Unraveling How Cats Control Their Metabolism During Life-Threatening Bleeding
A mysterious physiological response that sets felines apart in the animal kingdom
Imagine a cat struck by a car, bleeding internally. Unlike most mammals, whose hearts would race in a desperate attempt to survive, this cat's heart rate slows dangerously. Its body temperature drops, and its blood pressure plummets. This paradoxical response to hemorrhagic shock has long puzzled veterinarians and physiologists alike. For decades, the feline's unique reaction to blood loss represented a fascinating biological mystery—one that would only be solved by understanding the intricate dance between their nervous system and hormones.
When crisis strikes, most mammals rely on what's known as the "fight-or-flight" response—a dramatic surge of adrenaline that causes racing heartbeats and heightened alertness. Dogs and humans follow this predictable pattern. But cats? They march to the beat of a different drum, one regulated by a sophisticated neurohormonal system that has only recently begun to reveal its secrets 3 .
At the heart of this mystery lies the sympatho-adrenal system—the complex partnership between the sympathetic nerves and adrenal glands that controls how felines respond to life-threatening emergencies. By studying what happens when researchers selectively disrupt this system, scientists have uncovered remarkable insights into feline survival strategies that may one day transform how we treat critically injured cats.
The clinical picture of shock in cats is so distinctive that veterinarians refer to it as "the shock triad": hypotension (low blood pressure), bradycardia (slow heart rate), and hypothermia (low body temperature) 3 8 . This combination would signal imminent death in most species, yet in cats, it represents their unique adaptive response.
The answer lies in their specialized anatomy:
Within the wall of the cat's ventricle, mechanical and chemical volume receptors respond to distension. When bleeding reduces blood volume, activation of these receptors slows the heart rate through a cardiac inhibitory reflex, allowing ventricular contraction only when normal filling pressures are reached 3 .
Cats possess unique type-B atrial volume receptors that respond to atrial distension. During hypovolemia, reduced stimulation of these receptors leads to bradycardia rather than tachycardia 3 .
Hypothermia blunts the typical sympathetic nervous system responses, and increased parasympathetic outflow produces bradycardia and vasodilation through what's known as the Bezold-Jarisch reflex 3 .
These specialized features mean that the classic "fight-or-flight" response seen in dogs and humans is often replaced in cats by a more conserved energy state—possibly an evolutionary adaptation that prioritizes oxygen conservation during crisis.
To appreciate what happens during hemorrhage, we must first understand the two key players in the feline stress response:
The inner portion of the adrenal glands that secretes catecholamines—epinephrine (adrenaline), norepinephrine, and dopamine—into the bloodstream when danger strikes.
Specifically the splanchnic nerves that directly innervate abdominal organs like the liver and pancreas, providing rapid local control of metabolic processes.
Together, these components form the sympatho-adrenal system—the conductor orchestrating the feline body's emergency response. During hemorrhage, this system activates multiple survival mechanisms: releasing stored glucose for immediate energy, constricting blood vessels to maintain pressure to vital organs, and adjusting hormone levels to prioritize functions essential for short-term survival 1 .
But what happens when parts of this system fail or are experimentally disrupted? That's exactly what researchers set out to discover in a series of groundbreaking experiments that would reveal the remarkable redundancy and complexity of the feline survival response.
In 1982, a team of researchers designed an elegant experiment to tease apart the relative contributions of the adrenal medulla and the sympathetic nerves to the metabolic and hormonal adjustments during hemorrhagic shock in cats 1 . Their approach was methodical and revealing.
The study involved three groups of anesthetized cats subjected to two different levels of hemorrhagic hypotension 1 :
These animals served as controls, with their sympatho-adrenal systems completely functional.
These cats had their adrenal glands surgically removed, eliminating the contribution of adrenal catecholamines to the shock response.
These animals underwent both adrenalectomy and cutting of the splanchnic nerves, effectively disrupting both components of the sympatho-adrenal system.
The researchers then carefully monitored multiple metabolic and hormonal parameters in these cats as they experienced controlled hemorrhage, painting a comprehensive picture of how the body responds to crisis when its emergency systems are compromised.
The findings from these experiments revealed a sophisticated system of redundant controls for maintaining metabolic function during hemorrhage. When one pathway was disrupted, others compensated—up to a point.
Perhaps the most striking finding concerned the regulation of blood glucose during hemorrhage. In intact cats, hemorrhage caused very marked elevations of arterial plasma glucose—a crucial survival response that ensures the brain continues to receive energy despite dropping blood pressure 1 .
When researchers examined this hyperglycemic response more closely in related studies, they discovered that neither adrenalectomy alone nor hepatic denervation alone could completely eliminate it. However, when both systems were disrupted simultaneously, the hyperglycemic response was virtually abolished 6 7 .
| Experimental Group | Glucose Response | Proposed Mechanism |
|---|---|---|
| Intact Cats | Marked hyperglycemia (up to 500 mg% by 15 minutes) | Combined effect of adrenal catecholamines and hepatic sympathetic nerves |
| Adrenalectomized Cats | Attenuated but significant hyperglycemia | Hepatic sympathetic nerves assume greater role |
| Hepatic Denervation | Somewhat depressed but significant response | Adrenal catecholamines assume greater role |
| Combined Intervention | Virtually abolished hyperglycemic response | Both major regulatory pathways disrupted |
This elegant demonstration of redundant control shows that the feline body has evolved multiple overlapping systems to ensure the critical glucose release necessary for survival during hemorrhage. As one researcher noted, "The hyperglycemic response to hemorrhage is controlled by a redundant control system wherein either the adrenals or the hepatic sympathetic nerves can produce the response but elimination of both systems eliminates the response" 6 .
The hormonal changes observed during hemorrhage revealed an equally complex story. In intact cats, hemorrhage caused dramatic elevations of catecholamines (epinephrine, norepinephrine, dopamine), glucagon, and cyclic AMP (cAMP), while plasma insulin concentrations fell to only 20% of control values 1 . This hormonal profile favors the rapid mobilization of energy stores—exactly what's needed in an emergency.
| Hormone | Response in Intact Cats | Response After Adrenalectomy | Response After Splanchnicotomy |
|---|---|---|---|
| Catecholamines | Very marked elevation | Attenuated response | Further reduced response |
| Insulin | Fell to 20% of control | Normal inhibition abolished | - |
| Glucagon | Marked elevation | - | Possibly reduced response |
| cAMP | Marked elevation | Attenuated response | - |
The insulin response proved particularly telling. The normal suppression of insulin during hemorrhage—which prevents glucose from being stored instead of used—was completely abolished in adrenalectomized cats 1 . This suggests that adrenal catecholamines play a crucial role in regulating insulin secretion during crisis, ensuring that precious glucose remains available to vital organs.
The metabolic adjustments during hemorrhage extended beyond glucose regulation. Lactate and glycerol concentrations also rose significantly in intact cats, indicating increased anaerobic metabolism and fat breakdown, respectively 1 . These responses were similarly modified when parts of the sympatho-adrenal system were disrupted, revealing the far-reaching influence of this regulatory system on overall metabolism.
| Metabolic Parameter | Response in Intact Cats | Response After Experimental Manipulations |
|---|---|---|
| Glucose | Very marked elevation | Virtually abolished with combined adrenalectomy + hepatic denervation |
| Lactate | Marked elevation | - |
| Glycerol | Marked elevation | Further reduced after splanchnicotomy |
| Hepatic Glycogen | Significant depletion (3.1 g/kg/90 min) | - |
Understanding the complex interplay of metabolic and hormonal adjustments during hemorrhage requires sophisticated experimental tools. Here are some key reagents and methods used in this field of research:
| Tool/Reagent | Function in Research | Example Use |
|---|---|---|
| 6-Hydroxydopamine | Selective chemical sympathectomy | Used to achieve selective hepatic sympathectomy without physical cutting of nerves 6 |
| Adrenalectomy | Surgical removal of adrenal glands | Eliminates contribution of adrenal medulla to hemorrhagic response 1 |
| Splanchnic Nerve Section | Cutting of splanchnic nerves | Disrupts direct sympathetic innervation to abdominal organs 1 |
| Radioimmunoassays | Measurement of hormone concentrations | Used to quantify plasma catecholamines, glucagon, insulin 1 |
| Enzymatic Assays | Measurement of metabolic substrates | Used to determine glucose, lactate, glycerol concentrations 1 |
| Thromboelastography (TEG) | Assessment of coagulation status | Evaluates hyperfibrinolysis in cats with hemorrhage 5 |
The investigation into metabolic and hormonal adjustments during hemorrhage in cats after interference with the sympatho-adrenal system reveals a remarkable story of biological redundancy and specialization. The "redundant control system" that regulates glucose release during hemorrhage 6 ensures that cats have backup systems for survival-critical functions. The differential contributions of the adrenal medulla and sympathetic nerves to various aspects of the shock response 1 demonstrate the sophisticated division of labor within the stress-response system.
These laboratory insights have profound implications for clinical veterinary medicine. Understanding that cats naturally develop bradycardia and hypothermia during shock 3 8 helps veterinarians recognize these signs not as paradoxical responses but as characteristic features of feline shock syndrome. The knowledge that both catecholamines from the adrenals and direct neural control play crucial roles in regulating glucose metabolism suggests that supporting both systems might be important in treating shocked cats.
Perhaps most importantly, this research highlights the fundamental physiological differences between cats and other species—a reminder that medical knowledge cannot always be extrapolated across species boundaries. The unique feline shock response, with its specialized atrial receptors and temperature-dependent reactions 3 , represents an evolutionary adaptation that has both served cats well and made them particularly challenging patients in emergency settings.
As research continues, particularly into areas like the role of adrenal hormones in chronic diseases 4 and coagulation abnormalities during shock 5 , our understanding of the feline stress response will continue to grow—hopefully leading to ever more effective treatments for our feline companions in their moments of greatest need.