BIOL 460L 1st Edition Lecture 26 Outline of Last Lecture I. Blood Flow II. Regulation of Blood Flow in ANSIII. Paracrine Regulation of Blood FlowIV. Autoregulation Outline of Current Lecture I. Blood Pressure a. Hypertension II. Respiratory Systema. Respiration b. Lung c. Diaphragm d. Boyle’s LawCurrent LectureBlood Pressure1. Squeezea. Upstream pressure increasesb. Downstream pressure decreases2. “Squeeze” caused by resistance vessels (arterioles)3. Arterial BP ≈ Cardiac Output * PR4. Long term BP regulated by kidneys (regulate blood volume) and sympathoadrenal system5. Short term BP regulated by baroreceptor reflexa. Orthostatic hypotensionb. Stand quickly and get dizzyc. Slow baroreceptor reflex makes it worsed. Baroreceptors – aortic arch, carotid sinus (where carotid branches)e. Baroreceptors are constantly generating APsf. Higher pressure – more APsg. Send sensory information to medulla – vasomotor center (vasoconstriction/dilation) andcardiac center (heart rate, contractility)h. Beta blockers prevent this reflex – syncope (pass out)6. Sphygmomanometer – blood pressure cufa. Measured in mmHgb. Listening for Sounds of KortkofThese notes represent a detailed interpretation of the professor’s lecture. GradeBuddy is best used as a supplement to your own notes, not as a substitute.c. Listen at Brachial Arteryd. Increase in pressure above systolic pressure (about 140mmHg)e. Squeeze brachial artery shut – no soundf. Pressure decreases until it’s just below systolic pressure, every systole produces a surge of blood (first sound of kortkof)g. Sound disappears – diastolic pressure7. Hypertensiona. High blood pressureb. 1/5 of Americansc. Secondary  high BP as a result of a known cause (ex: atherosclerosis of renal artery)d. Primary (essential)  Idiopathic (poorly understood cause)e. 120/80 or less – no hypertensionf. Treating hypertensioni. Reduce stroke volume – thiazide diureticii. Beta 1 blocker – slows heart rate and contractility decreasesiii. Lose weight, which drops blood vessel lengthiv. Vasodilators – block alpha 1 receptors, ACE inhibitor (no angiotensin II, less aldosterol)Respiratory System1. Respirationa. External – exchange of respiratory gases between air and blood breathing movements, exchanged via simple difusionb. Internal – exchange between blood and tissuesc. Cellular – metabolic pathways that use oxygen and release CO22. Lunga. Alveoli (0.25-0.5mm)b. Type 1 alveolar cells (more common)i. Simple squamous, very thinii. Air/blood barrier, respiratory membraneiii. Gases must cross barrier for exchangeiv. Endothelium of capillary, basement membrane of capillary, basement membrane of alveolus, and type 1 alveolar cellsv. 2 microns in thicknessc. Type 2 alveolar cells (less common)i. Secrete surfactant (surface acting agent)ii. Surfactant composed of phospholipids and hydrophobic proteinsiii. Must have thin film of water on inner surface of alveolus (O2 must dissolve before difusing across air/blood barrier)iv. Surfactant prevents sides of alveolus from sticking because of waterv. Respiratory distress syndrome1. Hyliane membrane disease2. Type 2 alveolar cells not secreting surfactin3. Great risk in immature infantsd. Respiratory Zonei. Region of lung where exchange occursii. Alveoli plus respiratory bronchioles (smallest)e. Conducting zonei. Nasal cavity and mouthii. Pharynxiii. Larynx – opening called glottisiv. Tracheav. R and L primary bronchivi. Secondary and third bronchivii. Bronchioles form bronchiole treeviii. Terminal bronchioles lead to respiratory bronchiolesix. Warm, moisten, and filter are going into lungs3. Diaphragma. Divides coelom into thoracic and abdominopelvic cavitiesb. Layer of musclec. Media stinum (heart, thymus, etc) separates thoracic cavity into R and L pleural cavitiesd. Airspace in lungs – intrapulmononic spacee. Surface of lungs – serous membrane, secretes serous fluid to reduce frictionf. Serous membrane in lungs – visceral pleurag. Serious membrane in walls of pleural cavities – parietal pleurah. Intrapleural space – potential space because visceral and parietal pleura always in contact and connected via hydrogen bonds4. Boyles Lawa. P=1/Vb. Average atmospheric pressure 760 mmHgc. Inhalationi. Contract inspiratory muscles (diaphragm)ii. Increases volumeiii. Decreases pressure (757 mmHg)iv. Air moves from high to low pressured. Exhalationi. Expiratory muscles (rather unimportant in normal breathing)ii. Mostly elastic recoiliii. Volume down, pressure increases to 763 mmHgiv. Table 16.1 – intrapleural pressure always lower than intrapulmonic pressure, meaning lungs can never completely collapsev. Collapse1. Only in pneumothorax2. Air in intrapleural space3. Gunshot wound, stab wound,