Sphlanchnic Circulation and Intestinal Ischemia

Macrocirculation - anatomy review

splanchnic area gets 25% of cardiac output but makes up only 5% of body weight (muscle: 45% body weight Þ 20% CO; brain 2% Þ 20% CO)

celiac artery: suppliess stomach, 1^st part of the duodenum, head of pancreas, liver

superior mesenteric artery: supplies rest of pancreas, gut through the first 2/3 of the transverse colon

inferior mesenteric artery: supplies distal colon and proximal rectum

hemorrhoidal branches of internal iliac: supply rest of rectum

splanchnic circulation is highly anastamosed Þ collateral circulation

(i.e. left and right gastrics and gastroepiploics; intestinal arcades, marginal artery, etc)
this helps to prevent ischemic injury (must occlude a large vessel or several small vessels to induce ischemia)

‘watershed areas’ Þ the splenic flexure of the colon and the sigmoidal-rectal junction are less highly anastamosed

ischemic injury is more common in these areas

right angle of the celiac off of the aorta is thought to prevent embolus entry

Microcirculation

generally divided into three parallel circuits: mucosa, submucosa, muscularis externa

mucosa and submucosa receive 75% of flow (one of the best perfused tissues in the body)

each circuit can be divided into four parts

arterioles: major site of resistance; regulate blood flow
pre-capillary sphincters: regulate capillary perfusion
capillaries: highly fenestrated; allow exchange of nutrients, water, electrolytes
venules: capacitors; contain most of the blood volume

gastric blood flow is normally high; large reserve capacity Þ rare ischemic damage

countercurrent flow: in the small intestinal villi, the arteriole passes up to the tip of the villus and breaks into a capillary network that flows down the villus as a plexus that can exchange with the artery on its way up

countercurrent exchange allows the tip of the villus to be maintained hyperosmotic Þ easy water absorption

makes tip relatively hypoxic (O₂ diffuses to venous side before reaching tip)Þ injury if blood flow compromised

Regulation of GI Blood Flow

general cardiovascular factors: mean arterial pressure; cardiac output

intrinsic vascular factors:

autoregulation: analogous to autoregulation in kidney and brain – does not occur in stomach

escape: a vasoconstrictive agent will constrict for a time, then the system will return to basal blood flow

Þ reactive hyperemia: rebound effect after removing vasoconstrictor Þ increased mucosal blood flow

autonomic nervous system:

sympathetic: constriction via a -adrenergic receptors (dominant)

dilation via b -adrenergic (primarily seen when a receptors are inhibited)

parasympathetic: indirectly increases blood flow by increasing motility and secretions of the gut

Ý motility/secretion Þ Ý tissue metabolism Þ Ý vasoactive metabolites Þ Ý blood flow

changes in metabolic environment: vasoactive metabolites (NO, adenosine, histamine, prostacyclins) – Ý blood flow when nutrients are around

circulating substances:

vasoconstrictors: epinephrine, norepinephrine (exercise, stress); ANGII (congestive heart failure); vasopressin (shock)

vasodilators: gastrin (acid production; Ý blood supply to stomach), CCK, secretin (acid suppression; ß blood supply to stomach) – all three are released at mealtime

intestinal motility/distension:

motility: rhythmic contractions Þ increased flow (probably due to vasoactive metabolites)

distension: reduces blood flow to mucosa

Intestinal Ischemia

hypoxia: reduced blood flow itself rarely causes injury unless it is severe enough to effect oxygen uptake

mechanisms may include Ca influx and acidosis

reperfusion inury:

ischemia Þ xanthene dehydrogenase Þ xanthene oxidase

ATP Þ adenosine Þ hypoxanthene

reperfusion Þ hypoxanthene + O₂ Þ (xanthine oxidase) Þ superoxide radicals + H₂O₂

signs of injury dependant on length of ischemia; tip more susceptible due to countercurrent flow

mild: increased capillary permeability Þ diarrhea

moderate: sloughing of villi tips or entire villi Þ ulceration, bleeding

severe: damage penetrates muscle layer Þ perforation, peritonitis, air in abdomen, etc

small intestinal ischemia: acute ischemia is more dangerous because chronic allows for collateral flow to compensate

acute: arterial thrombus/embolus in MI, CHF

chronic: atherosclerotic disease; venous thrombus in patients in a hypercoagulative state

can develop into bleeding, necrosis, perforation, peritonitis Þ poor prognosis; surgery is necessary!

nonocclusive ischemic may occur with reduced cardiac output or shock

large intestinal ischemia: occurs in watershed areas; presents with diarrhea, bleeding

infrequent infarction; prognosis is generally good, surgical intervention is rarely necessary