of the cardiovascular system in the halothane-anesthetized dog during acute hypovolemia.

Exogenously administered vasopressors (sympathomimetics were evaluated in isoflurane-anesthetized dogs to determine the effects of these drugs on cardiovascular function before and after hemorrhage. Six dogs were anesthetized with thiamylal sodium (20 mg/kg of body weight) and isoflurane (1.25 minimal alveolar concentration) in 100% oxygen. After instrumentation, cardiac output, systemic arterial blood pressure, heart rate (HR), left ventricular pressure, pulmonary arterial pressure, and an index of cardiac contractility (dP/dT) were measured. Stroke volume, cardiac index (CI), stroke index (SI), rate-pressure product, and systemic vascular resistance (SVR) were calculated. Epinephrine (0.1, 0.3, and 0.5 micrograms/kg/min [low, medium, and high doses, respectively]) and dobutamine (1, 5, and 10 micrograms/kg/min [low, medium, and high doses, respectively]) were infused. Methoxamine was given in a bolus of 0.22 mg/kg, IV. All measurements were taken at 2.5 minutes after infusion, and were repeated after removal of 40% of the estimated blood volume. Before hemorrhage, administration of high doses of dobutamine and medium and high doses of epinephrine were equally effective at increasing CI and SI. The dP/dT was increase to the greatest degree by administration of high doses of dobutamine. Administration of the low dose of dobutamine increased dP/dT, whereas administration of the low dose of epinephrine increased CI, HR, and SI, and decreased SVR. The HR and SVR were not increased by administration of any dose of dobutamine or of the medium and high doses of epinephrine. However, methoxamine increased SVR and decreased HR. Methoxamine decreased CI, SI, and dP/dT, but increased systemic arterial pressure to the same degree as that attributed to administration of high doses of dobutamine and epinephrine. After hemorrhage, effectiveness of the drugs in eliciting a response was unchanged, except for a decreased ability of dobutamine to increase rate-pressure product. Further, when the results of this study were compared with those of an earlier halothane study, there were no significant differences in the response of a variable to drug infusion on the basis of the anethetic. The drugs were equally effective with halothane or isoflurane anesthesia. Results inidcated that dobutamine and ephinephrine are effective short-term treatments for hypovolemia during volume resuscitation, and that they work equally well with halothane or isoflurane anesthesia.

To investigate the potential role of sympathetic nerves in preventing pronounced increases in cerebral blood flow, we evaluated the effects of abrupt hypertension on the cerebral circulation of newborn pigs with intact cerebral sympathetic innervation and after cerebral sympathetic denervation. Epinephrine infusion was used to induce abrupt increases in mean (+/- SEM) arterial pressure (innervated pigs, 62 +/- 3 mm of Hg to 115 +/- 3 mm of Hg; denervated pigs, 71 +/- 4 mm of Hg to 132 +/- 4 mm of Hg) that remained increased for the 3 minutes of the study. Abrupt hypertension increased blood flow to all brain regions. In denervated pigs, the increased flow to the cerebrum was prolonged, compared with that in pigs with intact sympathetic innervation. Differences between pigs of the innervated and denervated groups were not apparent, with respect to blood flow to any other region (caudate region, brain stem, cerebellum). In newborn pigs, sympathetic nerves may attenuate hypertension-induced increases in blood flow to the cerebrum, but do not appear to affect flow to the rest of the brain.

Gas eructation function of the gastroesophageal sphincter (GES) was investigated in 6 conscious dogs before and after a sleeve was placed around the GES and gastric cardia and during IV infusion of a beta-adrenergic amine (epinephrine). To induce eructation, nitrogen gas was insufflated (351.4 +/- 2 ml/min; mean +/- SEM) into the stomach through 1 channel of a 4-lumen catheter. After baseline studies and epinephrine infusion studies were completed in each dog, surgery was done to limit partially gastric distension by intraluminal contents by placing a silicone rubber sleeve around the GES and the first few centimeters of the cardia. Gastroesophageal sphincter pressure was 31.8 +/- 2.2 mm of Hg in baseline studies, 17.3 +/- 1.3 mm of Hg during epinephrine infusion (P less than 0.003), and 30.3 +/- 2.2 mm of Hg after the sleeve was placed around the GES and cardia. During insufflation, gastric pressures before eructation increased to 5.74 +/- 0.41 mm of Hg before and to 15.15 +/- 1.63 mm of Hg after carida sleeve placement (P less than 0.001). Eructation occurred at intervals of 1.83 +/- 0.41 minutes before cardia sleeve placement, and eructations were not observed with the sleeve in place. Before the sleeve was placed, administration of epinephrine resulted in an eructation interval of 0.84 +/- 0.09 minutes, which was significantly different from that in the same dogs given no drugs (P less than 0.004). In vitro comparison of stomachs filled with fluid or filled with fluid and gas revealed that relatively small amounts of gas added to a partially filled stomach caused marked distension of the gastric cardia in comparison with no effects when fluid only was added. Seemingly, distension of the gastric cardia was the important stimulus for eructation. Limiting this distension prevented eructation and beta-adrenergic stimulation increased eructation frequency.

The arrhythmogenic dose of epinephrine (ADE) was determined in heartworm-infected and noninfected (control) dogs during thiamylal-induced and halothane-maintained anesthesia to assess the myocardial sensitization. The ADE in heartworm-infected dogs (2.42 +/- 0.26 micrograms/kg of body weight) was significantly lower than that for the controls (3.36 +/- 0.29 micrograms/kg). After 2 weeks, ADE was determined again in these dogs after atropine treatment. Atropine treatment lowered the ADE to 1.76 +/- 0.33 micrograms/kg and 1.77 +/- 0.19 micrograma/kg in heartworm-positive and negative dogs, respectively. After 2 weeks more the ADE was determined after administration of prazosin, an alpha 1-antagonist. Only 2 of 6 controls and 3 of 6 heartworm-positive dogs had arrhythmias after a threefold increase of ADE. The mean ADE in the dogs that responded to treatment were 7.4 micrograms/kg and 7.2 micrograms/kg for heart worm-positive and negative dogs, respectively. The findings of this study indicated that ADE in heartworm-infected dogs were lower than those in the control dogs, which makes the heartworm-infected dogs more vulnerable to arrhythmia during anesthesia. Atropine did not protect the dogs of either group. However, prazosin protected the dogs of both groups by significantly increasing the threshold of the ADE. On the basis of our findings, to reduce the risk of arrhythmia, we suggest that routine screening of dogs for heartworm infection be done before anesthetics are used.