Cutaneous T-cell lymphoma in a cat.

An 8-year-old castrated male cat was examined because of a chronic, nonhealing, ulcerative lesion on the left hind limb. Cutaneous lymphoma was diagnosed on the basis of the morphologic appearance of malignant cells and Pautrier's microabscesses on light and electron microscopic examination. The tumor was found to be of T-cell origin by use of a polyclonal antibody recognizing T-cell antigen. Results of serum ELISA for FeLV were negative. The gp70 antigen of FeLV was not detected immunohistochemically in tumor tissue sections, using polyclonal goat antisera and avidin/biotin/peroxidase complex technique. Presence of FeLV was demonstrated by the polymerase chain reaction procedure, involving amplification of a 166-base pair region of FeLV DNA. Although FeLV is reported to be the cause of most types of lymphoma in cats, cats with epitheliotropic cutaneous lymphoma have consistently negative test results for circulating FeLV antigen. In such cases, using the polymerase chain reaction method, tumor DNA may be assessed for integrated FeLV provirus and the presence of FeLV can be confirmed.

Pressoreceptor modulation of renal but not splenic sympathetic reflexes.

Influences of sinoaortic and vagally innervated vascular pressoreceptors on excitatory splenic and renal sympathetic responses to splenic receptor stimulation were investigated in anesthetized cats. These experiments demonstrated that these pressoreceptors have little apparent effect on the magnitude of splenic nerve responses to splenic receptor stimulation by capsaicin, bradykinin, or congestion. In contrast, activation of these pressoreceptors attenuated renal nerve responses to splenic receptor stimulation. Influences of sinoaortic and vagally innervated receptors on tonic sympathetic nerve activity also were evaluated. Stimulation of these receptors by small increases in arterial pressure (15-21 mmHg) caused equivalent inhibition of splenic and renal nerve activity; large increases (50-66 mmHg) caused significantly greater inhibition of renal than splenic nerve activity. These results illustrate that excitatory renal and splenic sympathetic responses to splenic receptor stimulation are not suppressed equally by pressoreceptor activation, vascular pressoreceptors can have greater inhibitory influences on tonic renal than splenic nerve activity, and vascular pressoreceptor influences on sympathetic reflexes are similar to those on tonic nerve activity.

Splenic and renal sympathetic responses to stimulation of splenic receptors in cats.

The effect of selective stimulation of splenic receptors on reflex responses of splenic and renal efferent nerves was studied in anesthetized, vagotomized, sinoaortic denervated cats. The following substances were injected into the artery or vein of vascularly isolated spleens: warm physiological saline (congestion), capsaicin (CAPS), bradykinin (BK), and norepinephrine (NE). Splenic congestion increased efferent activity of splenic and renal nerves, splenic venous pressure, systemic arterial pressure, and heart rate. CAPS and BK elicited responses similar to those produced by congestion but caused greater excitation of splenic than renal nerves. Reflex responses were eliminated by section of splenic nerves. Injection of NE increased splenic venous pressure but did not elicit reflex responses. Finally, in contrast to a previous report light- and electron-microscopic examination of splenic nerves revealed myelinated, as well as unmyelinated, fibers. These results have demonstrated that activation of splenic receptors elicits reflex cardiovascular responses and excitation of splenic and renal efferent nerves, contraction of the spleen does not produce reflex responses, the adequate stimulus for reflex responses is stretch of vessels and possibly capsule, and splenic receptors play a role in the reflex control of circulation.

Differential sympathetic responses initiated by angiotensin and sodium chloride.

Angiotensin II (ANG II) and NaCl act on central receptors to cause pressor responses that may be mediated in part by the sympathetic nervous system. The inhibitory or excitatory nature of effects on central sympathetic outflow are not well defined. This study was undertaken to evaluate further the potential contribution of the sympathetic nervous system to central actions of angiotensin or hypertonic NaCl. Experiments were performed using anesthetized, sinoaortic denervated, vagotomized cats. Intracarotid injection of NaCl produced increased splenic sympathetic nerve activity and decreased renal sympathetic nerve activity. Intracerebroventricular (icv) administration of NaCl caused slight excitatory responses in splenic nerves and no change in renal nerve activity. Intracarotid injection of ANG II caused significantly greater splenic than renal excitation. Administration of ANG II icv caused excitation of splenic nerve activity and no change in renal nerve activity. These findings illustrate that stimulation of sodium-sensitive and angiotensin-sensitive CNS receptors produces differential responses in sympathetic outflow. These differential sympathetic responses may contribute to the complex cardiovascular responses to increased plasma or brain concentrations of angiotensin or sodium.